Neuroradiology 0

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NEURORADIOLOGY
CONGENITAL LESIONS
A- Craniosynostosis:- (Premature fusion of Skull Sutures)
1- Fusion of coronal & lambdoid Sutures oxycephaly = tower like which may be associated
with: -8 th C.N lesion
-optic nerve compression
-mental deficiency, syndactly
( usually shows prominat convolutional markings)
2-Premature fusion of sagittal suture

narrow elongated skull= scaphocephaly =boat shaped

skull

NB: In microcephaly : small head d.t. premature closure of all the sutures+ primary mental defect
3-unilateral premature closure of coronal&lambdoid suture

assymetrical skull =

plagiocephaly = slanting skull

4-Premature Closure of metopic suture

triangular head

NB:. Prevent premature closure of sutures before 9 month

prevent mental defect

regain normal shape

(By excision of sutures & kept seperated by interposition of Tantalum)

B- Lacunar Skull : - In infants , disappear by 4-6 months, ch.ch. . by groups of round, oval or
finger shaped pits of the inner surface of vault (membranous part) seperated by ridges of bone
They lie in thickest part of frontal, parietal & upper occipital bone commonly associated with CNS
anomalis

myelomeningiocele, hydrocephalus

** NOTES:

Apeurts syndrome = Syndactyly + oxycephally.

Acrocephally = Summit skull (brachycephally) (same as tower skull).

Crourzons disease =( hereditary craniofacial dysostosis )is a form of acrocephally

+ facial bone hypoplasia, hypertelorism, exophthalmos, parrot-beak nose,
prognathism, MR & corepulmonale .
Carpenters synd rome = acrocephalopolysyndactyly

C- Cranial meningeocoele & encephalocoele:-Common in occipital and frontal region,usually diagnosed clinically , but difficult
in small lateral & basal meningeocele. Suspected if there is scalp swelling with underling bone
defects.
Encephalocele

Naso frontal region

Basal

-X- ray skull

-lateral view

hypertelorism

nasal obstruction

defect in sphenoid & spheno-ethmoid regions

soft tissue mass in the nasopharynx

-C.T.: may show 3rd ventricle extend down through pitutary fossa into the sphenoid

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empty sella

D- platybasia :A condition in which the base of skull appears relatively flattened . It include basilar
impression & basilar invagination.

*Basilar invagination:
-causes :- diseases producing bone softening( acquired)
{Pagets disease , Rickets , osteomalacia , ost. imperfecta & hyper parathyroidism}

*Basilar Impression:
Indicates an elevation of floor of the posterior fossa. commonly associated with
congenital anomalies of cervical spine . The foramen magnum may be abnormal in
shape and size.
***Lines & measurments of platybasia :1-Basal angle: A line drawn from nasion to tuberculum sellae in lateral view and a
second line drawn from tuberculum to ant. margin of the foramen magnum . This
measures between 125-142 . If > 142 , it indicate platyplasia.
2-Chamberlains line: from back of hard palate to posterior lip of the foramen
magnum in lateral view . Cd so if > odontiod peg lies above this line .
( see figure beside)

E- Hypertelorism:A condition in which the orbits seem widely separated.

F-Hamartomas:

Definition: mal arrangement of normal tissue

Pathology : Cong. Benign tumor

found in the affected part. It include

overgrowth of mature cells and tissues normally

glial lession , dermoid , epidermoid &nasal glioma.

Types: (1)Hamartoma of tuber cinereum (ganglioglioma) a specfic condition

associated with precocious puperty
(C.T. & MRI

Rounded suprasellar mass of brain denisty and occuping

inter- peduncular cistern

(2) In temporal lobes

presented with epilipsy & contain

calcifications

G-Hydrocephalus:- (see later)

PHAKOMATOSIS
(neuroectodermal dysplasia)
-Group of disease of different etiologies but having in common lesions of the skin , Retina and
nervous system and the fact that they are developmental
NB : developmental, neuroectodermal dysplasia

i.e. skin, retina &CNS

Tuberous sclerosis(+bone,resp.,kid.&heart)

Neuro fibromatosis(+skull,spine & bone)

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Sturge Weber

Von Hippel Landow

Ataxia Telangectasia

A) Tuberous sclerosis: Autosomal dominant, cl/p

epilepsy , MR , adenoma sebaceum

(may be---- skin, nervous, bone, respiratory, kidney & heart)

1 Nervous : Multiple area of heterotopia in the Brain ( area of abnormal glial tissue)
They contain calcification

widely scattered
small rounded discrete
may be paraventericular nodule near the foramen

of Monro( become large enough to produce obstructive hydrocephalus acquiductal by

developing into low grade of asterocytoma)

* CT c.c.c.(small nodular protrusions into ventricle e calcified foci +cerebellar atrophy)

* MRI Area of hetero topia , on T1 signal ,on T2 irregular areas of signal
subcorticaly , in the white matter , praventricular

2 Bone : skull

woolly & area of density (pelvis-spine)

spine

vertebral bodies sclerosis

pelvis

Flame shaped densities on iliac blades

NB : periostitis may be found in long bones ( metatarsals - metacarpals )

In hand cyst occur in phalanges( this is related to subungual fibromas)

3 Chest : common in female, Diffuse leiomyomatosis in (alveolar wall-small airways &

vessels- bronchial obstruction and distal destruction of alveolor wall)
*X ray

diffuse reticulation or miliary pattern progressing into honey combing

(pnemothorax is a common complication)

4 Kidney : show renal cysts as well as angiomyolipoma ( lesiones are multiple & bilateral)

B) Neuro fibromatosis : (Von Reckling Hausens)

*definition : Commen familial disoreder involve the skull ,spine ,CNS
*clinical picture : cafe au-lait spots , multiple cutaneous tumors , manifestation of Neurofibroma
.

1) Skull

Extensive calcfication of the choroid plexsus of the 3rd & lat ventricles
Abscense of greater wing of spheniod (bare orbit)

unilateral

exophthalmous
2) C.N.S

Glial tumor (parenchymal & optic nerve gliomas)

focal cerebral atrophy(MR)
Bil. acoustic neuroma with schwannoma of other cranial nerves
Cerebral artery aneurysm

3) Spine
4) Kidney

as neurofibroma (dumbell shaped), ant. thoraxic meningiocele

Renal artery stenosis or aneurysm
pheochromocytoma may be associated

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scoliosis (of short segment distribution thoracic)

5)Skeletal

Pseudo artherosis of long bone (sp.Tibia)

Abnormal rib tubulation, rib notching ( ribbon shaped)
Fibrous tumor of bone around knee (similar to non ossifying fibroma)

C)Sturge Weber Syndrome :

Trigeminal angiomatosis. I.C. calcification
D) Von Hippels Lindaus disease :
( Retrocerebellar Angiomatosis)
-multiple haemangiobastoma in the retina, cerebellum and the spinal cord.
- visceral tumor & cyst particularly renal & pancreatic
Question: Raised Intracranial Pressure ? ? ?
Causes :
(1)

A large intra-cranial mass(i.e. tumor ,

haematoma or abscess)
NB : cong.,traumatic,inflam.,neoplastic,vascular,others eg. benign

(2) Obstructive hydrocephalus , craniostenosis

(3)Cereberal oedma

around tumor or abcess

encephalitis

- cerebral edema
.

cerebral infarction, hypertenstion,A-V malformation

& large aneurysms

(4) Craniosynostosis
(5) Benigin Intra-cranial hypertension
Radiological Evidence of I.C.P :
No radiololgical evidence of I.C.P. seen before 6 weeks of the condition
* Effect of I.C.P :
(1) effect on sutures (chidren)

sutural diastasis + bulged fontanels + vascularity

(2) effect on sella (adult)

(3) expansion of skull(child)
(4) thining of bones of vault & base(child)+craniolacunae if associated with
meningeocoele
(5) widening of natural foramina.
(6) Pineal displacement.
(7) convolutional markimgs (silver beaten app.) which is of very little diognostic
.significance since it is commonly seen in nornal childien (4 -10 years)
A) Effect on sutures : (Sutural diastasis)
- In the 1st few weeks of life & up to 9 years( uncommon after 10 years) , an acute
rise in I.C.P sutures spreading with in a few days ( suture edge remain smooth )

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Infants & children= suture diastasis ,coronal & saggital are the most affected
- As condition become chronic

the lnterdigitations of sutures become exaggerated +

abnormalities of the sella + central part of the anterior fossa(cribriform plate) may be
displaced down in the lateral films
NB : increased vascularity (generalized or localized) = dilated emissary veins above int . occipital
protuberance also occurs in older children with chronic ICT

- After age of 10 years , suture diastasis is uncommon

B) Effect on sella turcica :
*Sellar Erosions : It is classified into
1- category I : erosions of lamina dura, parti cularly near the base of dorsum sellae.
2- category II : destruction of top of dorsum sellae with a tendancy to forword
displacement of the remaining portion of the dorsum ( usu ally accomapnied by
erosions of the lamina dura)
3- category III : combination of I & II in which erosions affect lamina dura and
extends to plannus sphenoidale
NB : Erosions of dorsum sellae is the cardinal sign of

ICT in adults as no suture diastasis now

Erosion commences as slight porosis of the anterior cortex of the dorsum & of the sellar
floor cortex (best seen in lateral films). It progresses to loss of definition of the cortex
also towards the Lamina dura- & eventually to frank erosion
* Sellar enlargement :
may accompany later stage of erosion, its type differes from that due to pitutary
tumors balloning & flattening (see figure beside )
C) Bones of vault :
* Infancy & childhood
- when I.C.P. occurs in ante nal peroid, the bone of skull vault become :
I- thinner than normal
.

II- may show defect in ossification = lacnura skull (craniolacunae )

- with long standing raised I.C.P

convolutional marking over the upper parts of

frontal & parietal bones. NO convolutional impressions over the lower 2 / 3 are of
diagnotic value ,as they represent bone growth in response to underlying brain.
NB : convolutional markings are of diagnostic value only if in the upper 1/ 2
*Adult
- When the cause of

I.C.P. is present since childhood enlarged skull and thinning

of calvaria .
- long standing hydrocephalus

Rounding contour of skull easily observed in anterior

fossa by depression of its midline anterior structures (cribriform plate)

(central part of the ant. Fossa may be displaced downwards in lateral films)

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D) Bones of skull base:

- occurs in long standing I.C.P. in late childhood & adult causing :
1- Thinning of bones in lesser wings of sphenoid , ant. Clenoid processes, greater
wings and floor of middle fossa .
2- Alteration of form of base depression of cribriform plate , ethmoid plates
and plannum sphenoidale.
E) Effecst on Forminae and venous channels:
- With chronic I.C.P. , the channels and foramina through which venous drainage
of brain passes tend to enlarge :
a- enlargement affects emissary foramina , foramen ovale
b- in extreme cases the optic canal becomes funnelled
c- diploic channels may be seen to increase in size
F) Pineal displacement:
Displacement of calcified pineal body > 3 mm from midline (in adult as not calcified in children)
NB :standard PA =TOWENS view of the skull
* Localizing evidence of cerebral tumors:
1- Intra cranial calcification
2- Skull erosion
3- Hyperostosis
4- Abnormal vascular markings

Intra cranial calcifications

A. Normal Intracranial calcifications:(1) Pineal calcifications :
- Age :In elderly patients
- Site: O.F. & towen s in the centre (>3mm from midline pathological)
(normal is within 3 mm of the mid line)
-lateral view

above petrous block & slightly behind it

- size: Variable , usually 3-5 mm

- shape: amorphous deposits which may be nodular or ring like
(2) Calcified Habenulla : (commisure)
- site: directly anterior to pineal body , directly related to back of 3rd ventricle
-shape: c- shape in lateral view
(3) Calcified choroid plexsus :
- site: (usually bilateral & symmetrical )
The choroid plexsus of lat. ventricles is frequently calcified
- lateral view

typically one inch above & behind pineal body

(parietal area)

- O.F. & Towms : Above & lateral to pineal

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- shape: faint punctate dots or dense circular areas

(4) Calcified dura:
- Age: middle age
- site: any where in skull vault (usually at falx, seen end-on in O.F.)
(5) Calcified ligaments:
- Petro-clenoid: best seen in Towens view , between apex of petrous bone and the
posterior clenoid process
- Interclenoid ligament: between anterior and posterior clenoids
(6)Calcified basal ganglia:
- usually pathological & may be idiopathic
- bilateral & symmetrical , at the head of caudate nucleus
(7) Pituitary calcification :
-commenly seen in pitutary adenoma
(8) Calcified lens :
(9) Pacchionian bodies: (arachnoid villi)
NB :intracranial calcifications may be

congenital, traumatic, inflammatory,

neoplastic, vascular & metabolic

B.Pathological Intracranial calcification:

I. Tumors: (slowly growing)
(1) Glioma :-high incidence of calcification occur as the tumor is slower in growth and
less malignant (calcifications occur in slowely growing tumors )
- calcification occurs in

5-10 % of gliomas
50% - 90% of oligodend roglioma
20% of posterior fossa glioma
rarel in medulloblastoma & malig. Astrocytoma

- Forms

serpiginous (in oligodendroglioma)

punctate dots
dense nodules
irregular linear streaks

(2) Cranio pharyngioma :- Incidence: in 75% of cases

- Age: mostly children , occasionally adults
- Forms: - vary from few punctate dots to a densy calcified mass
-when cystic

curvilinear calcification

- site: mid line just above the sella (c.c.c.)

(helping point ; the sella is bent forward as if pressed from above )
(3) Meningioma :- Incidence: 10% of cases show calcification

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- shape: ball like & amorphous

- site: parasaggital (or other typical meningioma site ; related to skull base)
- helping signs

hy perostosis ( involve vault or sphenoid ridge)

increased meningeal vascular markings leading up to the

site of attatchement & widened foramen spinosum

(4) Dermoid :- site: in post. fossa or near base of skull
-shape: ring like (similar to that of wall of an anuerysm)
(5) Teratomas :-site: pineal body & suprasellar region (children )
- helping sign: dental elements
(6) Epindymoma :-unusual calcification
- site: * children

post. fossa

* adults

supratentorial

(7) Pineal Tumors :(>3 mm away from midline)

(8) Choroid plexus papilloma :-Incidence of calcification 1:4 in children (1 with calc. & 4 without )
-site: lateral & 4th ventricle
- calcification differentiate its from medlulloblastoma
(9) Lipoma :-site: in relation to corpus callosum
-shape: bracket sign i.e. marginal calcification
(10) Chordomas :-site :near the clivus
- shape :irregular calcification
-associated R.A-

erosion at base of skull

soft tissue mass in pharynx

.
II. Vascular Lesions :
(1) Aneurysms :-Incidence: less than 1%

- site: in region of circle of willis

-shape: Ring , arc like , oval ,lobulated

(2) Angiomas :- Common
- Types:

few irregular calcified flecks

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few calcified ring shadows due to aneurysmal dilatation , usually on

the venous side of malformation
(3) Subdural haematoma :(after long peroid , calcification outline the subural membrane )
(4) Intra- cranial haematoma :- calcification in small I.C. Hge.
(5) Atheroma :- atheromateous carotid artery in the cavernous sinus

small flecks

superimposed on the sella

- near the carotid bifurcation in the neck
III . Infections :
(1) T.B. :- tuberculoma : 1% of cases
- healed T.B. mengitis: Intra cranial calcifications in the healed exudate at the
base of skull
(2)Toxoplasmosis :- multiple fleck like shadows in cortex
- linear streaks in basal ganglia
(3)cyto-megalic virus :-periventricula (out line dilated ventricle )
(4)Pyogenic abscess
(5) Hydatid Disease
IIII . Metabopalic & miscellaneous :
(1) Idiopathic basal ganglia calcifications (age related)
(2) Hypo parathyroidism , pseudo hypo parathyriodism
(3) Tuberous sclerosis
(4) Neurofibromatosis

Phakomatosis

(5) Sturge Weber syndrome (Trigeminal angiomatosis)

NOTES :
-bilateral & symmetrical calcifications
choroid plexsus

basal gang lia

Lipoma

-failure of appearance of sup. cortical vien in calcified cortex

* Erosions of the skull :1- Extracranial tumors
- Rodent ulcer , epitheliomas , nasopharyngeal carcinoma , glomus jugulare
-Bone tumous

secondary tumors (more common) , dermoid , haemangioma ,

chordoma , multiple myeloma , neuroblastoma , leukaemia , histocytosis

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2- Intracranial tumors
- pituitary adenoma, craniopharyngioma , optic glioma , meningiomas ,rarely gliomas
- osteomyelitis , TB , fibrous dysplasias
(i.e. infections, metabolic, neoplastic & dysplasia)
* Hyperostasis :1-Generalized
- marble bone disease
- Englmans disease
-craniometaphyseal dysplasia
- acromegally
- pagets disease
- thalassemia
2-Localized
-meningiomas
-osteomas
-ossifying fibroma
-fibrous dysplasia
-leontiasis ossia
-hyperostosis frontalis interna ( unknown cause postmenopausal + )
-sclerosing metastases
-chronic osteomyelitis
*Sturge -Weber- Dimitri Syndrome :=encephalo -trigeminal angiomatosis
=vascular malformation with capillary venous angiomas due to persistence of usually
transitory plexus stage of vessel development (developmental neuro-ectodermal
dysplasia of unknown etiology involving skin-CNS-eye)
-Clinical picture :
Seizures(90%)
Facial port-wine stain along sensory branch of trigemial
Mental deficiency (50%)
Crossed hemiparesis

hemiatrophy ( within 2 years)

-Radiological findings :
(1) Plain films
A.Tram line calcification(i.e. along vessels )
-site ; in occipital bone(cortex) in the surface of atrophic branches of trigeminal
B. thickened meninges
C. ipsilateral thinning of the skull & orbit (reaction to brain atrophy)

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D. enlarged ipsilateral sinuses

-shape ; parallel lines representing the sulci seen end on
(2) Angiography
-leptomeningeal venous angioma
-capillary blush(excessive vascularity of meninges ) microanuerysms
-abnormal deep medullary vein drain into internal cerebral vein
-failure to opacify sup. cortical vien in calcified region
(3) CT&MRI

asymmetry of lobes

* Q :discuss radiological & imaging diagnosis of a case of recent head injury

Q

( as if you are reading CT )

Effects :( can be seen in plain film )
1. Early

haemmoraghe(all kinds) + calcifications (late)

brain edema
foreign body
fracture

2.Late
- Infectian : abscess
- Infarctian : atroply , porencephally
- Cephalhaematoma
- Leptomeningeal cyst
- Hydro cephalus
- Cortico cavernous fistula & sersiod anuerym
-

Calcification
N.B. for any hemorrhage mention :
(shape

attenuation ,edema, mass effect, enhancement, origin & site)

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Head Injuries.
* Diagnostic methods:(1) plain x-ray : lateral, lateral with horizontal ray, O. F., base, towens
(2) C.T.
(3) Angiography
(4) U/s : through anterior fontanellae in infants
(5) MRI
* Radiological manifestations (plain film) :A. Displacement of calcified pineal body
-may occur with the presence of intra cranial haematoma

confirmed by CT

B.Fractures
1- Linear fractures of vault:- may carry possibility of an extradural haematoma
Appearance:
- It shows as black line & have sharp edges .
- line crosses vascular markings
- If it diverted into a suture

localised diastasis of suture & the fracture may

pass out of suture into another bone

(linear lucent line ; in some cases where fracture lines overlap in relation to
x-ray beam , they may appear as lines of increased density )
Differential diagnosis:
(1) Vascular channels
- wider

-less translucent

- tend to taper as they branch

(2) Internal suture line
- may appears as a straight line along course of suture
- linear & not serrated as external suture
(superimposed on a serrated suture, while a fracture will be deviated far at its some parts )

Healing : usually complete

2- Depressed fractures of vault :*Enface

It is seen as an irregular ring comminuted with radiating levels

*Tangential

if area is large
if area is small

loss of contour of vault

white line representing inner & outer

tables of the fragment w appear discontinuous e rest of vault

N.B. -defect in the parasagittal region is difficult to see
-depressed fractures may need tangential views to show their exact relationship , but
are better seen by CT

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3-Fractures of base of skull :Views

Lat. with horizontal rays , O.F. , base & towens

* Importance of lateral view with horizontal rays :

- to reveal any air which may enter head as a result of dural tear, this air seen as:
1- small bubble in subarachnoid space over frontal lobe
2- extensive shadows over the cerebrum
3- an aerocele which invades brain & may perforate into ventricular system
ventriculogram
-to reveal presence of a fistula between sphenoid or ethmoid sinuses & subarachnoid
space by seeing a fluid level shown in one of these sinuses + clinical manifestations
of C.S.F. rhinorrhoea
-fracture of sphenoid bone may extend into petrous or mastoid temporal bone with
dural tear

otorrhoea & such localization of fistula is attempted by C.T.

4- Fractures of facial bones:5- Foreign bodies:-more than view may be necessary to confirm the diagnosis other wise C.T. is
recommended
NOTES :
-pneumocephalus & aeroceles result from fractures involving frontal or ethmoid sinuses
-obtained by views with head brow up & horizontal x-ray beam to demonestrate possible air
fluid levels
-this view is also uesful to detect air fluid level in sphenoid sinus which indicates fracture in
the skull base
* Late effects of head injury :(1) Calcification in subdural & extradural haematomas :Sub-dural It appears as an incomplete shell conforming to the general shape of the
collection.
Extra-dural

not extensive , occurs as a result of a small collection of blood & it

appears as a complete shell continous with inner table

(2) External cephal haematoma:- a haematoma which occur at birth between pericranium and outer table
- ossification occurs at edge of the aerea where pericranium is lifted from the
underlying bone
- a complete shell of bone may develop over surface of haematoma in about 4 weeks
-this lesion tend to disappear with growth
(3) Cephalhydrocele (acute leptomeningeal cyst): = post traumatic cysts involving meninges
-usually occurs in childhood when a fracture of vault is accompanied by extensive

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dural tearing escape of C.S.F. from subarachnoid space a very large swelling
of tissues of scalp which become distended by C.S.F (atrophy of overlying bone
margins may occur & large bone defect may follow )
-after a few weeks the fracture line begins to widen by thining & erosion of bone
& large bone defect may be seen
-clinically there is a superficial cystic mass
-radiologically there is elongated area of lusency with or without a fracture
extending into it
* C.T. in cranial trauma :Indications
1-deterioration in patients condition
2-suggestion of an expanding intracranial haematoma
Complications of trauma
A) Acute : (1) Intracranial haemorrahge or haematoma extracerebral,
extra-dural, subdural, subarachnoid, intracerebral
(2) cerebral edema & contusion
(3) fractures
(4) F.B.
NB ; CSF otorrhoea or rhinorrhoea both need

CT cisternography
Radio nuclide scanning

=fracture in petrous
or mastoid bone
B) Late :-

=fracture in the
skull base
(+ post traumatic sequaele )

(1) Effects on cerebrum

infection : empyema, meningites

atrophy , infarction , porencephaly
hydrocephalus

(2) Effects on cranium

growing fracture = leptomeningeal cyst

depressed
secondary effect of atrophy or expansion

(3) Miscellaneous

ch. extra cranial haematoma

cirsoid aneurysm
cortico cavernous fistula

* Extra dural :a)attenuation & edemas

-

clearly defined biconvex , high attenuation lesion

deep to skull vault

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(i.e. casting blood density)

- no surrounding edema
b) mass effect (+ ve)

compression of contralateral umderlying hemisphere

c) enhancement

no

d) others
-origin : usually arterial bleeding from meningeal vessels (serious)
-site: most commonly in tempro parietal region & tend to be localised
-associated skull fractures
* Subdural :- ( Its appearance depend upon the stage)
a) Acute subdural hge.(first 48 hrs)
1.

attenuation & edema , high attenuation blood spreads over

surface of brain takes
form of concave - convex form ( < 2 weeks )
2 . mass effect

swelling of ipsilateral cerebral hemisphere

effacemet of ipsilateral sulci
shift of mid line
compression of ipsilateral ventricles

3 . enhancement

no

4 . others
-origin : more commonly of venous origin but may be arterial
arising from a tear of vein bridging subdural space
-small lesion : less than 1cm may not be detected , so detection may be
increased by tilting head to affected side
b) Subacute hge (2 - 4 weeks)
1. attenuation & edema isodense , if there is evidence of a capsule a line of
high attenuation is seen along its medial border
2 . mass effect

displacement of choroid plexsus , pineal body or other midline structures

ventricular assymetry
effacement of sulci & or sylvian fissure on affected side

3 . enhancement

no , but if capsule is present it may enhance

4 . others
* Bilateral isodense hge ( difficult diagnosis, the clue may be ) :
-ventricular assymety ; as the lesions are not of same size in both sides
-lack of normal wider sulci in older patients
-the frontal horns lie more closer together > normal
(termed
c) Chronic subdural hge ( > 4 weeks )
1. Attenuation & edema

rabbits ear appearance )

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-appears as concavo-convex cresent of low attenuation overlying cerebral hemisphere

-may be capsule of high attenuation

-unusual calcification
2. mass effect

the underlying brain appears atrophic in most of chronic cases

(It may be normal )

3. enhancement

no & if enhancement occur possibility of infection is

considered (i.e. empyema )

N.B. contrast causes brain enhancement & lesion is seen against enhanced brain

4. others

if there is chronic haematoma with recent hge into them ; dense

attenuation posteriorly as the patient is lying supine with low attenuation anterior to it
* Subarachnoid :1. attenuation & edema

high attenuation , diffuse than that occuring with

spontaneous subarachnoid hge from an aneurysm of circle of willis

2. mass effect

no

3. enhancement

no

4 . Others

Site: in basal cisterns & sites of aneurysms, intracerebral &

intraventricular along side of falx

+Associated

traumatic lesion
areas of infarction due to arterial spasm
hydrocephalus due to blood in subarachnoid space

* Intra cerebral :a) traumatic in origin

b) spontaneous occuring with

hypertension & atheroma

anuerysm
angioma
anticoagulants
tumors

1. attenuation & edema multifocal hyperdense lesions & may be surrounded by areas of low
attenuation ( dueto blood clots & damage of blood brain barrier) 50-90 H.F. (+ associated low
denisty areas of perifocal -little- edema with brain swelling )

2. mass effect
3. enhancement

little
no, but may occur after weeks around a clot due to damage
to B.B.B & new vascularity develops

4. others
- classical sites

hypotensive (60% basal ganglia & 40% pons)

temporal & frontal lobes

- examination of post. fossa. for possibility of pontine hge

Neuroradiology 16

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- resolulion of haematoma denisty take place from the periphery

* Intraventricular :-usually accompanies other traumatic haematomas & appear as high attenuation
inside the ventricles
NB : Value of CT is to detect

where is blood extending

cause e.g. anuerysm
complications

* Cerebral contusion :A- Haemorraghic contusion

-site

mostly in temporal and frontal lobes

-attenuation
mass lesion of mixed attenuation (high & low) predominantly hypodense
usually multifocal (he occuring 24 hrs or later )
at first hours after injury , attenuation usually hypodense with mass effect
but later , there may be multiple he with high attenuation
B- Simple (non hgic) contusion
-attenuation

hypodense ( shows enhancement after c.m. injection & this is

important to differentiate it from cerebral edema )

-mass effect

occurs

* Cerebral edema :types :a)focal

similar to simple contusion d.d. by

-contusion enhanced after i.v. contrast due to impaired B.B.B.

-contusion involving cortex more than white matter
b)generalised

difficult diagnosis & known by

-exaggeration of low attenuation of white matter

-mass effect

very small lateral ventricle (slit like)

-effacement of the sulci

* Fractures :-The value of C.T. is for demonstrating
1-Basal fractures

in cases of rhinorrhoea , otorrhoea

collections of C.S.F. e.g. in ethmoid sinuses

2-Orbital fractures may be associated with retrobulbar or subperiosteal

haematoma (i.e. high density lesions within the orbit or applied to the bone )
3-Depressed fractures

to assess the underlying brain.

* Foreign bodies :-Value of C.T. is

accurate localisation

Neuroradiology 17

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intra ocular f.b. (accurate localisation by C.T. than plain film)

* Cerebral infarction :- (traumatic)
-Cause

vascular occlusion or spasm caused by trauma

-Appearance

similar to those dt. thr-embolic lesions but usually involve frontal lb.

-Attenuation

region of low density (10-30 H.U.) at first ill defined , but by the
second week , it becomes well demarcated

-Mass effect
-Edema

in about 25% of cases

occurs in white matter & swelling of affected area

-Enhancement

in about 50% of infarcts during 1st week

in about 90% of infarcts during 2nd & 3rd weeks
it is caused by extravasation of c.m. due to breakdown of B.B.B.

-Shape

in about 50% co edged, may be rounded

* Post traumatic atrophy :Types

focol (common)
Generalised (diffuse)

Cause

trauma at birth or early childhood

under developed hemisphere

C.T. criteria
-enlargement of fissures & sulci
-dilated ventricles
-associated porencephalic cyst
* Porencephalic cyst :-it is due to degeneration of damaged portion of the brain
-it usually communicates with ventricular system
-of low attenuation value (=C.S.F.)
-MRI appear as signal void rounded area at the site of anatomical vessel & after i.v.
gadolenium the lumen of vessel doesnt enhance since rapid flow of blood prevent the
effect of contrast (this is very important & characterestic )
* Hydrocephalus :-incidence

one of most common complications of severe head injuries and can be

treated surgically

-CT appearance
1. earliest sign is dilatation of temporal horns
-differential diagnosis

2. ventricular dilatation

brain atrophy

* Leptomenigeal cyst :- or growing fracture

-pathology

as before (fracture

dural tear

CSF leak

-C.T. appearance
1.underlying brain damage
2.expansion of subjacent portion of ventricular system

swelling)

Neuroradiology 18

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3.subarachnoid space is widened & communicates via fracture w an extra-cranial

collection
4.bone is thinned from

within the skull

without i.e. underlying the collection

* Angiography in cranial haematoma :* Extradural haematoma :-It can be demonestrated by

1)displacement of normal intracranial vessels away from skull vault
2)displacement of saggital sinus downwards
* Subdural haematoma :-angiography should be restricted to difficult cases
* Intracerebral haematoma :1)for diagnosis of basal ganglia or capsular hge
-lateral displacement of middle cerebral artery (A.P.view)
-displacement of lenticulostriate artery medially or laterally
-displacement of anterior cerebral artery & internal cerebral vein to the
opposite side
2)for diagnosis of thalamic haematoma
-upward & medial bowing of thalamostriate veins
* Ultrasound :-before closure of anterior fontanelle in which haematoma may be detected by shift of
mid-line structures.

Neuroradiology 19

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NOTES :-Localisation of the vessel ruptured in subarachnoid haemorrahge is by site e.g.

hge in medial frontal lobes ,septum pellucidum or corupus callosum is from the
anterior cerebral artery
hge at sylvian fissure is from middle cerebral artery
hge at external capsule is from internal corotid or middle cerebral
MRI in subarachnoid hge :- It is seen within sulci and systerns best by FLAIR tech (Fluid attenuated Inversion Recovery)
-It is less sensitive than CT & it depend on giving relatively high signal than C.S.F
-If the clot has liquified and been dispersed throughout C.S.F it is difficult to detect it.
MRI of intracerebral hge (stages) :Time

Hyperacute
Acute

Hemoglobin type

Magnetism

MR appearance

T1w

T2w

< 24 hrs

Oxyhemoglobin

Diamagnetic

T1w = T2w

black

Black

1-3 days

Deoxyhemoglobin

Paramagnetic 4

Low T1w, low T2w

Intermediate black

Very black

unpaired electrons,

Surrounding edema

(+ surr edema black)

(+ surr edema white)

however it cause

has high T2w

Black + blacker acute

no shortening

Early
subacute

4 -7 days

Late
subacute

2wks to
8 months

Methemoglobin

Paramagnetic 5

high T1w, high T2w

White + black acute

(intracellular)

unpaired electrons

Central lowT2w d.t.

center

center

central deoxyhg

(+ surr edema black)

(+ surr edema white)

high T1w, high T2w

White + black acute

White + blacker acute

Methemoglobin

Paramagnetic 5

(extracellular so only

unpaired electrons

causing changes in

center

center

(+ surr edema black)

(+ surr edema white)

T2W images)

Chronic, rim

+ 14 days

Hemosiderin

Diamagnetic

(> 8 mth)

Macrophages e

Outside black

Outside black

hemosiderin =

(+ surr edema black)

(+ surr edema white)

Low T2w + low T1w

Chronic,
Central

+ 14 days

Hemichromes

Diamagnetic

high T1w, high T2w

Acute black central +

Acute blacker central +

surrounding white

surrounding white subacute

(>8 mth)

subacute

- Subacute blood is always white on T1 whether early or late

- Blood in MRI never ever to be black in T1 and white T2 as CSF, whatever is its type.
- Gd has 7 unpaired electrons, so is the largest paramagnetic substance, MR Gd-Edta > 1w will
give rim enhancement.
- T1 (short TR, short TE ), T2 (long TR, long TE ) and PD - (long TR, short TE ) or better FLAIR w shows
CSF egression, periventricular demylignation: M.S., or any white pathological vessels.

MRI of cerebral contusion :1) T1 region of poor grey / white matter discrimination
2) T2 ill defined areas of hyperintensty
3) cisterna around brain stem is obliterated

Neuroradiology 20

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MRI of subdural haematoma :-MRI is superior in demonestration of extracerebral collection although initially it may
be isointense with adjacent brain
1.the lateral margin is well seen unobscured by bone
2.the displaced cortex is clearly evident
3.the adjacent mass effect is well shown than CT
4.the collection becomes progressively more hyperintense on T1

VASCULAR LESIONS

Intra cranial hge

aneurysms

arterio-venous

arterio-venous

malformations

fistula

embolus-stenosis
& thrombosis

1-Non Traumatic Intra-Cerebral Hemorrhage:

Spontaneous I.C.H. occurs with stroke syndrome: hypertension, rupture aneurysm or A.V.M, and
anticoagulant therapy.
N.B.: All thalamic Hge > 3 cm in diameter are fatal and 70% of pontine Hge are fatal.

CT appearance:
1. Density:
Recent hge: rounded high density lesions with smooth margins. Enlarging size in successive scans
denote active bleeding.
Old haematoma: gradual diminution in density isodense and can be detected only by mass effect.
Weeks later: a denser pre-contrast ring may locate the margin of a organizing haematoma.
2. I.V Contrast: enhancement: in acute recent Hge no need for C.M.
Ring enhancement may be seen around resolving haematoma, DD from tumors or abscess.
3. Mass effect: is attributed directly to size & location of lesion.
4. Location: 20% of hypertensive haematomas occur in the supratentorial compartment putamen,
thalamus, head of caudate N. and external capsule. In posterior fossa, the pons and cerebellar
hemispheres are other usual sites of hge.
Ventricular and subarachnoid extension:
Capsular or thalamic hematomas may dissect medially and rupture into ventricular system or into
the Sylvian fissure subarachnoid spaces

2-Aneurysms:
-Sites of aneurysms:(around circle of Willis: 75%)
1. Posterior communicating artery (27% )
2. Junction of anterior communicating with anterior cerebral (27% )

Neuroradiology 21

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3. Bifurcation of main middle cerebral (20% )

4. Terminal , supra clinoid segment of the internal carotid (large) ( 6% )
5. Basilar Ar tip (large), posterior cerebral artery , vertebral
- Clinically + complications:
a)

Subarchnoid hge:
- Plain: ring calcification (late)
- CT is the 1st choise for large aneurysms (> 1cm) shown as high density rounded lesions at base
of brain, enhance immediatly & strongly after contrast (may be thrombosed: isodence center) +
marginal calcifications & d.d.: Suprasellar mass (meningioma, carniopharyngioma, pitutary
tumor) or large basilar aneurysms (clivus chordoma or meningioma).
-MRI shows area of signal void (residual lumen) along course of named arteries close to the circle
of Willis, if large clear extra axial mass + surrounded by areas of variable signal clot. Mri
helps in dd aneurysm from tumors and meningioma.
-Angiography:

1-

To find aneurysms smaller than 5mm in diameter (only detected by angiography) may
require
Injection of both internal carotid & may need vertebral with AP, lateral & oblique transorbital
(also Towens for vertebral

2 -Following recent bleeding, vessels in the region of the rupture of aneurysm is in spastic &
narrow state ischamic effect (spasm localasition).
2-

Localise aneurysms neck, they are always multiple and 5-15%, largest one almost bleeds &
this
if severe intracranial haematoma displacement of vessels, mass effect & stretch of vessels
B. Pressure upon cranial nerves leading to orbit:
-Commonest nerve is 3rd , but 4th 5th & 6th may be involved
-This is usually caused by aneurysm intracavernous sinus or affecting the PCA
- Occasi.ly suprasellar aneurysm may involve optic chiasma or optic nerve
C. Large mass: either supratentorial (rare) or infratentorial
-They simulate an intracranial tumor
1.basilar rare & simulate tumor & vertebral angioma
2.large aneurysm of internal carotid bulgs forward in the orbit, erode sphenoidal fissure &
cause proptosis ( d.d. 2ry deposits meningioma )
3.area of vein of galen in infants & children seizures, hydrocephalus & it
shows calcifications at the wall

3-Angiomatous malformations: (cause: congenital AVF but present in adults of 20-40 yrs)
-Definition

blood is passing directly from arteries to viens with no

Neuroradiology 22

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intervening capillary circulation, seen at parietal/ temporal lobes.

-Rare types

cavernous angioma
venous angioma
capillary taelangectasia
spinal angioma

-Pathology

communication between the artery & vein lies over the surface of

brain but , if large they extent down in the brain substance in a manner of inverted cone
in shunt area It is symptomless but in motor cortex or occiptal cortex
Jaksonian epilepsy or cortical field defect + headache which is migranous in nature &
also may rupture subarachnoid haemorrahge
-Radiological findings
A.

Angiography:must do both carotids (external) to find feeding vessel which may be a

meningeal artery esp. supratentorial angiomas which are commoner )
1.Ccc drainage vein fill in the normal arterial phase
2. Compensatory hypertrophy of the afferent vessel supplying it
3. Increase in size of vien draining it.
4. Blood diverted away from normal cerebral vessel resulting in ischaemia.
5. If rupture

heamatoma

displacement of vessels
mass effect
stretched vessels

B. CT:
1.Serpigenous, serpentine high density shadow (thrombosed enlarged vessel)
2.Calcification

ring like - curvilinear - serpigenous

3.Multiple vessels in large lesion

it area of low denisty

mottled appearance with adjacent or around

ischemia.

4.After I.V contrast tortous vessels are obvious

5. AVM with intraparenchymal hge or subarachnoid hge or intraventricular hge.
C. MRI:
1.variable but it may have punctate appearance specially on T2 at signal void
2.large artery & draining vein are characteristic feature and usually shown as
signal void (+ brain atrophy, local mass effect & intra cerebral haematoma )
Differential Diagnosis:
1.
Infarction.
2.
Vascular tumors.
3. Partially calcified masses e.g. oligodendroglioma and granuloma.
4. Glioblastoma multiform may have prominent draining vein similar to those seen with A.V.M.

4-

Arterio-venous fistula : (Traumatic or rupture of a diseased artery into a vein)

- Occur commonly on dura and drain extradural via superficial viens w may be visible in the

Neuroradiology 23

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dura , orbit or scalp. Dural AVF are malformation between meningeal branches of ECA & ICA
and dural veins near cavernous sinus (= dural shunts resulting in increase IOP & proptosis).
- Intra cranial (rare):
1- Drain by superior opthalmic vein, superior pertrosal sinus & basal vein
2- Seen in cavernous sinus (cortico-cavernous fistula )

5- Infarction: (Thrombotic or embolic)

CT Appearance:
Cardinal sign of infarction is an area of diminished density involving both white and gray matter e a
vascular distribution.
1. First few hours: the infarct area is isodense with brain tissue so that the C.T appears normal.
2. From 12-24 hours:
CT: Mild hypodensity with mottled appearance and focal obliteration of the sulci.
CT+c: No enhancement.
Haemorrhagic infarction appear as:
CT: An area of marked increased density and is surrounded by an area of mixed or low density
with corresponds to rest of infarction.
N.B.: Enhancement of a very recent infarction after a double dose on a delayed scan may suggest that
such an infarct is prone to bleeding and they there is relative contraindication to an anticoagulant.

3. From 2nd to 5th day:

CT: same but decrease in density
CT+c: No enhancement.
4. From end of 1st week through 3rd or 4th week:
CT: area of infarct appears to be less prominent than in the pervious stage foggy effect.
CT+c: about 70% enhancement.
5. After the first month:
CT: The density of infarct to be similar to C.S.F attenuation (encephalomalacia).
CT+c: No enhancement.
N.B.: The possibility of re-infarction should be considered when enhancement occurs several months
after stroke.
NB: Water shed infarcts seen at margins of major vascular territory e.g. post. frontal and pareito-occipital zones
(subcortical & cortical).

Mass effect: small superficial early infarcts may be identified by sulcal obliteration, larger infarcts
may show some degree of mass effect for even a month.
Location: ACA- MCA- PCA
MRI :
- Infarcts commonly seen more extensive than on CT. T1 & T2 are prolonged in infarcted &
severely ischemic tissue.
- MRI + Gd enhancement towards the end of the 1st week.
- Occluded artery signal void.
- MRI may be less sensitive than CT at detecting areas of hemorrhage within the first few days.
Scheme for Brain Tumors:
1-Def origin
2-Incidence
3-Age
4-Pathology and sites

Neuroradiology 24

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5-Clinical picture (increased ICT, Hormonal effects)
6-Radiological appearance:
-PXR: Calcification, displacement of pineal body, increased ICT, abnormal vascular
markings, erosions or hyperostosis.
-CT:
Attenuation before contrast, enhancement after + Odema, necrosis, hge + Calcification
Mass effect (mid line shift ventricular compresion - hydrocephalus)
-MRI: Low on T1, high signal on T2, enhance after Gd-EDTA
-Angio: vessel diplacement, pathological vessels.
7-Complications: increased ICT, hydrocephalus, hge, lateralization

Brain Tumors
A. Supratentorial tumors :1. Gliomas

astrocytomas

low grade I- II (bengin)

high grade II-IV (glioblastoma multiformis)

(30% )

oligo-dendroglioma
ganglioglioma

calcification
3rd ventricle ( bengin)

optic
2. Secondary deposits

metastasis

(20% )
3. Sellar tumors

lymphoma , leukaemia
see later

4. Supra sellar tumors

see later

5. Neuroblostoma
6. Tumors in & adjacent to 3rd ventricle

colloid cysts
germinos = pineloma
teratomas
pineoblastomas
pineocytomas

7. Tumors of developmental origin

dermoid
teratoma
lipoma

8. Tumors from ependymal cells

colloid cyst
choroid plexsus papilloma
ependymoma

9. Meningioma
B. Infratentorial Tumors :1. Intracrainal

brain stem
cerebellum

glioma
secondaries
primary

astrocytoma
medulloblastoma
hemangioma, ependymoma

2. Extracranial

meningioma (CPA tumors)

chordoma

Neuroradiology 25

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neuromas (CPA tumors)

glomus tumor (CPA tumors)
cholesteatoma (CPA tumors)
secondaries

General Notes :0-5 years

Brain stem glioma, optic nerve glioma

5-15years

Medulloblastoma, astrocytoma, pineoloma, craniophrayngioma,

choroid plexus papilloma

15-30years

Ependymoma

30-65years

glioma, meningioma, acoustic neuroma, pituitary tumors

> 65 years

meningioma, acoustic tumor, glioblastoma

*Gliomas: (commonest brain tumor, 40-50, more in males)

*Cerebral astrocytomas :Low grade I - II
-incidence

15-20% of all gliomas

40-50 years, may be in children (

-PXR

calcification 5% , signs of increased ICT, signs of tumor

Abn. vas. markings Skull erosions Hyperostosis Pineal displacement Calcifications

-MRI

low T1, high T2, DTPA

-angiography
-CT

enhance (general)

vascular displacement, rare

pathological vessels

attenuation, calcifications, enhancement, mass effect & edema

-pathology

solid tumor grow by infilteration

variable cysts may be found

-site

frontal, parietal & temporal lobes

thalami & hypothalamus are more frequently involved in children

-CT picture
1.attenuation poorly marginated, non homogenous, low attenuation area
merging with the surrounding cerebral parenchyma (cystic glioma is well
defined area of low attenuation )
2.edema little or no (edema affects white matter rather than grey & often
extends with finger-like processes subcortically & into corpus callosum,
external & internal capsules)
3.contrast enhancement no (so it is not possible to differentiate between it and

Neuroradiology 26

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the surrounding oedmatous white matter ) & reccurance is known by biobsy

N.B. follow up CT after surgery & radiation of glioma is complicated by radiation
necrosis & give rise to mass of mixed attenuation which may show marked enhancement ( =
disrupted BBB) & radionecrosis may occur after months or even years after radiotherapy

4.calcifications

uncommon.

5.haemmorahge & necrosis

uncommon

6.mass effect if large

compression of ventricular system

displacement of mid line structures
contralateral hydrocephalus

- Differential diagnosis

acute cerebral infarction

1.similarity

hypodense with littel or no contrast enhancement

2.difference

less mass effect (in infarction )

more prominent invasion of grey matter
sharpely delineated from adjacent normal brain

Glioblastoma multiforme( grade III IV)

-incidence

represent 1/3 - 1/2 of all gliomas

50 60 years

-pathology

involves cerebral white matter

grow rapidly

invasion of cropus callosum and contral-

lateral hemisphere

butterfly glioma

central necrosis of tumor with a rim of viable tumor

small cysts may be found in solid tumors
-CT
1.attenuationpoorly marginated or lobulated , non homogenous hypodense
area invading the cerebral white matter & multiple, patchy areas of normal or
slightly hyperedense nodules may be seen intermixed within or around the hypodense area

2.edema

virtually all glioblastomas are associated with perifocal

edema in white matter

3.contrast enhancement

enhancement of peripheral viable rim

ring enhancement

( this who it differs from benign )

enhancement of central portion (necrosis) after

20 - 60 minutes from injection i.e. delayed filling

4.mass effect

when large

5.calcifciations

no

6.haemorrahge & necrosis

-differential diagnosis

carcinomatous metastasis
pyogenic cerebral abscess

*Oligodendrogliomas :-incidence

5%

30-40%

Neuroradiology 27

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-pathology

solid tumors invading mainly cerebral cortex of frontal

lobes & deep structures may be involved

-calcification in 90% (frequently tumor may contain foci of astrocytoma called

mixed glioma )

-CT :

1.attenuation

poorly marginated hypodense mass invading both cortex &

white matter
isodense or slightly hyperdense nodules may be seen at
margin of tumor

2.edema

no

3.enhancement

no (peripheral nodules may show enhancement)

4.calcifications

charachterestic (see intra cranial calcifications)

5.mass effect

if large (it is slowely growing & less malignant )

6.haemorrahge

no

7.cystic degeneration

in large tumor

*Gangliogliomas :-incidence
-pathology

uncommon (20-30 years ) benign (hamartoma)

origin is neural & glial tissue

floor of 3rd ventricle

site mostly at region of the anterior of 3rd ventricle

temporal lobe

-CT
1.attenuation
2.edema

. small isodense or slightly hyperdense mass

no

3.enhancement
4.calcifications
5.mass effect

homogenous in non cystic type

foci of calcification
as above

6.haemorrahge

as above

NB : charachterestics are sites & being benign

*Optic gliomas :-incidence
-pathology

1% (childhood )
from optic nerve or chiasma
low grade astrocytoma infilterating along the fibre tracts & nerves
typically involve intracranial & orbital portion of optic nerve
usually associated with neurofibromatosis

-CT
1.enlargement of the optic canal
2.enlargement of intraorbital & inrtracranial portions of optic nerve(enlargement

Neuroradiology 28

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is usually diffuse & uniform, occasionally enlargement may be irregular and fusiform )

3.wide optic nerve or chiasma has the following features

attenuation

isodense & large tumor invading hypothalamus may

contain irregular hypodense masses

enhancement
edema

variable
no

calcification

tiny calcifications may be seen

haemorrahge & necrosis

mass effect

no
obstr. of 3rd ventricle

large suprasellar tumor

-differential diagnosis
1.optic nerve sheath meningioma (old age, fusiform, calcified, tram-track )
2.optic nerve neuritis
(NB: charchterestics are child, tubular, diffuse enhancement)
*Secondary deposits :* Metastatic brain deposits :(The brain is common site of haematogenous metastasis from

bronchial

carcinoma, breast, renal, GIT & melanoma )

-Site at junction of cortex with underlying white matter (the penetrating arteries
branch & narrow at this level, so easy to be obstructed by the circulating tumor cells)
Leptomeningeal carcinomatosis (meningeal metastasis)
-mechanism either

direct haematogenous metastis into meninges

parenchymal neoplasm

breeching of the ependymal

lining of ventricles
parenchymal neoplasm

breeching of the surface of

cortex with seedling of tumor cells into CSF, so

implants on meningeal surface.
-CT appearance
A) Small

(rounded, homogenous nodules of variable density )

1.attenuation
2.edema

majority are isodense or slightly hyperdense

extensive edema of white matter

3.contrast enhancement
4.mass effect

mass effect

universal, intense(v.imp.)
++

Neuroradiology 29

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B) Large

the same as small & differs in

-central necrosis

hypodense (lucent) central zone with

peripheral isodense or slightly hyperdense rim of irregular thickness

- Differential diagnosis from glioblastoma

-cut line
-contrast enhancement

Large metastasis

Glioblastoma

regular-spherical

irregular

homogenous

non homogenous

melanoma secondries are hyperdense

NB

Calcifications are rare & against diagnosis except

bone sarcoma
colon cancer

-special sites of metastasis

1.calvarial

irregularly marginated osseous destruction (bone window)

2.epidural

bond like soft tissue thickening simulate appearance of epidural or

subdural haematoma
the association of overlying destruction of calvaria is diagnostic

3.leptomeningeal
-thick, sheet like, homogenous contrast enhancement obliterating major intracranial subarachnoid cisterns is diagnostic (simulate picture of gross subarachnoid
haemorrahge in non contrast films)
-nodular, homogenous enhancing masses may be seen in quadrigeminal and pineal
region
4.ependymal and subependymal
-tumor spreads in the wall of ventricles sheet like or nodular plaque
like intense contrast enhancement
- differential diagnosis from ependymits, complicating rupture of cerebral
abscess
Lymphoma & leukaemia :-old name is microglioma (1ry is more common than 2ry)
-in both leptomeningeal infiltrations of meninges by tumor cells occur firstly and then
spread along the space of Virschow to penetrate the brain
-They are similar to metastasis but

less or no edema
central necrosis is not a feature

tend to lie more deeply in basal ganglia or paraventricular regions

-CT
-MRI

appearance & enhancement are similar to that of metastasis

typical lymphoma give same signal as grey matter on T1&hyperintense on T2

Neuroradiology 30

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Meningioma:
- It is commonest benign intracranial tumors but can turn malignant usually vascular angioblastic
type (others are fibroblastic & calcified types) - recurrence after surgery is not uncommon
- Multiple in 5% in association with neurofibromatosis
Types of meningiomas:

a)Sellar
b)Supra-sellar ( infratentorial )
c)Cerebello-pontine angle
d)Intra-orbital w can be either:
-Primary: - extra-dural meningioma (within orbital cavity away from optic nerve)
- optic nerve sheeth meningioma foraminal, intra-canalicular, intra orbital.
-Secondary: orbital extension of meningioma arising at greater wing of sphenoid or
supra-sellar or floor of anterior cranial fossa
e)Spinal meningioma: extradural extramedullary - intradural extramedullary
Sites: - Most common: para-sagital, convexity, falcine

- Strategic sites: intraorbital, supra-sellar, diaph sella, CPA & cerebellar convexity
- Others: sphenoid ridge, pterion, tentorium, olfactory groove, spinal, intraventricular
DD of meningoma: optic nerve glioma neurofibroma - acoustic neuroma
meningioma differ from acoustic neuroma in that meningioma is larger than neuroma with broad base on the petrous, by
CT It is hyperdense homogenous intense enhancement + normal internal auditory meatus, hyperostosis +calcifications &
cystic changes. By angiography shows dense homogenous blush.

Radiological appearance:

Plain X-ray:
Occipito-frontal view: signs of ICP, intra-cranial calcification (ball like 20%
amorphus) - intra-cranial erosion - hyperostosis affecting apex of
orbit & ant. clenoid process (in primary orbital meningioma)
pineal displacement & hydrocephalus
Lateral view

enlarged meningio-vascular markings

enlarged diploic vascular markings
sclerosis of pituitary fossa but it may cause its expansion & erosion

Neuroradiology 31

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hair-on end skull vault only when it breaks through outer table(ch.ch.)
orbital calcifications (1ry orbital meningioma)
Base

long nerve sheeth.

wide foramen spinosum (hypertrophy of middle meningeal artery)(ch.ch.)

density of skull base (ch.ch.)

Optic

enlargement of optic foramen in foraminal sheeth meningioma (ch.ch.)

CT appearance:
-On unenhanced scan meningioma usually appear as homogenous intense high density mass
with rounded well defined margins
-Calcifications are found in 16-20% of cases (either irregular or uniform calcifications)
-Marked & uniform enhancement post C.M., heterogenous if large: central dots of necrosis
-Absent or minimal edema with or withiut cystic changes & mass effect in 10%
Angiography:
-Carotid angiography (selective external carotid DSA) it is of little role except when tumor
is adjacent to saggittal or other major sinuses w are well shown by intravenous DSA
-Ccc angiographic features are: ( presurgical embolization may be done)
hypertrophy of meningeal artery supplying tumor
hypertrophy of branches of external carotid supplying tumor
localization of the tumor in its characteristic sites
invasion of the arterial wall evidenced by cuffing or narrowing
the presence of typical meningoma blush + the above features
(blush peripherally supplied by anterior & middle cerebral arteries = internal carotid artery)

in orbital meningioma displacement of the opthalmic vessels in most of cases, but a

minority of cases show a pathological circulation on carotid angiography
MRI:
-Superior in diagnosis (inversion recovery better > than spin-echo)
-It detects dural sinus invasion better than CT, T1 hypointense or isointense & T2
hyperintense (isointense in 90% on T1 & T2)
-Gd-DTPA: diffuse homogenous enhancement, even if big (good in demonstration of
meningioma en plaque) + enhancement along above + below - of dural i.e. dural tail
w represents a dural reaction. Black areas may be seen w are central calcifications, or
peripheral signal void vessels, or white T2 breakdown necrotic areas.
Germinomas (pinealomas):

2072

-Pineal tumors = pinealomas = any tumor in pineal region part of PNET (primar neuroectodermal
tumors w also include dysgerminomas & medulloblastoma)
1.Pineal cell tumors: pineoloblastoma - pineocytoma
2.Glial tumors: astrocytoma glioblastoma
3.Germ cell tm: germinoma (pineloma)- teratoma - embryonal cell tumor - choriocarcinoma
4.Epidermoid dermoid metastases (v.rare)
- Age: 2nd & 3rd decades

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- Highly malignant similar to testicular seminomas, most common is near 3rd third ventricle, in
pineal region is ectopic pineloma arising from floor of 3rd ventricle indenting back end of 3rd
ventricle obstructing aqueduct (suprasellar type) (this is how small tumors are detected )
- CT: spherical, hyperdense, sharply defined mass (solid-cystic-mixed) e homogenous intense
enhancement, no edema + may displace calcified pineal body & obstruct aqueduct leading to
hydrocephalus. Calcification are unusual.

Intracranial cystic lesions:

Colloid cyst:
- Etiology: derived from paraphysis (post lip of F. of Monroe) w is a tumor in a gland normally
found in human fetus at one stage of development (other theory is that it is neuroeptitheleal cyst
w lies on roof of 3rd ventricle directly behind foramen of Monro & contains gelatenous (colloid)
material ( usually around 1-2cm size )
CT : 1.site
spherical sharply marginated masses located at ant. portion (roof) of third
ventricle (dd: tuberous sclerosis w is in midline)
2.attenuation: commonly hyperdense due to its mucoid (high protein) contents &
fibrous capsule, occasionally isodense.
3.edema + calcifications + no post-CM enhancement: absent
4.mass effect: it causes the following: obstruction of foramen of Monro e dilatation of
lateral ventricles or widening of adjacent septum pellucidium
inferiorly e slight separation of postero-inferior portionsof frontal horns
- Only white cyst containing protinacious material, centered in midline at foramina of Monroe
(anterior part of 3rd ventricle) so may cause hydrocephalic changes.
- By MRI, high signal in T1 & T2 + no enhancement with Gd-ETDA.
Dermoid tumor: (inclusion tumors)
-Pathology: 1- Cystic lesions close to mildline in following sites para sellar regions, posterior
cranial fossa and inferior frontal.
2-May rupture into subarachnoid space or adjacent ventricle; severe granuloma,
meningitis, ependymitis & hypdrocephalus
- CT 1- Smoothly marginated rounded mass of mixed density (+teeth)
2- Attenuation: wall is isodense, except if curvilinear calcification, hyperdense contents
hypodense due to fat contents (-10 to -300 HU) + no enhancement & edema
3- Mass effect : hydrocephalus with fat fluid level (lighter fat float over CSF) (fluid
occurs if ruptures into a ventricle )
Porencephalic cyst: cyst communicating e dilated ventricle, either congenital or aquired post
trauma, infarction (chronic infarction is totally liquified leading to a ve mass effect) or resolution
of infection. Black in T1 & white in T2.
Arachnoid cyst: usually in relation to greater wing of sphenoid along the temporal bone. Grey in
PD, black on T1 won't enhance & white in T2. DD e epidermoid via location.
Epidermoid cyst: (inclusion tumors)
- Sites: CPA creeping along tentorium to suprasellar and quadrigeminal cysterns - parasellar region.
- CT: large hypodense area e no enhancement or edema, +ve mass effect, calcification is possible

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- By MRI: grey in PD, black on T1 & white in T2

Hydatid cyst: multiple lesions, almost never calcifies, associatted e other lesions in the body
Cystic astrocytoma: rare to be mutiple, almost never calcify, more common than hydatid.
- It may show 3 patterns of enhancement: marginal e non-uniform wall thickness or cyst with no
enhancement or cyst with enhancing nodule (post fossa).

Intracranial lesions (non-cystic):

Lipomas:(inclusion tumors)
- Sites: between frontal lobe in > 50% & associated e agenesis (partial or complete) of corpus call.
- Quadrigiminal region

-Hypothalamus

-CT: hypodense (-50 to -150 HU) sharply defined irregular mass, non-enhancing, no edema, linear
calcification are frequently seen.
Rathkes cleft tumor: suprasellar, benign, uniocular cyst, dd: craniopharyngioma

So generally MRI of brain tumor:

1- All of them are black in T1 & white in T2 except lipoma, colloid cyst, melanoma, cystic
craniopharyngioma (variable: white if high cholesterol, black if high keratin), haemangioblastoma
w are white in T1 & black in T2.
2-High packing tumors (low H20 content) will have intermediate signal in both T1 & T2: as
meningioma, medulloblastoma and lymphoma, they will enhance e GD-EDTA (black area would
be in such cases central calcification or peripheral signal void vessels).
3- MRI Gd-EDTA differentiate edema from tumor (edema hyperintense on T1)
4- Any tumoral haemorrahge will give high signal in T1 & T2
5- Calcification is black in T1 & T2 (non-mobile protons) except in minute periventricular
calcification w aren't seen or faint calcifications w appears white in T1 & black in T2 (as fat).

Pituitary tumors
- Pituitary gland, beam like structure e concave upper border (depth: 1.4 cm - AP: 1.6 cm height < 0.8cm) only
occupies posterior of sella turcica while ant. part of sella is filled with CSF.
- Pituitary gland is connected to hypothalamus via infundibular (at anterior surface of pituitary, near posterior clinoid
process) stalk w should be in midline (not seen until its end d.t. traversing optic chiasma).
- Above pituitary: is diaphragma sellae above w is suprasellar cystern containing circuit of Willis & above is anterior part
of 3rd ventricle.
- A depression post. to cavernous sinus is called "Rickle's cave" containing ganglion of trigeminal seen in post. cuts.
- MR protocol include: sagittal T1, sagittal T1+Gd-EDTA, coronal T1, axial T2, pituitary gland is of intermediate
signal in T1 & T2 but post. lobe is usually > white in T1 d.t. its higher fat content, pituitary stalk appears homogenous
enhancing as for normal pituitary tissue. ICA appears signal void while cavernous sinus enhances post contrast d.t. its
sluggish circulation. Sphenoid sinus (normally black in T1 & T2 d.t. air content) appears white if filled e fluid.
- T1W could be enough e no need for T2W i.e. all images enhance except for AVM & aneurysms.

Neuroradiology 34

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Types of lesions related to sella:

Intrasellar tumors:
1- Micro & macroadenoma
2- Rare lesions: pituitary apoplexy pituitary carcinoma pituitary teratoma - deposits - abcess
Supra sellar tumors:
1- Craniopharyngioma
2- Meningioma (from diaphragma sella)
3- Glioma from infundibular stalk (diffuse non-uniform increase thickness), hypothalamus, optic chiasma
4- Aneurysms from circuit of Willis.
5- Empty sella syndrome (suprasellar or sellar).
6- Arachnoid cyst - Dermoid cyst sarcoidosis rare ectopic pineloma (dysgerminoma ant. to 3rd ventricle)
7- Lesions from orbit e.g.: optic nerve meningioma, glioma, neuroma and retinoblastoma
Parasellar tumors:
1- Cavernous sinus thrombosis
2- Carotid cavernous fistula
3- Trigeminal neuroma
4- Internal carotid artery aneurysm (intracavernous or supracavernous portion)
Infrasellar tumors:
1- Mucocele and carcinoma of sphenoid sinus
2- Metastasis to the skull base.
Radiological ideas:
- Origine of tumor: Intrasellar lesions find it easier to extend upward, after destroying sella, to wider
suprasellar space. Suprasellar lesions won't erode sella & will increase in size in all directions.
- Non-specific signs: plain X-ray: intracranial calcification, ICP, obstructive hydrocephalus, abnormal
vascular markings, lateral pineal displacement, skull erosions, hyperostosis of skull.

- Specific signs: sellar deformity, enlargement, compression, acromegally, special skull changes,
hormonal effects, effect on optic chiasma.

Intrasellar lesions:
1-Pituitary adenomas 2080-81
1- Macroadenomas (non-functioning) >1cm
- Was previously termed the chromophobe adenoma
- It attains large sizes, grows slowly, presents late by signs of increased ICT + visual
disturbances (bitemporal hemianopia) + pan hypopituitarism.
- Called invasive adenoma if extending supra & infra + cavernous sinus.
2- Microadenomas (functioning adenomas) <1cm
a- Acidophil adenoma:
- Increase growth hormone: acromegaly in the mature & gigantism in adolescents.
b- Basophil adenoma:
1- Is usually a microadenoma with no sellar enlargement

Neuroradiology 35

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2- It gives rise to cushing disease with increased ACTH (from bone.)

3- In cases of cushing disease treated by adrenalectomy enlargement of an
adenoma may result in 2ry pituitary hyperplasia + 2ry enlargement of
sella: Nelsons $.
c- Prolactinomas:
1- Are microadenomas presenting e amenorrhea, galactorrhea (no sellar enlarg.).
2- Serum prolactin: may be 10 1000 times the normal (N: 0-15 ng/ml).

Radiologically:
- PXR: increased sellar size acromegaly features cushing - increased ICT.
- CT: - Macroadenomas: -Isodense mass, extending to the suprasellar cistern, it shows areas of
necrosis or calcification
-Best way to see bony extention & erosion.
-Cavernous sinus invasion in parasellar extension (as can't be removed surgically)
- Microadenomas: small hypodense area in the pituitary gland, height > 8mm, contralateral
displacement of pituitary stalk and a convex upper border of pituitary gland.
(normally in young females upper pituitary gland is convex = hyperplasia)
- MRI:
1- T1-Gd EDTA: homogenous small adenoma or heterogenous large adenoma e central necrosis.
2- Only way to diagnose invasion of optic chiasma (stretched or absent CSF space)
3- Dilated lat. ventricles = suprasellar compressing optic chiasma & ant.part of 3rd V(F. Monroe)
4- Cavernous sinus invasion e signal void ICA, w should be symmetrical on both sides
5- ICA weither invaded or not, narrowed or occluded.
- Angiography: elevation of the transverse portion of the anterior cerebral Ar. in P.A.

2-Pituitary apoplexy
Def: hemorrhage inside a normal gland or in a pituitary tumor.
C/O: increase ICT + blurring of vision, usually presents in subacute phase because vague symptoms
CT: best seen by MR as subacute blood is seen in CT isointense
MRI: white in T1 & T2 in subacute stage (be sure it is not a contrast image) to be dd from dermoid
cyst via T2 images in w dermoid is black d.t. its fat content.

3-Empty sella syndrome 2082

Def: - Extension of a subarachnoid recess into the pituitary fossa through the diaphragma sella.
- Recess is filled with CSF compressing the pituitary gland to the postroinferior part of sella.
- Though the gland is compressed, pituitary function is often normal or decreased, may
present with increased ICT, visual field defect due to prolapsed chiasma.
Aetiology:
1- Developmental defect in diaphragma sella, prolapse of a small fluid-containing pocket of
arachnoid into pituitary fossa + transmitted CSF fluid pulsations from suprasellar (contains
circuit of fluid) to intrasellar CSF leading to suppression of gland & decrease in its size +/-sellar
enlargement.
2- 1ry pituitary shrinkage:
a- Following necrosis of a tumour.
c- Post-radiotherapy
b- Post-operative.
d- Sheehans $ (Panhypopituitarism)
Radiological appearance:
1- PXR :
- Enlarged, deepened, globular sella.
- No erosion of lamina dura.
- No displacement of dorsum sella.
- Normal outline of the sella.

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2-CT: is diagnostic as the pituitary gland is seen depressed with herniation of the suprasellar cistern
downwards + pituitary stalk dipping below level of posterior clinoid process.
3-MRI:
a) Coronal cuts (best): infundibulum is seen traversing the CFS-filled sella, to be inserted
into posteriorly displaced pituitary.
b) Axial T2: white area filling sella (CSF filling it)
DD: intrasellar arachnoid cyst

4-Arachnoid cyst: (rare)

To d.d. from empty sella syndrome must judge on the following:
1-Infundibular stalk position: w if seen inside sella then it is empty sella syndrome if not it is then
pressed or diplaced via an arachnoid cyst.
2-Lumbar myelography (old tech.): in w dye will only enter sella in case of empty sella syndrome.

5-Carcinoma of pituitary gland:

- Is extremely rare & appear to be locally malignant only.
- It causes erosion of the bony walls of the sella.

Parasellar lesions:
1-Meningioma:
- Homogenous enhancing parasellar lesion ccc by bone sclerosis (osteoblastic activity)
- Passes along meningeal reflections (tentorium & petrous apex) causing typical dural tail.

2-Neuroma:
- Homogenous enhancing parasellar lesion ccc by bone erosion + cl/p of fascial neuritis.
- Lesion passes along nerve from infratentorial origin in pons to prepontine cysterns & up to
parasellar region.

3-Cavernous sinus thrombosis:

- C/O: ophthalmoplegia + proptosis
- Relative increase in size of sinus compared to other side.
- ICA inside sinus enhances (white) & cavernous sinus remains black (thrombosed)
- Sup. ophthalmic vein is dilated (but less than in a fistula) S-shaped curving around superior rectus
muscle, so appears as 2 bright dots inside orbit (cut twice).
NB:Sometimes thrombosed sinus may be totally black but may be heterogenous because it drains so
many veins that after contrast injection some flow can be seen within it.

4- Carotid cavernous fistula:

- Mostly unilateral fistula between artery & cavernous sinus leading to increase in pressure sinus &
marked increase in its size homogenous enhancement (totally white)
- Markedly congested superior ophthalmic vein.

5-Internal carotid artery aneurysm:

- Marked increase in cavernous sinus size homogenous CT enhancement of both sinus + aneurysm.
- MR will show signal void in middle of enhanced sinus except if huge aneurysm (=turbulence)
their will be whorly appearance of enhancement.
- It thrombosed aneurysm it will appear white (subacute blood) inside lumen of aneurysm.

Suprasellar lesions:
1- Craniopharyngioma 2082 (w)
- Age (2 peaks): children: 5-15 yrs & adults: 60-70 yrs.

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- Origin: from remnants of Rathkes pouch.

- Site: mainly suprasellar but may be intrasellar: rounded expansion of the sella.
- Clinically: 1- Signs of increased ICT.
2- Obstructive hydrocephalus
3- Visual disturbances.
4- Hypopituitarism (if infrasellar) Frolichs $ (if suprasellar)
- Types: 1- Cystic (cholesterol content): slowly growing e a capsule but adherent to surrounding.
2- Solid with calcifications.
- Radiological appearances:
1- Plain X-ray:
- Increased ICT
- Increased vascularity
- Calcifications (75%): midline suprasellar, > solid type: punctate clots or densily calcified
mass or with cystic type: currilinear.
- Skull changes:- Erosion and forward bent of dorsum sella
- Flatenning from above if tr. is intrasellar: round sellar expansion.
2- Angiography: avascular tumor with upward displacement of the ACA.
3-CT: - Partially cystic lesion, matrix calcification +/-solid enhancing components.
- Suprasellar or intrasellar w arises in midline and may go to right or left.
- Enhances intensely or shows ring enhancement around the cysts.
- If it obliterates foramen of Monro, so hydrocephalus + deformity of the 3rd ventricle.
- If huge, may rarify dorsum sella + expand sella + cause brain edema.
4- MRI:
- Defines soft tissue content, so cysts containing cholesterol (white in T1 & T2) and
subacute hemorrhage (same).
- Calcifications appear as signal voids (in solid or cystic areas).
- Determine the extend of the tumor w may be seen infiltrating the floor of the 3rd ventricle
and merging with the infundibulum making surgical removal difficult.
D.D. of purely cystic craniopharyngioma: arachnoid cyst dermoid cyst -epidermoid cyst

2-Meningiomas:
- Adult females, it arises from diaphragma sella & ccc by homogenous midline suprasellar
enhancement + lobulated surface & may calcify.
- Occurs in children (rare) in association of NF-II w is associated e gliomas & neuromas
- In early cases not surrounded by edema as suprasellar cystern is a wide space between it & brain.

3-Gliomas:
- Homogenous !! enhancing lesion e lobulated surface affecting pituitary stalk, hypothalamus or
optic chiasma or all of them.
- If it extends along pituitary stalk & make it thick it will have ccc figure of 8 appearance.

4-Aneurysm:
- From vessels of suprasellar cystern, perfectly rounded homogenously enhancing lesions
- Off midline as arise from vascular junctions, may be bilateral, +/-marginal calcification.

5-Sarcoidosis:
- Suprasellar lesion that can affect pituitary stalk or optic chiasma
- Midline, non-lobulated lesion in a middle age pt., +ve chest x-ray & +ve systemic symptoms.

Double floor of the sella

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Def: sellar floor is normally composed of a single dense line but sometimes 2 lines are seen.
- It is usually an abnormal finding, frequently seen in intrasellar tumors particularly adenomas.
Normal causes of a double sellar floor (pseudo-double):
1- Central depression in the floor of the sella
2- Asymmetric development of the sellar floor
3- Uneven development of the sphenoid sinuses
4- Groove for cavernous sinus and its ICA (carotid groove)
5- Incorrect patient positioning (not true lateral).

Posterior fossa tumors (infra tentorial)

Most important in post fossa lesions is to correlate them to 4th ventricle (well seen by angiography)
1-

Anterior lesions: i.e. brain stem will press posteriorly

2-

Posterior lesions: i.e.vermis will press anteriorly

3-

Cerebellar lesions located postrolateral press it anterior & to contralateral side.

4-

CPA lesions located antrolateral press posterior and to contralateral side

5-

Lesions inside the fourth ventricle will result in its dissapearance.

1-Cerebello pontine angle lesions:
a) Intra-axial : Hge, infarction, SOL

b)

Extra-axial:- Meningioma
-Aneurysm, AVM
- Lesions +/- eroding petrous bone as cholesteatoma & glomus tumor w arise from
chemoreceptor cells in jugular bulb (glomus jugular, carotid body tumor, glomus
vagale, tympanic tumor)

- Pearly tumours: epidermoid & dermoid ccc by keratin, fat, cholesterol content so
low density non-enhancing e CT, very low signal T1 & high T2 +/- flui dlevel
- Acoustic neuroma (50%) 72, 104, 2088, 2277
- Female > male 2:1
- Origin: neurilemma of acoustic nerve = vestibular
shwanoma (rarely the trigeminal), it grows by expansion.
- Site: CPA + internal auditory canal, unilateral and
bilateral with NF-II
- Clinically: decreased hearing dizziness headache
increased ICT.
Radiologically:
- PXR: widenning of int. auditory canal > 2mm, erosion of tip of petrous pyramid
(Stenver's-Town )
- CT:
Isodense mass, compression with
displacement of 4th ventricle
Hydrocephalus displaces brain stem to other side
Unilateral enlargement of internal auditory canal.
- CT with CM: well defined, markedly enhancing , homogenous at the posterior
surface of petrous pyramid.
- Angio: post-inf. Displacement of anterior inferior cerebellar artery.
- MRI:
- Intermediate signal on T1 e high signal on T2W contrasted against
lower signal of CSF - Gd-edta for small intracanalicular extension
(not done if seen in non-CM images)
To d.d. intra from extraaxial lesions:

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1-

Extra axial lesions compress brain parenchyma keeping pontine and ambiant cyterns wide
compared to other side.

2-

Extra axial lesions extending in petrous bone are eroding (intra axial aren't)

3-

AVM will show serpiginous enhancement will epidermoid cyst will not.

4-

Lesions ccc:

- Meningioma's dural base + don't enters IAC but can scallope it if sizable.
- Intracanalicular (IAC) extention of neuroma along 8th
nerve course, center of the lesion corresponds to it
(not in meningioma) + history of SNHL + best is thin
cuts MRI over petrous: intermediate signal in T1 &
T2. (in past CT ventrilography was used)

Dilated vessel of aneurysm + along its course.

2-Brain stem lesions:
- They are like does of the brain, m/c are gliomas, metastasis and tuberculoma.

a)

Brain stem hemorrage: acute (white) blood.

b)

Infarction (basilar Ar. Br occlusion), d.d.: low grade glioma

c)

Calcifications: periventricular :CTCT, enhancing oligodendroglioma, and non enhancing

tuberculoma (NB: active tuberculoma: as an abcess e a very thick uniform wall with marginal
enhancement called 'button hole")

d)

Meningioma: along dorsum sellae and clivus (rare sites)

e)

Lymphoma: not common but possible in association with other body lesions

f)

Basilar tip aneurysm: associated with dilated basilar Ar.

g)

Glioma: (usually missed d.t. interpetrous artifact, it flattens 4th V. anteriorly {dd lacunar
infarct}

Adult type : aggressive but usually does't cause

supratentoriel hydrocephalus but invade locally causing presenting
symptoms.

Cystic astrocystoma: ring enhancement + non

uniform wall thickness

Glioblastoma multiform: child + 4th ventricle

compression + heterogenous enhancement

h)

Metastatic deposits: variable degree of enhancement (homo-hetero-ring)

i)

Abcess: usually related to ear infection (post op.) + marginal uniform ring enhancement

j)

AVM: serpiginous enhancement along surface of brain stem and cerebellum

3-Cerebellar lesions:

a)

Haemorrage: 2nd most common site for CVS after tempro-parietal region

b)

Infarction: hypodense area + little mass effect

c)

Calcifications: 2 types .scheme, Sturge Weber limited to supratentorial region (dd

from blood by bone window)

d)

Meningioma: homogenous enhancement + bone erosion as post fossa is a tight place

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e)

Infratentorial lymphoma: only diagnosed if other body lesions

k)

Abcess: usually related to ear infection (post op.) + marginal uniform ring enhancement

l)

Cerebellar AVM & aneurysms (rare)

m) Cerebellar astrocytoma: 2074
- Age: young male
- Site: one hemisphere & usually extending to cerebellar peduncle or midline
hydrocephalus is common & more marked with vermal lesion
- Radiologically: calcifications are common, areas of mixed attenuation (high if solid & low
if cystic) often cystic or cystic e mural nodule & edema is present enhancement is irregular, low grade tumors show no enhancement & 2/3 of
cases dont enhance making d.d . very difficult.

- Diff. Diagnosis : Epidermoid cyst w is not limited (as astrocytoma) to infratentorial region
Dandy Walker Arachnoid cyt
n) Haemangioblastoma: 2075
- Age: 35 45 yrs it is solitary or multiple, mostly in posterior fossa.
- Pathology: vascular tumors but may develop large cysts w can mask underlying vascular nodule
- Radiologically:
1- CT: - solitary nodule with large cyst (can be mistaken for glioma or gliomatus cyst)
-mural nodule is identified in post enhancement scan (tumor nodule is isodense or slightly
hyperdense & enhances strongly after contrast media)
- multiple tumors are very small & may be easily missed
2- MRI : cyst & nodule are well demonstrated on T1, it causes homogenous low signal. Nodule is
low in T1 & T2 (may need Gd-EDTA), large vessels are frequently seen adjacent to tumor
3- Angiography: highly vascular, dense & early blush of contrast commencing at arterial &
continuing at venous phase - They may show A-V malformations (commonly AV
shunting) - vertebral angiography is indicated in every case since it is accurate
method to demonstrate multiple small lesions (which are missed on CT & MRI)
NB: In Von Hippel Lindau $: may show multiple hemangioblastoma of cerebelum, retina sp.cord.

4 Fourth ventricle lesions: in general one of first two:

a)

Choroid plexus papilloma (in young: lat V. adult: 4th V.)

- Generally produces hydrocephalus (over productive not obstructive type)
- Periventricular hypodensities of retrograde transependymal CSF permiation.
- May present as over calcification of choroid plexux w wont be over productive, no hydroceph.

b)

Ependymoma: 2075 (in young 15 yrs: 4th V. adult: lat V.+ cerebrum) "it is a type of
glioma"
- CT: -Hyperdense homogenous lesion w markdly enhance & causes hydrocephalus via
obstrution of 4th V.
-Can calcifie w is ccc in 30 % & spread via seeding (or serosal) through CSF to cysterns
causing another enhancing area in CSF on the surface of the brain & basal cysterns.
- MRI: low T1 and high T2

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c) Medulloblastoma: 2074
- Age: child < 5 yrs male neuronal in origin (primary neuroectodermal tumor = PNET)
- Ccc: -Midline, malign. tm from roof of 4th V. and grows inside it & rarely arise in adult from
cerebellar hemisphere & not from vermix.
-Invades brain stem & obliterates 4th ventricle so hydrocephalus is common & metastasy
via CSF into cerebrum ( do a brain MRI)
-Calcification in medulloblastoma occurs in 13% of cases.
- Radiologically: heterogenous enhancement, ident ventricle, e minimal perifocal edema
c)
d)
e)

Intraventricular hemorrhage (free or ependymal)

Astrocytoma: marginal non-uniform enhancing cystic lesion + enhancing nodule.
Meningioma.
NB: 3 tumors spread via CSF: ependymoma medulloblastoma & glioblastoma multiforme.
Complications of brain tumors:
1.Brain edema
- Vasogenic edema: (grey matter is resistant to edema)
- 2ry to tumor, abscess or infarction
- Caused by destruction of blood brain barrier leading to extravasation of protein & fibrin.
-CT appearance

wide , hypodense white matter obliterating at 1st sylvian fissure

finger like projection of white matter into gyri
thinning & compression of grey matter with effacement of sulci & gyri

- Administration of corticosteroids will decrease edema

- Cytotoxic edema:
-2ry to hypoxia and water intoxication d.t. damage of Na/K pump leading to swelling of
the cells mainly occurs in infarction.
interstitial edema

(subependymal)

-2ry to acute obstruction of flow of CSF

escape of ventricular fluid across the

microscopic breaks in ependymal lining of ventricle

-CT appearance

poorly circumscribed periventricular hypodenisty

it is seen at anterior superior margin of frontal hornes

loss of

sharp definition of margins of the horns

-no effect of corticosteroid but with shunt operation
2.haemorrahge
3.herniation
-mechanism expanding mass within cranial vault caused by tumor & edema causing
compression & distortion of adjacent normal brain tissues.herniation of brain under the
relatively rigid falx through tentorial incisura or through foramen magnum
-types

Neuroradiology 42

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descending tentorial herniation caused by temporal tumor

displacement of

uncus & parahyppocampal gyrus (which is on medial aspect of temporal lobe)

ascending transtentorial herniation caused by posterior fossa tumor herniation
of cerebellar vermis
tonsillar herniation caused by posterior fossa tumor

displacement of cerebellar

tonsills through foramen magnum

* Lesions of skull base :*Primary

(see figure beside)

(arising in bone itself)

primary osseous lesions

a)primary bone tumors

1.cartilagenous tumors (chondroma chondrosarcoma)
2.epidermoid (congenital cholesteatoma)
3.osteoma
4.plasma cytoma
5.osteogenic sarcoma
b)metastatic bone tumors

osteolytic
osteoblastic
mixed

c)diffuse boney lesions

fibrous dysplasia
Pagets disease

*Secondary lesions

(arising from soft tissues surrounding skull base)

endocranial lesions

growing down to invade skull base

exocranial lesions

growing up to invade skull base

secondary lesions

a)congenital lesions

encephalocele (fronto-nasal encephalocele)

arachnoid cyst (middle cranial fossa-anterior to temporal bone

..

smooth marginating pressure effect on skull base)

Arnold chiari malformation
b)neurogenic tumors

acoustic neuroma
trigeminal neuroma
9th, 10 th & 11th neuroma

c)chordomas
d)meningiomas

mention the types

e)sellar lesions

as before + empty sella

f)lesions of petrous bone

tuberculosis
tumors

g)lesions of PNS

mucocele
squamous cell carcinoma

widening foramen ovale

widening of jugular fossa

Neuroradiology 43

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h)lesions of nasopharynx

juvenille angiofibroma (may invade skull base)

squamous cell carcinoma of nasopharynx

i)trauma with CSF fistula

(CT with metrezamide + coronal cuts to demonstrate the bone defect

and leakage of contrast through this defect)

cephalhaematoma
skull fractures

rhinorrhoea + pneumocephalus
otorrhoea + pneumocephalus

PNS fracture
petrous fracture

CT brain
( lesions are congenital-traumatic-inflammatory-vascular-neoplastic-other; atrophy)

1- Congenital:
HYDROCEPHALUS: classification :-

1.non obstructive

ventricular dilatation due to reduced brain substance

2.obstructive

obstruction in CSF flow

within or inside ventricular system

outside ventricular system i.e.subarachnoid space

(non communicating)

or basal cisterns (communicating)

*Causes :a)non obstructive hydrocephalus

1.congenital

neonatal brain atrophy (developmental or due to birth injury)

2.atherosclerosis & infarcation

3.degenerative

senile dementia
familial cerebral atrophy

4.inflammation

following encephalitis

5.traumatic

local scar following head injuries

6.neoplastic

choroid plexsus papilloma

b)obstructive hydrocephalus
Non communicating

1.causes of aquiductal steonsis

congenital
acquired

-tumors

seedling from ependymoma or ventricular glioma

tumor in posterior fossa

lateral displacement of 4th ventricle

kinking of the duct

local tumor in brain stem

-late complication of TB meningitis & meningioencephalitis

acquired stricture

-tuberous sclerosis
2.causes of 4th ventricular obstruction
-adhesive arachnoiditis

occlusion of foramina of Magendi & Luscka

normal 4th ventricle & cerebellum

Neuroradiology 44

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-Dandy Walker syndrome

atresia of foramina of Magendid & Luschka

dilatation of the 4th ventricle with may be hugely balloned

associated with hypoplasia of vermis & cerebellum with expanding enlargement

of posterior fossa + meningeocoele + cropus callosum defect
(important to differentiate from mega cisterna magna & arachnoid cyst)
-Arnold Chiari malformation

prolapse of medulla , pons & tonsils through

foramen magnum into upper cervical canal causing occlusion of

ambient cistern
communicating type

aqueduct

non communicating type

Arnold Chiari malformation :Type 1

least obvious clinically

-tonsillar herniation through foramen magnum + normal 4th ventricle present in adults
(herniation till 3mm is normal but 10-15 mm = malformation)
-70%

syringomyelia & 5%

Type 2

boney dysplasia

presents in neonates & infants

-accompanied by dorsolumbar myelomeningiocele

-caudal herniation of tonsills, medulla & vermis
-elongated & caudally displaced 4th ventricle

(non comm.)

(comm.)

-hydrocephalus may be due to associated acquiduct stenosis or occulsion of ambient cistern

-associated

hypoplasia of corpus callosum, flax & deformed mid brain

Type 3
-major deformities with cerebellar hyoplasia
Type 4: accompanied with high cervical or occipital encephalocoele
Communicating

(see figure beside)

-due to over production of C.S.F & absorption (this is a rare cause due to the presence of a
choroid plexsus papilloma)
-the cause is usually at tentorial hiatus
1.arachnoidal

chronic arachoniditis following meningitis

occlusion of the

basal cisterns
2.subarachnoid space

subarachnoid hge

adhesion & occlusion of basal cisterns

superior saggital sinus thrombosus

CSF absorption

via the arachnoid villi

-Communicating i.e. free communication between vetnricles & basal cisterns with obstruction
to CSF flow in subarachnoid spaces or basal cisterns dil.of all ventr. & basal cisterns.
NOTES
@Arnold Chiari

I (tonsillar herniation + normal 4th + syringomyelia)

II(tonsillar-vermal-medulla + displaced 4th + meningeocoele + hydroceph.)

non communicating

acquiductal

communicating

ambient

Neuroradiology 45

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III-IV (anomalies + occipital encephalocoele)

@Dandy Walker

balloned 4th ventricle

obstruction of Luscka & Magendi

Radiological features of hydrocephalus :*Plain film

signs of ICT
craniofacial ratio

1)infants

thining out of skull vault

widening of sutures
bulging of soft tissue shadow at anterior fontanelle
+ flattening of sella turcica
2)in eldry patient

finger prints
resoprtion of dorsum sellae

calcification

in cause of hydrocephalus e.g.

calcified ependyroma
pinealoma
tuberous sclerosis

* CT
-CT detects

effects of obstruction
site of obstruction

leak = haze
parenchyma

cause of obstruction

atrophy or not
sulci or not

follow up the shunt operation

non obstructive hydrocephalus

(as if brain atrophy)

ventricular dilatation
brain tissue
enlarged subarachnoid system & sulci
no periventricular haze (only type with no haze)
when unilateral

ventricular displacement to affected side

obstructive non communicating

1)it can define site or level of obstruction e.g.
-dilated single lateral ventricle obstruction at foramen of Monro
-both lateral ventricles obstruction in 3rd ventricle
-both lateral ventricles & 3rd ventricle

in aquiduct
or 4th ventricle

2) it can diagnose cause of obstruction as brain tumors

-obstructive hydrocephalus associated with smooth uniform dilatation of ventricles
with periventricular haze around frontal horns d.t. passage of CSF thr. ependyma (subependymal leak)

obstructive communicating

all ventricles are dilated

+ enlarged basal cisterns (charechterestic)
may be enlarged sylvian fissure

Neuroradiology 46

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periventricular haze
absence of enlarged sulci (to differentiate between brain
.

atrophy & obstructive communicating hydrocephalus)

*Ultrasound

before closure of anterior fontanell

in uteruo
1)it can detect congenital hydrocephalus in uterus in 17 weeks
2)it can diagnose midline shift in unilateral hydrocephalus
3)it can diagnose Dandy Walker syndrome
4)follow up of shunting operation
5)can diagnose intracranial haemorrahge
*Angiography

in absence of CT

-ventricular dilatation can be diagnosed by stretching anterior cerebral artery in lateral view
-downward displacement of internal cerebral vein
* MRI

has value as CT but of high cost

* Isotope scanning
Agnesis of corpus callosum :-usually partial but sometimes complete
-CT appearance wide separation of medial borders of lateral ventricles between which the 3rd ventricle may
extend upwards + enlarged occipital horns (complete type)
-In partial agenesis it usually involves posterior part & anterior part may remain normal, frontal horns + bodies are
laterally displaced & small
-enlarged rounded occipital horns due to associated white matter hypoplasia
-lipoma may sometimes be found at site of the absent corpus callosum

Arachnoid cyst :-arise in the brain (or spinal cord)

-intracranial but extra cerebral
-age

infant but may present in adult

-site any where specially

middle & posterior cranial fossa

supra sellar region
behing 3rd ventricle

-pathology

contain clear fluid lined by arachnoid tissue

differential diagnosis

subdural hygroma
post-inflammatory locules

-clinical picture

if large

mass effect

hydrocephalus

associated hypoplasia of cerebral tissue

-CT & MRI

cyst at sites ,of CSF density, no enhancing wall or adjacent calcification

-differential diagnosis

suprasellar

Rathkes cleft cyst - craniopharyngioma

quadrigeminal cistern
NB:-tumors of posterior fossa & CPA

brain stem glioma

dilated suprapineal recess

Neuroradiology 47

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epidermoid

cerebellar

secondaries

primary(haemangioblastoma-medulloblastoma-astrocytoma)
rd

-tumors of 3 ventricle

colloid
ependymoma

teratoma
-tumors of sella

pinealoma
meningioma

adenoma
glioma

craniopharyngioma

*Hydranencephaly major perinatal destructive process resulting in massive intracerebral

cavitation & falx is present (differential diagnosis to holoprosencephaly)
*Lissencephaly

(=agyria=smooth brain) disorder of neuronal migration

absence of sulci

& convolutions in the cortex

*Heterotopias

arrest of migrating neurons in the form of small masses of grey matter in

wh.matter e.g.of cerebellum or subcortically (i.e.abnormal glial tissue) occur in tuberous sclerosis
*Porencephaly

congenital

localised agenesis of cortical mantle

cavity lined by

ependyma (see figure beside)

acquired or false porencephaly
.
*Schizencephaly

(post traumatic or post infarction)

secondary to cerebral destructive process

encephalomalecia (see figure beside)

(see figure beside)

* Holoprosencephaly: The cerebral ventricles are represented by a single cavity often expanded
posterior as a thin walled sac. The falx cerebri is absent.

Neuroradiology 50

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B. Intra-cranial tumors: see before.

C. Vascular lesions: see before
D. Infections and inflammatory diseases:
1. Bacterial infections:
Leptomeningitis - Meningioencephalitis - Epidural and subdural empyema.
Cerebritis - Cerebral abscess - Ventriculitis.
2. Granulomatus lesions: T.B, and sarcoidosis.
3. Fungal infections.
4. Parasitic infestations: cysticercosis, hydatid & toxoplasmosis w is cccc by:
Congenital extensive brain damage bilateral chorioretinitis
Adult form in pts. e impaired immune system; multiple brain lesions involving BG & subcortical
regions (focal multiple, density) + intracranial calcification.

5. Viral infections: Herpes simplex virus.

6. Vascular inflammatory lesions: cerebral arteritis, mycotic aneurysms, venous
thrombosis.

1. Leptomeningitis and Meningio-Encephalitis:

Leptomeningitis is an inflammatory reaction of the meningeal layers.
The disease is characterize by congestion of superficial cerebral & pia vessels followed by
production of exude in subarachnoid space obstruction to C.S.F Hydrocephalus.
CT appearance:
Early normal CT scan, then there may be enlargement of cortical subarachnoid spaces and increased
density of basal cisterns and interhemispheric fissure and enhancement of cortical gyri.
Increased density of dural sinuses or cortical veins & lack of normal intraluminal enhancement
detected by CT (delta sign) due to spontaneous (or associates inflammation) venous & sinus
thrombosis infarction2112.
- The main value of CT in meningitis is to detect complications:
1. Hydrocephalus

2. Subdural effusion.

3. Arterial and venous thrombosis infarcted areas related arterial or venous distribution
4. Focal zones of encephalomalacia and atrophy.

Encephalitis: Types:
1-Acute disseminated encephalomyelitis (ADEM): white matter ring or punctate enhancement in MRI+Gd
2-Acute haemorrhagic leukoencephalopathy: late evidence of petechial haemorrhage in MRI
3-Subacute sclerosing panencephalitis: post measles ccc by cerebral atrophy + white matter involvement.
4-Progressive multifocal leukoencephalopathy (PMLE): rare to enhance in MRI+Gd, hypodensities in CT.
5-Herpes simplex: multicystic encephalomalecia in infants / hypodensities in temporal lobe in adults.

Neuroradiology 51

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2. Epidural and Subdural Empyema:

Epidural empyema is commonly found in the frontal region due to proximity of the frontal sinus.
The most common location of subdural collections is the cerebral convexity2097.
CT: Crescent or lenticular shaped, hypodense extra-cerebral collection associated with
compression and displacement of the ipsilateral cortical sulci and lateral ventricle.
CT+ C: The margins of subdural empyema usually enhance. There is significant variation in the
thickness and irregularity of the enhancing zone.

3. Cerebritis and Cerebral Abscess:

Pathologic picture: vascular congestion, cerebral softening, petichial hge and edema. If cerebritis
doesn't resolve e ttt, area of cerebral will undergoes liquefaction e abscess formation.
Route of infection:
a) Direct: local infections superficial
b) Metastatic: bronchiectasis, endocarditis, dental sepsis deep
CT appearance:
Early C.T2096:
Normal or poorly defined hypodense white matter areas with marked edema.
Edema in white matter surrounding lesion is an almost constant finding with significant mass effect.
N.B. Abscess appears as central hypodense zone surrounded by slightly high density capsule. + C ring
enhancement.

DD: Primary or metastatic brain tumors, tuberculoma, and syphilis gumma.

4. Ventriculitis or Ependymitis:
Ccc CT enhancement of ependymal layers along ventricular wall.

5. Tuberculomas: It may be single or multiple in number.

Sites: In children; usually infratentorial, supratentorial tuberculo. are usually parietal or parasagittal.
CT Appearance: They appear as area of hypodense or isodense or slightly hyperdense, on
enhancement, the lesion extensively enhanced.
DD: extra axial tuberculoma attached to dura from meningioma, intra axial tuber from glioma

6. Sarcoidosis: (rare)
It can occur in C.N.S as: diffuse granulomatous meningitis Or

Intracerebral mass lesion.

Appears as: peripherally located, slightly hyperdense, homogeneously enhanced.

Neuroradiology 52

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Demyelinating disorders

2101

Abnormal formation or maintenance of myelin.

1-

Congenital leukodystrophies: in childrens, low density white matter in CT, white T2W
symmetrical lesion usually spearing capsular region, well seen by FLAIR tech.
2- Canavan's disease, Alexander's disease: begins in frontal and extends towards occipital lobes.

2-

Metachromatic leukodystrophy & adrenoleukodystrophy: begins in occipital lobes extending

towards frontal + enhancement near the periphery.
4- Pelizaeus-Merzbacher disease: almost complete failure of myelination with signal hyperintensity.
5- Secondary demyelination: post inflammatory, vascular, toxic, and neoplastic.

Disseminated sclerosis

2102

Unknown etiology; mostly slow virus. Multiple sclerosis is destruction of normally formed myelin.
Sites: in acute cases mostly periventricular, while in chronic cases mostly in optic pathway, brain
stem, cerebellum, spinal cord.
Radiological findings:
1-CT: low density plaques of white matter w can or not enhance if acute.
2-MRI: x 10 more sensitive: multiple hyperintense plaques, periventricular & in peripheries lies
within the convolutions, lesion are well seen in T2, FLAIR, DW images and they enhance
for long periods with Gd-EDTA (Dawson's fingers: perpendicular ovoid lesions to the
ventricles).

Causes of generalized attenuation of white matter:

1.
2.
3.
4.
5.
6.
7.

Senile
Uremia
LCF
HT crises
Malignancy
Muscle dystrophy
Vasogenic edema surrounding a brain tumor.

SPINE
Topics of comment on plain film of the spine:
1. General alignment

6. Post. I.V. joints.

2. Vertebral bodies

7. I.V. foramina.

3. I.V.D

8. Ribs

4. Pedicles & lamina

9. Spinous process

5. Transverse process

10. Para-vertbral soft tissue shadow.

Neuroradiology 53

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Topic of comment on myelogram:

1.

Flow of contrast in subarachnoid space:

normal (free)
arrested partial
complete at which level.

2.

Indentation of contrast column & its level.

3.

Position of cord in the theca:

central
displaced.
4. Relation of margin of the contrast column to pedicle normal equidistant.
N.B.: The cord terminates at L1/L2 in adult and L2/L3 in children.
Termination of subarachnoid space (thecal sac) is variable, usually S1/S2.

Developmental abnormalities of spine:

1. Coronal Cleft Vertebra: see orthopedics
2. Sagittal cleft vertebral butterfly vertebra: see orthopedics
3. Congenital Vertebral Fusion: see orthopedics
4. Sacralization and lumbarization: see orthopedics
5. Spina Bifida: Failure of fusion of neural arch of vertebra in the midline 2150-2220.
Etiology: Unknown, genetic factor.
Pathogenesis:
Normally the neural grave starts to close around 21st day, beginning in thoracic region & then
proceeding in both a cranial and caudal directions. It the neural tube does not close, the adjacent
mesoderm fails to develop and the neural arches dont fuse posteriorly.
Types of spina bifida:
1. Spina bifida occulta:
Definition: It is an unossified minor bony defect of spinous processes & laminae eout any
overlying skin abnormality. No ossifying cartilage. Commonest site is at LS junction.
Association:
- When associated with an overlying cutaneous abnormality, there is often underlying
myelodysplasia.
- The cutaneous abnormality may take form of: pigmentation, skin dimple, abnormal texture of hair.
Skin dimple is usually found in mildline in lumbo sacral region.
- It may be connected with dermal sinus. If open, infection leads to recurrent attacks of meningitis
- A fibrous band may be attached to the meninges or underlying cord and spina bifida. This fibrous
band may tether cord and prevent its normal ascent.

Neuroradiology 54

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Radiologically:
1-A small defect in neural arch.
2-Absence or deformity of spinous process.
3-There may be a little local widening of I.P.D at the affected level.
4-Associated spinal tumor may be at a higher level than S.B at lumbo-sacral junction on plain film.
N.B. In a patient with a neurological deficit: One should keep in mind that there is an association between Spina Bifida
Occulta with cutaneous abnormality. Also an association between congenital spinal tumors and a lipoma or dermoid
cyst of the filum terminalis or conus medullaris.

2. Meningocele or meningomyelocele
It is spina bifida with herniation of :
dural sac + leptomeninges meningocele.
dural sac + leptomeninges + elements of the spinal cord meningomyelocele.
Types of meningiocele:
1- Lateral thoracic meningiocele:
It is herniation of meningeal sac through wide I.V.F at margin of dorsal vertebra mostly due to
neurofibromatosis posterior mediastinal mass.
Plain: Well-defined, rounded para-vertebra soft tissue mass in the posterior mediastinium.
Myelography: Outlines the sac.
CT: confirms the diagnosis.
2. Anterior Sacral Meningocele:
It is herniation through a large bone defect in the anterior sacrum into pelvis.
Plain: Soft tissue mass in the pelvis.
Barium Enema: Displacement of recto-sigmoid.
Myelography & CT: Confirm diagnosis.
3-Meningo-myelocele:
A.P.: spina bifida + bony defect of neural arch, widening of the spinal canal (wide I.P.D)
Lateral: Soft tissue mass is outlined
Dysraphism : d.t.:
1. Adhesions bet ectoderm & endoderm of embryonic disc prior to formation of the notochord at the 3rd week of gestation.
2. Derangement of normal sequential closure of the neural tube & its separation from the dermis, followed by in-growth of
mesoderm to form meninges. Eg: Myelomeningocele - Lipoma - Epidermoid & dermoid tumors -Dermal sinus-Diastematomyelia

Diastematomyelia:2169

2 unequal cords + increased width of spinal canal e medial convexity of

hydromyelia.

Narrowing of the disc space at same level and intra-laminal fusion

pedicles +/-

Neuroradiology 55

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A bony spicule dividing canal is confirmatory.

Spinal infections
Spinal infections include cord affections & bone affection (mainly in dorsal spines).
Inflammatory disease of spine (now called discitis osteomylitis) include involvement of disc
together e opposing parts of vertebral end plates, it include --> non specific discitis & Pott's disease
(T.B of spinal but staph can affect spine). N.B. no spinal bony affection without disc affection.
1. Non specific discitis
- Low grade inflammation e no aggressive spinal affection & non-significant abscess formation.
- Narrow (inflamed) disc space + eroded vertebral end plates.
- Occurs mostly as a post-operative complication, mostly in lumbar region (look for laminectomy)
2. Pott's disease of the spine
a- PXR: aggressive infl. process resulting in narrow disc space + eroded vertebral end plates.
- Multiple level affections usually occurs, mostly in dorsal region.
- Significant abscess formation occurs in back muscle region, paravertebral region (on both sides),
prevertebral region (iliopsoas to groin) +/- inflammatory granulation tissue in epidural region
(intraspinal) that enhance after IV contrast. Abcess formation is best seen non axial images &
eroded end plates on lateral x-ray and sagittal MRI.
b-CT images:
- Once vertebra above & below disc level are affected in an inflammatory process, disc will be
affected even if no significant radiological changes are seen in it:
- Affection of disc is very mild occurring in form of: non significant bulge - haziness
- Affection of vertebral and plates above & below disc level: eroded end plates e rarifactions
(sclerosis may also occur in low grades of inflammation as there is chance for healing).
So on CT search for level of disc then go one level above and one level below the disc lesion.
D.D:
1-Multiple Schmorl's nodes: occurring in vertebral end plates (above & below disc) but they are of well
defined margins + sclerotic margins.
2- Metastatic deposits: ccc by normal disc in between, mostly affects pedicles & body (not end plates) +
history of 1ry malignancy (no history of spinal operation).
N.B: most intraspinal lesions are neoplastic but other may occur w are haematomas or inflammations.

c-MRI: (dd: Modic type I degeneration)

- Sagittal images are important in evaluation to know operation done, search for spinous process
absence and presence of intraspinal granulate tissue, arachnoiditis, discitis).
- Eroded end plates and narrowed disc space (d.t. edema): black T1(edema enhance + C), white T2.
N.B.: In contrary of brain edema & any other edema, marrow edema is the only type of edema that
enhance after IV contrast whether it's cause is (degeneration, inflammation or neoplasms).

- T2W: white disc + white end plate is not truly homogenous (as patient while under ttt there will
be part responding and ports not responding).
- Axial cuts + coronal cuts: detect paravertebral abscess. If this abscess press on cord = myelitis if
white in T1W+Gd, and = edema if white on T2W.

Neuroradiology 56

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- So in ?? spinal infection on MRI --> see sagittal T2W --> diffusely white disc (due to
inflammation) & ensure that they are black on T1 images + white on T1W+Gd.

Neuroradiology 57

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Spondylolithesis :
1845

Definition:
Forward slipping of one vertebra above on a vertebra below due to a fracture in pars interarticularis,
i.e. forward sublaxation of vertebral body, pedicles, & sup. articular processes, while lamina,
spinous process and the inferior articular process main in normal position.
Reversed spondylolithesis: may occur in following: rheumatoid arthritis, ankylosing spondylitis,
trauma, OA of apophyseal joint.
Spondylolithesis: usually leads to adjacent disc degeneration or prolapse (sublaxation annular
tear spondylitic changes).
Spondylolysis: pars interarticularis defect without vertebral slipping.
N.B: In all types of spondylolithesis the I.V.D at the level of the slip projects posterior to the plane of the
displaced body. This should not be misinterpreted as a significant disc prolapse or protrusion unless there is
considerable encroachment of the epidural fat between the disc and theca rost sheath.

Site: Commonest at LS junction with forward sublaxation of LV5 on SV1.

Pathogenesis:
1.

Incomplete fusion of inter-articular part of N. arch.

2.

Fibrosis rather than bony union between the separate ossific centers.

3.

Developmental weakness of pars interarticularis.

4.

Forward sublaxation rupture of annulus fibrosis disc lesion.

Predisposing factors:
1. Congenital hypoplasia of articular processes.
2. Trauma: stress fracture of pars interarticularis, acute fracture of pars interarticularis
3. Degenerative O.A changes in apophyseal joint.
4. Pathological fracture i.e. T.B, Pagets disease.
Radiologically:
A.P.:
Bow line extensive form. Owing to the associated lordosis of L5 vertebra, it is viewed in AP view
to be super imposed on sacrum bow line.
Lateral:

Grade I: forward displacement of 1/4 of width of upper surface of sacrum.

Grade II: forward displacement of 1/2 of width of upper surface of sacrum.

Grade III: forward displacement of 3/4 of width of upper surface of sacrum.

Grade IV: forward displacement of full width.

Oblique view:

Neuroradiology 58

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- Will show if defect of pars interarticularis is present and whether it is bilateral or unilateral.
- Defect appears as a gap in neck of Scottie dog.
- Margin of defect are well defined & width of then gap varies with degree of forward displacement.
- When displacement is progressive 2ry deformities of body of 5th lumbar and 1st sacral segment.
- Eye: pedicle
- Ear: superior articular process.
- Nose: transverse process.
CT:
Look for the pars at the level of the pedicle at disc level you will see apophyseal joint.
1. fracture of pars interart. (sclerosed, irregular margins).
2. disc state.
Myelography: For any evidence of indentation or disc protrusion.
MRI of spondylolisthesis:
1. Degree of slip & neural compromise.
2. Lack of signals from sclerotic but intact bone which may simulate a break.

Inter vertebral disc prolapse:

Definition: A herniation of nucleus pulposus through tears or rupture of the annulus fibrosis.
Etiology:
1. Trauma:

Single trauma history.

Occupational micro-trauma.

2. Degenerative:

Of the nucleus pulposis

Posterior longitudinal ligament weakness

3. Congenital weakness of annulus.

The presence of spinal canal stenosis help disc protrusion to become symptomatic
Pathology:
It can occur in any direction:
Prolapse through anterior or antro-lateral margin of annulus pain but no neurological

1.

signs.
Prolapse into an adjacent vertebral body corticated erosion of vertebral body [Schmorls

2.

node].
3.

Prolapse through post. or postero-lateral margin of annulus pain with neurological signs due
to:
pressure on spinal cord. Or pressure on nerve roots in I.V. foramen.
4. Calcified disc prolapse especially in dorsal region may simulate a meningioma.
Site:

Neuroradiology 59

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The commonest site for disc prolapse is L4-L5 then L5-S1 then L3-L4 (maximum anglulation,
weight bearing.)
Lower cervical: C5-C6 & C6-C7 ( most mobile).
Stages: read
a)Disc bulge:
- outside disc space,
- inside disc space pressure: schmolers node sclerosing margins (i.e. protrusion without
focality).

Ligaments and annulus are intact.

b) Protrusion: focal annular weakness nucleus protrudes

Posterior

Posterior lateral

Infra lateral

Rupture annulus.
c)Migration: Herniated nucleus ascends or descends from original disc space
migrated disc has the same CT density & MRI signal on both T1 & T2.
d) Sequestration: Same as migration but with loss of connection of migrated protruded nucleus
from original nucleus.
Fragment has high signal on T2 W.
Radiology Appearance:
A. Plain findings:
1. Completely normal in acute disc prolapse.
2. Narrowing of I.V.D space (symmetrical or on one side).
3. Alteration of the spinal alignment (flattening or scoliosis) due to reflex spasm of paravertebral muscles to tension on the nerve roots being stretched over protruded disc.
4. Blunting of edges
5. Sclerosis of edges of adjacent body
6. Vacuum sign (degenerated disc material traps nitrogen gas from blood).
7. Calcification in disc.
8. Spondyolitic changes in body or facet joint: osteophytes.
9. Cause (trauma, fused vertebra....).

B. Myelographic findings:
I. General: cardinal signs :The cardinal signs are considered diagnostic provided it is constant.
I. In. lateral film:
Indentation (Extradural) of anterior margin of omnipaque column, seen with posterior disc
herniation rather than lateral disc herniation the level of affected disc.

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2. AP view:
A) Post. disc: hour-glass constriction of the ominipaque column, (central disc + lig. flavum hypertrophy.)
horizontal, serrated defect of the ominipaque column
B) Lateral disc lateral indentation in ominpaque column.
C) Obliteration or deformity of affected nerve root sheath (amputation of root sleeves) d.t. edema.
D) Block defect either partial or complete to subarachnoid spaces if large disc protrusion:
asymmetrical filling lat film Rt. & Lt.
CT findings:
Disc herniation diffuse or localized, encroachment on the epidural fat with entrapment of nerve
root at the exit foramina.
MRI:
- Annulus fibrosis, spinal ligaments dura matter and cortical bore low signal
- Vertebral bodies, nucleus pulposus high signal (white).
1- It is only non-invasive technique that shows nucleus of the disc.
- Epidural and paraspinal fat good delineation of dura high signal of the fat around low
signals of dura.
2- C.S.F has long T1 & T2 low signals (block) using short echo delay time.
- A shelf of annulus causes a low signal horizontal band gives a characteristic bilocular appearance
of the nucleus.
- With normal aging intensity of signal of nucleus.
3- Nucleus pulposus of normal IVD, high signal or T2 weighted, which is surrounded by the low
signal of the annulus which also partly divides the nucleus giving the characteristic biocular
appearance of the adult nucleus pulposus.
4-. The signal returned from the degenerated nucleus is low due to dehydration associated with degeneration
with indentation of the thecal sac by the protruded disc.
5-On T2 weighted MRIs the disc returns to a higher signal than the scar, in which signal decreases with
aging. Recent scars enhance immediately but old scars enhance more slowly and much less. Gd enhanced
MRI is more accurate than CT in this assessment.

Focal Varicosities:
Caused by disc compression on vertebral venous plexus focal dilated veins. It may also occur in
angiomas & spinal canal stenosis. Normal myelogram + narrow disc = anterior protrusion.

Spondylosis
Definition:
- It is a bony overgrowth in adjoining vertebral margins due to long standing herniation or
degeneration of an intervertebral disc. It is a descriptive term referrning to defects in the region or

Neuroradiology 61

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the pars interarticularis or a vertebra. It most commonly occurs at the 5th lumbar vertebra.
- Elevation of periosteum from edge of vertebral body allowing osteoblasts to lay down new bone
so a bulge is formed compress nerve root i.e. starts as lipping due to friction caused by
flattening of bodies then redundancy in ligaments bone laying.
N.B. Spondylosis degeneration
Spondylysis pars defect without slippage.
Spondyelythesis pars deject with slippage.
Radiological appearance:
1. Schmorls node: Traumatic or developmental defect in the cartilaginous end plate vertical
herniation of nucleus pulposus indentation of adjoining margin of vertebral body with s
sclerosing margin which is seen in the lateral film.
2.

Osteophytic rim: May be seen on the posterior margin of vertebral bodies extending to
I.V.F compression of nerve roots at their exit from spinal canal.
3. Subchondral sclerosis and irregularity of the surface of vertebral body adjoining the disc space.
4. Lateral films with flexor & extensor sublaxation & abnormal mobility.
5. Calcification in nucleus or annulus. More in thoracic vertebra and differentiated from thoracic
meningioma.
6. Narrow disc space with marginal sclerosis and osteophytosis.
7. Post indentation of omnipaque column by thickened ligament flavum.
8. Vaccum phenomena: radioluncent collections of gas crested by abnormally altered disc spaces.

Spinal Canal Stenosis

Causes:
1.

Congenital: short pedicles, achondroplasia

2. Ligamentum flavum hypertrophy.
3. Posterior osteophytosis.

4.

Facet joint arthropathy.

5.

Annulus protusion.

6.

Calcification of posterior longitudinal ligament

Radiological appearance:
A) Plain:
1. Narrowing of A.P diameter of canal < 1.5cm. (it is measured in lateral view from mid body to the
root of spinous process).
2. Narrow transverse diameter is not reliable i.e.I.P.D.
3. Low spinal index < 4-5.
Spinal index:
A.P diameter mid body

same tr. diameter A-P diameter,

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AP diameter canal
4.

Pedicles:

canal trans. diameter.

hypertrophied, bulky & short.

5. Apophyseal joints: Vertically oriented, distinct joint space, present inside pedicles.
6. Inferior articular process: convergent., encroaching on AP diameter of the canal (lat view)
B) Myelographic findings:
1. Suggestive data:
a. Difficult lumbar puncture with the best hand.
b. Pain with injection of dye.
c. Whole dural sac of lumbar vertebra is filled with less than 6ml of dye in the standing position.
2. Definite data:
a. Beading of dural sac opposite disc spaces.
b. Post. scalloping of the opacified column.
c. Crow dening of the nerve roots.
d. Worm like appearance of the venous channels.
C) C.T findings:
1. Absent epidural fat & short bulky pedicle .
2. Medially placed epipth at the pedicular.
3. Bony surface area < 1.42 cm.
4. Soft tissue surface area < 100 mm.
5. Mid Sagittal diameter is less than 10mm in cervical 12 mm in lumber.

Causes of Lower Back Pain

1. Lumbar disc prolapse or pure lumbar canal stenosis.
2. Spondyloilthesis
3. Spondylosis.
4. Spinal tumors: 1ry or 2ry.
5. Inflammation: Potts disease.
6. Pelvic causes of intra pelvic malignancy infiltrating roots.
7. Sacra-ileitis referred sciatica.
8. Muscular skeletal pain.
9. Psychogenic.

Spinal Injuries: types:

I. Hyperflexion:
1. Dislocation of post intervertebral joint (unstable).
2. Wedge fracture of post intervertebral joint (stable).
3. Clay shovellers fracture .
II. Hyperextension:
1. Hyperextension dislocation
2. Avulsion fracture of anterior arch of atlas.
3. Laminar fracture.

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4. Extension teen drop fracture.

5. Traumatic Spondyloilthesis.
6. Pillar fracture.
III. Vertical compression:
1. Jefferson bursting fracture
2. Burst fracture of lower C. spine.
IV. Atlanto-occipital dislocation.
V. Fracture odontoid process of axis.

Radiographic assessment of cervical injures:

Two questions must be answered.
1. Is a fracture or dislocation demonstrated?
2. Is the lesion stade or unstable?
Technique:
1. AP view of CS
2. Lateral view with horizontal beam method.
3. Oblique or swimming views.
4. Lat. film inflexion & extension to detect instability.
CT: Value:

Elucidate the degree of spinal cord compression.

Fracture of neural arches & vertical fracture of vertebral bodies.
F.B herniated disc, haematoma.

I. Hyperflexion injuries: (commonest).

A. Dislocation of posterior intervertebral joints: unstable.
1. Loss of smooth posterior line of vertebral bodies, (or ant. wall of spinal canal) with hyper
kyphotic angulation.
2. Loss of normal cervical lordosis.
3. separation of spinous processes at affected level.
N.B. If a vertebral body is displaced forwards by > 1/2 of its AP diameter both apophyseal joints must be
dislocated.

B. Wedge fracture:stable.
1. in anterior vertebral height of involved body.
2. Disruption of anterior cortex of involved body.
3. + haematoma para vertebral soft tissue shadow.
C. Clay shavellers fracture:
Stress fracture of a lower cervical spinous process in coronal plane.

II. Hyperextension injuries:

A. Hyperextension dislocation:

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1. Normal alignment of cervical spine.

2. Diffuse prevertebral soft tissue swelling.
3. Avulsion fracture of anterior aspect of inferior end plate.
4. Vacuum defect: widening of inter-vertebral disc space at the site of injury.
B. Avulsion Fracture of Arch of Atlas. :
Anterior arch: Horizontal fracture with prevertebral soft tissues swelling
Posterior arch: No prevertebral soft tissue swelling.
C. Laminar fracture:
Lateral view: disruption of laminae of lower cervical spine.
D. Extension Tear Drop Fracture:
Typically involves axis.
The fracture segment is located at anterior inferior corner of the body of axis.
E. Traumatic spondylolisthesis: (Hangmans Fracture of axis)
Type I: Isolated hairline
Displace C2 body.
Normal disc space C2-C3.
Type II: Displaced anterior segment.
Abnormal disc space.
Type III: as above
Displaced posterior fragment.

F. Pillar Fracture:
It is vertical fracture of articulmass (pi) resulting from impaction of involved mass by
ipsilateral superior articular mass during hyperextension & rotation.

III. Vertical Compression Injuries:

A. Jefferson Bursting fracture:
Due to symmetrical transmission of force through occipital condyles to superior articular
surface of lateral masses of atlas.
A-P: (open mouth). Separation of fragments where lateral masses of atlas overlap those of axis.
B. Burst Fracture of Lower Cervical Spine:
Lateral view: Comminuted vertebral body
Interruption posterior spinal line.
CT:

Demonstrates vertebral body fracture & posterior arch fracture.

Cord. compression

IV. Atlanto-Occipital Dislocation:

Usually fatal displacement of occipital condyles from superior articular facets of atlas.

Neuroradiology 65

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It is mostly associated with atlanto-axial dislocation.

V. Fracture Odontoid Process of Axis:

Best seen in A-P with open mouth. CT: best demonstration.

Atlanto-Axial Subluxation:
- The maximum normal distance between the cortical margins of the arch of atlas and the odentoid
is 2.5 mm in adults and 5mm in children. In atlanto-axial subluxation and dislocation may cause
acute or slowly progressive quadiparesis.
It may be secondary to:
A)

Separation of odontoid process due to a fracture or congenital anomaly. Fractures of the

dens are common, usually caused by hyperextension injury, which generally fractures the
posterior arches of atlas allowing ring enlargement with no cord compression.

B)

Erosions of the atlanto-axial joint by an inflammatory disease, most commonly Rheumatoid

Arthritis, or occasionally anklosing spondylitis, TB or pyogenic abcess.

C)

Presumed laxity of the joint capsules and ligaments:

In association with laryngitis or pharyngitis especially in children.

A.O. ass

MPS, hypoplasia of dens is seen frequently.

Spinal Tumors
A. Extra dural:
1. Benign:
1. Meningioma
2. Neurofibroma
3. Dermoid
4. Lipoma
5. Extradural cyst, abscess, haematoma.
6. Vertebra: Hemangioma
Osteoblastoma
Aneurysmal bone cyst.
2.
Malignant:
1. Primary vertebral tumors: Solitary myeloma
Chordoma
Chondro-sarcoma
2. Secondaries:

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3.

- breast, lung due to wide venous and lymphatic connections of extradural space.
- lymphoma.
Non neoplastic:
1. Prolapsed disc
2. Spondylosis,
3. Extradural archnoid cyst
4. Pagets disease: by vertical compression of softened vertebra
5. Osteomyelitis
6. Trauma
7. Extra medullary haemopoiesis.

B. Intra dural:
I. Extra-medullary:
1.
Benign:
1.Meningioma,
2. Neurofibroma,
3. Lipoma,
DD with extradural causes
2.
1.

Malignant:
Seedlings of metastatic deposits from glioma or carcinoma via the CSF.

II. Intramedullary:
1.Neoplastic:
1.
Gliomas: astrocytoma,
ependymoma.
2. Haemangioblastoma.
3. Teratoma,

2.
3.
4.
5.

2. Non neoplastic:
1. Syringomyelia
Arnold-Chiari Malformation.
Haematoma
Post radiation myelopathy
AV malformations
Thick dura: Syphilitic pachymeningitis, metastases, mps deposition
Multiplicity: neurofibromatosis, metastases from CNS. metastases from other tumors, meningioma
(rarely).
Radiological Approach:
I. Plain: only in 20% of patients.
A. A-P.
1. Bone destruction and erosion.
2. Destruction of pedicle.
3. Expansion of the vertebral canal (wide I.P.D., thin flat pedicle).
4. Para-vertebral soft tissue mass.

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5. Lateral scalloping of vertebra.

6. Concave medial border instead of being flat or convex
B. Lateral:
1. Concave post. border of vertebral body.
2. A-P scalloping of vertebra
3. Destruction.
C. A-P & lateral:
1. Sclerosis & destruction of adjacent body or appendages.
2. Disc destruction & collapse.
D: Oblique:
Wide, eroded I.V.F (dumb-bell tumor) mainly in neurofibromatosis.
II. Myelography:
A. General:
1. Shows the degree of spinal cord or nerve root compression.
2. Shows the size, shape and limit of the mass.
3. Shows whether the mass is extradural, intradural extra or intra medullary.
4. Distinguishes (with plain & C.P) between tumor and degenerative spinal cord disease.
B. Special: see later.
III. C.T see later.
IV. Spinal angiography:
The spinal cord is supplied mainly by the longitudinal midline ant-spinal artery with is anastomatic
chain between vertebral, deep cervical, intercostal and lumbar arteries.
Spinal angio is done by catheterization of femoral artery and inject through:
vertebral & costocervical trunk (for cervical region),
intercostal (for upper dorsal region),
Intercostal & lumber (for lower region).
V. MRI: Is best method for diagnosis of spinal masses as regards to its site, extent and nature.
Signals as before.
VI. Isotopes:
Intrathecial injection of radioactive agent TC99m DTPA.
Normally within 24h. upward diffusion of agent through subarachnoid space to reach the basal
cisterns is seen by camera. If trace does not reach the cisterns and brain covixity within 24h
suspect obstruction to flow.

Special features:
I. Extra-dural
A. Benign

Plain

Myelography

Usually extension from intradural component

1. Vertical compression of abnormal
softened bone flattening of vertebral body
and constriction of vertebral canal convex
bulging of the vertebral body in lat. View
2. Extradural cyst widening of spinal canal
:

A. Extradural masses (B.M)

1. A-P view: gap is produced by mass
between contrast. column and pedicle.
2. In lat. view displace most of thecal
contrast col.
away from vertebral body or disc.
3. Obstruction. of contrast column flow :

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a. Flattening of pedicle.
b. Thinning
c. Wide I.P.D
d. Scalloping of post. vertebral margin
in lat view

B. Malignant

II. Intradural T. A.
extra-medullary

B. Intra-medullary:
(ependymoma
is
commonest).
in children

Criteria of malignancy :
1. In metastatic disease normal I.V.D
d.d from T.B
2. Erosion of pedicles (or destruction)
3. Abnormal sclerosis of vertebral body
4. Destruction of Vertebral bodies &
appendages
5. Pathology. fracture.
6. Soft t. mass with myeloma
chordoma calcification
7. Cord compression by 1ry vent. tumors
Meningioma :
1. Normal
2. Bone erosion (rare)
3. Flat one pedicle
4. Calcification D.D with calcified
I.V.D.P narrow I.V.D calcifc.
opposite disc osteophytic lipping of
vert. margin.
5. Angioneurofibroma hourglass,
dumb-bell tumor.
a. Bone erosion
b. Expansion of I.V.F (oblique view).
c. Wide vert. (I.P.D)
d. para-vert. Mass
e. Erosion of vert. endo of ribs.
f. Post. scalloping g-scoliosis
Uncommon
1. Fusiform enlargement of the spinal
cord and sometimes of the vert. canal.
2. Ependymoma great expansion and
erosion of lumbo-sacral canal (giant
tu. of cauda equina).
3. Glioma minimal erosion expansion
of the vert. canal due to shorter
history & neurological disability is of
rapid onset.
- It occurs anywhere in the cord.

a. Small mass no obstruction

b. Large mass complete obstruction
horizontal cut off contrast column at
level of lesion.
In lateral view , the edges are seen
serrated by the compressed N. roots
B. extradural cyst :
The dye may entered & remain in cyst
cavity while the remaining subarach.
contrast travel through spinal canal on
tilting bde

Both meningioma & neurofibroma

produce the same myelographic picture.
The cord is normally outlined occupying
central half of contrast column. Intradural
extra-medullary tumors
1. Displacement of cord within theca
to opposite side away from tumor
2. Spinal block
a. Complete: concave cut off of
column, as the capsule of tumor is
outline by contrast.
b. Incomplete: the contrast flow
round and outline with of tumors.
Dural ectasia in neurofibromatosis

Can distinguish between extra & intramed masses

- Myelogram shows
1. Fusiform enlarg. of the cord &
vert. canal.
2. The cord is central in column and
is not displaced.
3. The contrast column is in normal
in relation to pedicles equidistant
4. Obst. to flow of the omnipaque
partial complete dilated vessels
on surface of the cord.

N.B.Meningioma:
Angio nidus which is central with radiating vessels (star) vascular blush.
N.B. Calcification is like small gr& usually dat the periphery.

Role of C.T in Spinal tumors: with or without intra-thecal contrasts.

1. Bony affection: Erosion, destruction, fracture.
2. Preserved of para vertebral soft tissue mass.

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3. Mass as regards to: site of origin, (extra-dural, extra-medullary, intra medullary), nature (density)
4. Density by CT:
a. High attenuation: Meningioma, haematoma, calcifications.
b. Low attenuation: Lipoma, cystic disease, congenital tumors.
c. C-S.F attenuation: Syringomyelia, hydromylia.

Neurofibroma
-

Familial, AD, equals in both sexes

Origin: neurolemal + fibrous tissue elements of nerves (peripheral nerves, Cranial ns 5, 8)

- Gradual onset , progressive painless swelling.
Types : 1- Generalised = Von Reckling Housens
- multiple tumors from many nerves (cutaneous , muscular, spinal (post nerve
roots) & cranial sp.5-8)
- cafe au lait patches
- no sensory or motor paralysis, if found

sarcomatous change ( Neurofibro sarcoma ) + Painful

2- Solitary neurofibroma .
3- Acoustic neuroma ( 8th CN ) deafness & ICT
Plain X-ray findings:
i. Bone erosion (DD with meningioma.)
ii. Scalloping of posterior border of vertebral body.
iii. Expansion of inter-vertebral foramina.
iv. May expand into para-spinal mass called hourglass or dumb bell tumor. It may then
cause splaying apart or erosion of vertebral ends of ribs.
v. Expansion of spinal canal (widening of inter pedicular space & thinning of pedicles).
vi. Myelogram: same as meningioma except for lack of sex or site preference &
calcification.
vii. Occurrence in cauda equina giant tumor of cauda equina.
CT:
- Neurofibroma is larger than meningioma, occurs at any level with erosions.
- No calcifications (meningioma: califications at the periphery).
- IV contrast: enhances of the tumor more than in meningioma.
- Both tumors: Flat cord and displaced, widening of the subarachnoid space.
MRI:
- 2/3 are intradural and the rest are either entirely extradural or having an extradural componant.
Low on T1 and high on T2 and enhances on Gd injection.
- Upper & lower borders are outlined against extradural fat behind spinal cord after gadalium
tumor enhance & its outer border is compressing dura is evident.
Associations : *MEN IIb

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* Carcinoid tumor
* Gardners syndrome ( Familial polypi + Osteoma )
* Tarcots syndrome
Complications: 1- infection

2- cystic change

3- malignancy

4- pressure effects e.g. Acoustic neuroma

SYRINGOMYELIA imp
Partial mechanical obstruction to C.S.F outflow from 4th ventricle thus C.S.F is funneled into upper
part of central canal of spinal cord (instead of passing into cisterna magna) leading to cystic
cavitation of the cord. Hydrocephalus is unusual.
Causes of foramina obstruction:
1. Chiari malformation (90%) with downward prolapse of cerebella = tonsils through foramen M.
2. Basal adhesive arachnoiditis (1/3 of cases).
3. Dandy-Walker syndrome.
Syringomyelia behaves like intra medullary tumors (cystic degeneration & gliosis in the central
canal leading to cord expansion).
Radiological appearance:
1. Plain film is normal is most cases.
2. Thinning of pedicle and widening of inter pedicular distance.
3. +ve contrast myelogram:
a. Prone expanded cord with free flow of myodil (usually cervical).
b. Supine outlining of herniated cerebellar tonsils.
4. Air myelogram: phenomenon of the collapsing cord
Head down: Cx cord appears swollen (cavity full with fluid).
Head up: Cx. cord appears thin (cavity empty).

ANGIOMA
A.V malformations usually on dorsal aspect of the cord
Pt usually presents with progressive cord malacia.
Radiological appearance:
1. Plain film: normal.
2. Myelogram: tortuous serpiginous linear defects in the opaque column extending over several
segments (mainly due to dilated feeding arteries & draining varies).

Hydromyelia:
It is a simple dilation of the central canal of the spinal cord. It may communicate with the fourth
ventricle with or without imperforate foramen of Magendi. It is a congenital lesion usually
associated with:
Chiari II malformation manifest dysraphism (if hydrocephalus has responded to treatment).

Neuroradiology 71

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Or

Congenital lesion leading to fourth vent dilation Dandy-walker syndrome (especially if

hydrocephalus has not been adequately treated in infancy).

- Hydromyelia extends from and usually is confined to lower segment of spinal cord. It may be
associated with occult spinal dysraphrism especially diastematomyelia.
- The cord does not expanded as the surrounding gray & white matter are atrophic. The size of the
cord may change with posture, with the patients head down the cord is normal or enlarged, or
the patients head up ribbon like.
Radiological Appearance:
Plain film:
It is impossible to distinguish between syringo or hydromyelia and an intra-medullary tumor on
plain film unless there are associated developmental abnormalities such as:
basilar impression
occipitalization of atlas
fused cervical vertebrae
- Widening of spinal canal usually due to Arnold-Chiari malformation.
CT: delayed C.T scan revealed pooling of C.M. into spinal cord by diffusion effect.

ARACHNOIDITIS:
Infiltration of the meninges with chronic inflammatory cells and fibrosis.
Causes:
1.

Chemical damage to meninges by: Myodil, Ionic C.M, Spinal anesthetics.

2. Subarachnoid Hemorrhage
3. Infections: pyogenic, TB, B, sarcoidosis.
Myelography:
1. Shortening & incomplete filling of nerve root sheaths.

2.

The sacral cul de-sac is shortened and the outline of the theca is smooth.

3.

Nerve roots in cauda equina is adherent to each other single irregular longitudinal
structure.

4.

Irregular opacifications of the subarachnoid space.

Paraspinal soft tissue shadow (Posterior mediastanal mass)

Usually in the dorsal region, It may be desc. aorta especially if tortuous if it is on the side.
1. Neural lesions: Extradural cyst, hygroma or myelocele, neurofibroma and ganglion neuroma.
Scalloping of posterior margin of vertebral bodies.
Increased interpedicular distance.
Enlarged intervertebral foramen.
Widened intercostal space.
Sympathetic chain tumors

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2. T.B of the Spine:

Fusiform, involving many segments.

Collapsed intervertebral space & vertebral body

Calcification in the adjacent soft tissues.

3. Extra Medullary Haemopoiesis:

Chronic anemia.

Abnormal bone pattern is most marked in hands.

4. CT tumors:

Lipoma, fibroma.

5. Loculated Pleural Effusion:

Lateral view characteristic

Mediastinal effusion mediastinal widening.

6. Sequestrated Lung segment:

Triangular, usually Left sided.

Blood supply from Descending Aorta.

May rupture into bronchus fluid level.

7. Aneurysm of Descending Thoracic Aorta:

Erosions of antero-laterial aspects of vertebral bodies.

Marginal calcifications.

8. Hiatus hernia: (fixed): Bochadalek hernia, pseudopancreatic cyst.

Fluid levels

Lateral view in front of the spine.

9.Metastasis & multiple myeloma:

Vertebral osteolytic and sclerotic reaction.

Vertebral body collapse.

DD of collapsed vertebra (vertebra plana):

(this part was in orthopedic old papers)

I. Neoplastic diseases:
A. Metastasis: breast, bronchus, prostate, kidney .
Incidence: accounts for majority of patients with a solitary spinal metastasis.
Type: Lytic, scleroor mixed
I.V.D are preserved. Associated pedicle destruction.
B. Plasmacytoma :
The vertebra is a common site of plasmacytoma.
- May mimic an osteolytic metastatic lesion expansile & resemble an neurysmal sipt.
- Intact I.V.D spaces.
- Associated para verterbral soft tissue shadow.
C. Lymphoma:
Types: as metastasis.

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-Intact I.V.D.S.
Associated features: involvement of other bones i.e. pelvis.
D. Benign tumors:
1. Haemongioma.
2. Aneurysmal bone cyst.
II. Trauma:
1. Discontinuity of trabeculae.
2. Sclerosis of the fracture line.
3. Disc space usually preserved.
4. Usually no soft tissue mass.
III. Osteoporosis:
- Reduced bone density
- Vert. body may be wedged or biconcave (fish shapes)
IV. Infection:
Destruction of end plates adjacent to destroyed disc.
Pyogenic

T.B.

1. Rapidly progressive.

1. Slower

2. Marked sclerosis

2. Less sclerosis

3. Less vert. collapse.

3. Marked collapse

4. Small or no para-vert. abscess.

4. Large P.V. abscess.

5. Early bridging of affected vert.

5. Not early

IV. Histocytosis:
1. Eosinophilic granuloma is most common causes of solitary vertebral plana in a childhood.
2. Affected vert. body tends to bulge laterally.
3. Para-vert-soft tissue shadow.
4. Disc spaces remain intact & may be widened.
VI. Sickle - cell anemia:
- Generalised depression of central portion of the vertebral plate.
- Sometimes, depression is flat & sides slope obliquely
VII. Scheuermanns disease:
1. Irregular end plate.
2. Numerous schmorls nodes in thoracic spine.
3. Disc spaces narrowed.
4. Degenerative changes.
5. Progressive to sever kyphosis

Erosion, destruction of a pedicle :

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1. Metastasis; Early involvement of pedicle in metastatic carcinoma.

Late involvement multiple myeloma.
2. Multiple Myeloma .
3. Intra-spinal mass with widening of I.P.D
4. T.B with a large para vertebral abscess.
5. Aneurysmal bone cyst.

Solitary dense pedicle:

1. Osteoblastic metastases no change in size.
2. Ost. osteoma.
3. Osteo-blastoma.
4. 2ry to spondylolysis.
5. 2ry to congenital absent contra-lateral one.

Enlarged vertebral body:

Generalized: gigantism, acromegaly
Localized: (single or multiple)
Pagets disease, Aneurysmal bone cyst, haemangioma, Hydiatid.

Squaring of one or more vertebral bodies:

1. Ankylosing spondylitis

2. Pagets diseases.

3. Psoriatic arthropathy

4. Rheumatoid arthritis.

Block vertebrae:
1. Isolated congenital:
- Failure of segmentation, the ring epiphyses of adjacent vertebra dont develop
resulting a large AP diameter.
- Most common in the lumbar region.
- The articular facets, neural arches, spinous processes may be involved.
2. Klippel - Feil syndrome (cervical)
2. Rheumatoid Arthritis spinous processes dont fuse.
3. Ankylosing spondylitis
4. TB
6. Post traumatic or operative union.

Ivory vertebral body: Imp

Neuroradiology 75

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Single or multiple very dense vertebrae

1. Metastasis: as before (osteoblastic).
2. Pagets disease.
1. Lymphoma.
2. Low grade infection.
3. Haemangioma.

I.V.D. Calcifications: Imp

1. Degenerative spondylosis.
2. Alkaptonuria:
widespread disc calcification, osteoporosis, disc space narrowing & osteophyosis.
4. Ankylosing spondylitis: Square vertebral bodies + syndesmophytes.
4. Gout.
5. Haemochromatosis.
9. Idiopathic: A transient phenomenon in children.

Anterior vertebral body beaks: Imp

Central: Morquios syndrome (MPS)
Lower 1/3: Hurlers syndrome
Achondroplasia.
Cretinism.
Downs syndrome.

Widened I.P.D: flattening of inner side of pedicle

1. Meningomyelocoele:

Fusiform distribution of widened I.P.P.

Narrowed I.V.D.S.

Spinous process & laminae are not identifiable

scoliosis in 50-70%.

2. Neurofibromatosis.
3. Intra-spinal mass : esp. ependymona.
4. Diastematomyelia.

Intradural, intramedually spinal masses: (oral)

1. Syringomyelia

2. Tumor

Neuroradiology 76

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a) Chiari Malformation confirms diagnosis

b) No bony abnormality

Bone erosion & expansion. More marked

with Ependymoma than Glioma.

c) No dilated vessels on the surface of the

cord.

c) Dilated vessels on the surface of the cord

with complete obstruction.

d) Smooth outline of the cord.

d) Irregular outline of the cord.

3. Haematoma: caused by contusion of the cord.

4. Post-radiation myelopathy: may cause symmetrical expansion of the cord.
Atlanto-Axial Subluxation:
When the distance between the posterior aspect of the anterior arch of atlas and the anterior aspect
of odontoid process exceeds 3cm in adults & 5mm in children.
1.

Trauma

2.

Arthritides: Rheumatoid arthritis, psoriatic arthritis, SLE, ankylosing spondylitis

3. Congenital: Downs syndrome, Morquios syndrome, congenital hypoplasia or absence of
Odontoid

SCOLIOSIS:
A. Idiopathic:
1. Infantile: before 4 years of age, 90% are thoracic and concave to the right.
90% resolve spontaneously.
2. Juvenile: 4 to 10 years of age, more common in females, progressive.
3. Adolescent: more common in females, majority are concave to left in thoracic region.
B. Congenital:
1. Failure of formation:
a.

Incarcerated hemivertebra: straight spine

b.

Free hemivertebra: progressive

c.

Multiple hemivertebra.
On the same side severe
Hemivertebra on opposite sides may composite each other.

d.

Central defect: butterfly vertebra.

2. Failure of segmentation:
a. Bilateral Block vertebra.
b. Unilateral unsegmented vertebra.
Severe progressive curve with kyphosis or lordosis depending on the position of bar.
3. Mixed: e.g. at unilateral unsegment bar + hemi-vert.
Indications of Serious Progression are:

Neuroradiology 77

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1. Deformity present at birth.

2. Sever deformity of chest wall.
3. Unilateral unsegmented bar.
4. Thoracic abnormality.
C. Neuro-Muscular Diseases:
1. Myelomeningocele.
2. Poliomyelitis
3. Cerebral palsy
4. Muscular dystrophy.
D. Mesodermal & Neuroectodermal Diseases:
1. Neurofibromatosis classically a sharply angled short segment. Scoliosis with severe kyphosis.
2. Marfans syndrome typical double structural curves.
E. Post-Radiotherapy:
Wedged and hypoplastic vertebra.
F. Painful Scoliosis:
1. Oste. Osteoma.
2. Osteoblastoma.
3. Intra-spinal tumors.
4. Infection.

Lucency in skull vault with no surrounding sclerosis:

A. Adult:
1. Neoplastic:
a. M. Myeloma: punched out appearance
affects the mandible.
b. Metastasis; usually, irregular & ill defined.
c. Hemangioma; may have soap bubble or Hair-on-end appearance.
d. Neurofibroma; usually at occipital bone.
e. Adjacent malignancy: e.g. rodent ulcer.
2. Traumatic: burr hole very well defined.
3. Idiopathic:
a. Osteoporosis circumscripta; occurs in active Pagets
b. Sarcoidosis
4. Metabolic; Hyper parathyroidism pepper- pot skull
5. Infective:

Neuroradiology 78

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a. T.B. rarely produces punched out lytic lesion

b. Hydatid.
c. Syphilis: moth-eaten appearance.
B. Child:
1. Neoplastic:
a. Metastatic. e.g. neuroblastoma, leukemia
b. Histiocytosis X.
2. Traumatic:
a. Leptomeningeal cyst.
b. Burr hole.

Lucency in skull vault with surrounding sclerosis:

1. Fibrous dysplasia.
2. Developmental:
a. Epidermoid: scalloped appearance within sclerotic margins. Expansion to both inner and
outer tables. Commonly in squamous portion of occipital or temporal bone.
b. Meningocele: smooth margin with overlying tissue mass.
3. Neoplastic;
a. Haemangioma rare with sclerotic margin
b. Histiocytosis X. in healing phase.
3.

Infective:

a.

chronic osteomyelitis

b.

frontal sinus mucocele.

Multiple lucent lesions in skull vault :

a. Neoplasm: metastasis, m. myeloma & histocytosis.
b. Osteomyelitis.
1. Acute: multiple, small ill defined lucencies associated frontal sinusitis, scalp wound or
infected bone flap. No surrounding sclerosis.
2. Chronic: sclerosis.
c. Avascular necrosis of bone flap: identical appearance to acute osteomyelitis.
d. Radiotherapy.
e. hyperparathyroidism,

f. Sarcoidosis.

Generalized increase in density of skull vault:

1. Pagets disease.
2. Sclerosing metastasis.

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3. Fibrous dysplasia.
4. Myelosclerosis: spleenomegaly.
5. Renal osteodystrophy.
6. Fluorisis: mottling of the tooth enamel, axial skeleton is most frequent site.
7. Acromegaly.
8. Chronic haemolytic anaemia.
9. Congenital: a) osteopetrosis; bone-in-bone appearance.
b) pyknodysostosis: wormian bones especially in base + wide sutures.

Increased density of skull base

A. Localized
1. Fibrous dysplasia,
2. Meningioma
3. Sclerosing metastasis.
4. Chronic mastoiditis.
B. Generalized:
1. Pagets
2. Fibrous. dysplasia
3. Other causes of general increase in bone density

Hair on end Skull vault:

1. Chronic hemolytic anaemias: thalassaemia, sickle cell
2. Neoplastic: hemangioma, meningioma, metastasis, osteosarcoma
3. Others; congential heart disease d.t. erythroid hyperplasia
4. Iron deficiency anaemia: severe form

Large head in infancy:

1. Hydrocephalus.

5. Neurofibromatosis.

2. Chronic subdural haematoma

6. Achondroplasia.

3. Megalencephaly

7. Hydranencephaly

4. Storage diseases.

Wide sutures:
Birth to 1 month suture width > 1cm, after > 3 month suture width > 3mm
1.

I.C.P: S.O.L, Hydrocephalus,

2.

Infiltration of suture: Neuroblastoma, leukaemia, lymphoma

3. Defective ossification: Rickets, renal osteodystroph.

Arachnoid cyst:

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Arachnoid

Perineural

Extradural

Intradural

Herniation of arachnoid via

Duplications of arachnoid or

In relation to dural ostea of

dural defect ; surgical or

abberent

of

spinal nerves commonly at

traumatic

subarachnoid spaces usually

S2, S3 of large erosion of

thoracic congenital

related

septations

neural

canal

(DD

neuro fibromatosis)
N.B.: Arachnoiditis: arachnoid matter is devoid of blood vessels so, no inflammation can occur. However, inflammatory process
involves subarachnoid space & pia matter to with arachnoid becomes adherent via organization of the exudate.

On myelography :
1. Complete black with irreg. configuration
2. Smooth featureless thecal sac in which the roots or root sleeves are visible
3. Irreg. opacification of subarachoid space
4. Thickened roots or nor filling of sleeves.

Expanded Pituitary Fossa:

Normal size:
Height: 6.5-11mm
Length: 9-16mm, = 14 AP.
Breath: 9-19mm
1. I.C.P: due to dilated 3rd ventricle.
2. Intra-sellar masses.
3. Para-sellar masses.
4. Empty sella syndrome.
5. Nelsons syndrome

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ORBIT
- A.P. diameter (globe) = 22 mm, optic nerve thickness = 4mm
- Conal = structure inside muscle gp of eye, extraconal lesion will be outside as lymphoma
- Lamina paparecia is lateral wall of ethmoid sinus & medial wall of orbit along which inflammation
of ethmoid sinus extends to orbit
How to think on a film ?
- Child: retinoblastoma, rhabdomyosarcoma, metastases from neuroblastoma, optic n. glioma
- Adult: haemangioma, orbital meningioma
- Old age: lymphoma, pseudotumor, metastases
~ Special features: pulsation (AV malformations aneurysms)
increase on straining (orbital varices), thyrotoxic
Investigations:
1-PXR
2-CT: location of lesion if orbital, paraorbital and demonstration of calcifications+enhancement
3-Ultrasound + doppler
4-MRI
5-Orbital venography + carotid angiography

DD of optic nerve enlargement:

1- Optic nerve glioma (90%)
2- Optic nerve meningioma (10%)
3- Optic neuritis: diffuse, smooth expansion of optic nerve +CT e C: may show tram-tract sign .
4. I.C.P widening of subarach. space around optic nerve.
5. Pseudo-tumor in w control trial of steroids should be done, chronic inflammation.
6. Secondary to: lymphoma, retinoblastoma, T.B, toxoplasmosis.
NB: dd is difficult & sometimes biopsy is needed

DD of unilateral exophtalmos: (Proptosis):

1- Intra-cranial lesions
1.Orbito-sphenoidal meningioma2245:2ry orbital meningioma w is orbital extension of
meningioma at greater wing of sphenoid (commonest origin), or from suprasellar or floor of
anterior cranial fossa, it is ccc in CT by hyperostosis of lat. wall & roof of orbit + marked
enhancement after Gd-EDTA injection in T1w images.
2.Glioma, infra-clinoid aneurysm, C.S.Thrombosis

2- Lesions of PNS or nasopharynx

1.Mucocoele of frontal sinus extending inferiorly
2.Neoplasms as carcinoma of PNS osteoma
3. Dermoid causing expansion of superolateral part of orbital roof, bone defect expanding +
sclerotic margin by PXR and CT show fat attenuation.

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3- Thyroid disease commonest cause 15 %

Grave's orbitopathy2238: CT + MRI findings:
1-Bilateral symmetrical or unilateral enlargement (less common) of recti muscles,
enlargement of medial rectus will cause indentation on medial orbital wall.
2- Enlargement (fusiform) involves belly of muscle rather than origin or insertion (dd pseudo
tumor of muscle)
3- In minority of cases increase fat content of orbit with little or no muscle affection
forward displacement of eye ball, intraconal space, angulation of lat. rectus ms

4- Downward displacement of opthamic vein (coronal view) d.t. sup. rectus++

4- Intra orbital S.O.L:

1- Vascular anomalies:
1- Ophthalmic artery aneurysm is rare & mostly at junction of ophthalmic artery e ICA
2- AVM: uncommon, either congenital or following trauma to anterior orbit
C/P: pulsating exophthalmos + audible bruit
Carotid angiography: external + internal is essential to diagnose feeding vessel (may be ECA)
3- Haemangioma: (commonest retrobulbar intraconal tumor in adults)
1.Capillary in infants causing unilateral exophthalmos often e superficial capillary neavus

Carotid angiography: fine vascular network + diffuse pathological circulation

2.Cavernous in adult it is benign encapsulated neoplasm or hamartoma within muscle cone
to dd from venous malformation.
CT: well demarcated mass e rounded margin, lateral to optic n. + ccc intense C.
Carotid angiography: venous pools within ms cone in both capillary & venous phase
4- Orbital varices:
a) Primary
1. Congenital venous malformation:
- Proptosis since birth or early childhood w by in venous pr. of head on straining
- Associated venous anomalies in scalp on same side + anywhere in body.
- PXR: gross orbital enlargement (as since birth) + phleboliths + prominent vascular markings
- CT: phleboliths (intraconal & extraconal) - rounded mass (intraconal or extraconal)
2. Traumatic varices: d.t. tear in sup. pphthalmic vein w is best seen by orbital venography
b) Secondary: Carotico-cavernous fistula - Dural AV shunt in middle cranial fossa - Intracranial AV
malformation in anterior/ middle cranial fossa best demonstrated by carotid angiography.

2. Tumors of orbit:
1- 1ry orbital meningioma - Orbito-sphenoidal meningioma(see before):
~ Meningioma of optic nerve sheaths:
- From meningioblatic rests in dura matter covering optic nerve, it cause proptosis before
compression on optic n. (it doesn't infiltrate it) + decrease VA + constriction of field of vision.

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a) PXR:
1- Localized / generalized orbital enlargement
2- Hyperostosis of orbital walls
3- Changes in adjacent sinuses: pneumosinus dilatans2250: it is a sign of presence of occult
meningioma when detected on plain film you must go to CT or MRI occurs in form of abnormal
dilatation of one of PNS containing only air & lined by normal epithelium.
Commonly seen in sphenoid sinus in cases of meningioma of tuberculum sellae or planum sphenoidale

b) CT:
1- Before C: diffuse enlargement of optic nerve + thickenned
2- Marked contrast enhancement (> optic glioma) after C injection
3- Optic canal narrowed if hyperostosis is present or optic canal enlargement in cases of invasion.
4- Calcifications (psammomas) mau be visible along course of optic nerve.
5- Must look at intracranial portion of optic nerve to exclude extention.
c) MRI: low on T1 & T2 with strong enhancement after Gd-EDTA, excellent to show
extension through optic canal, fat suppression technique could be used for better
evaluation.
1- Optic Nerve Glioma

2- Meningioma

i) Age: child, male

i) Age: adult, female
ii) CT:
ii) CT:
a)Margin; Well defined
a)Margin;> infiltrative. Tubular thinking or fusiform enlargement.
b)Calcification; rare
b)Calcification; common.
c)Orbital hyperostosis; None
c)Orbital hyperostosis; Present
d)Enhancement; mottled d.t. mucin deposition
d)Enhancement; Diffuse, homogenous
e)Optic Nerve; kinking of optic nerve
e)Optic Nerve; Straight optic nerve.
f) Opic canal; widened 90%
f)Optic Canal; widened 10%
g) Associated neurofibromatosis; 25% NF1
g) Associated neurofibromatosis; rare NF1

2- Retinoblastoma
-AD, most common intra-occular malignancy in childhood arise from retinoblast & in 1/3 of
cases is bilateral
-Age: 18 m
a) Ultrasound:high echogenic mass e shadowing in posterior globe + doppler: increased flow
b) CT: diagnostic procedure & only 10% of retinoblastomas lack calcifications, it is seen
as a partially calcified intra-occular (intra-conal) mass involving retina which shows marked
contrast enhancement & thickening of optic nerve may indicate extension of tumor to the
perineural subarachnoid space
c) MRI: high T1 & low T2 (opposite to normal) & it is the best in evaluation of transscleral or
perineural spread
- In absence of dissemination; enucleating & radiotherapy may be curative but extension into
predicts a very poor prognosis & recurrence rate is high, must look in all familly members.
3-Malignant melanoma 2233
- >50 yrs, usually unilateral
a) U/S: mass causing scleral thinning + >1mm elevation + doppler
b) CT + MRI: post globe affection, high T1w, low T2w signals.
c) Bone scan could be done to evaluate metastasis to long bones + liver + lung.

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4-Rhabdomyosarcoma
-Rare, muscular malignant orbital tumor in children
-Cl/p: rapidly progressive exophthalmos + superficial swellings of eyelids & canthi
a) PXR: progressive enlargement of orbit +/- bone destruction e extension to temporal fossa, PNS.
b) CT+MRI: bulky tumor mass with anterior location in orbit involving an extra-occular muscle
(isodense on CT ) & may extend intra & extraconally + strong enhancement
+ bone destruction + extension to infra-temporal fossa & cranial cavity.
5- Lymphoma
- Non-Hodjikin lymphoma, from anterior orbit outside muscle cone, > 50 yrs.
-CT: mass in anterior orbit extraconal in position enveloping globe, no bone erosion
ressembles rhabdomyosarcoma.
- DD: pseudo tumor metastasis Myeloma.
6- Metastasis
- From neuroblastoma (w is the commonest cause of proptosis in children + Histocytosis X),
Ewings, Wilms & leukaemia in children
- Osteolytic lesions are commonly seen, osteoblastic from cancer prostate, breast, lung & stomach
(in elderly)
- DD: pseudo tumor metastasis Myeloma - rhabdomyosarcoma.
a) PXR: ill defined lesions with osteolysis or sclerosis of orbital bones
b) CT: bone involvement, soft tissue mass, extra ocular muscles may be involved especially
medial rectus ms, marked contrast enhancement
7-Neurofibromatosis
- Enlarged orbit + optic canal (associated optic nerve glioma in NFI)
- Elevation of sphenoid ridge to level of orbital roof , MRI: intermediate signal in T1 & T2.
- May cause large defect in greater wing of sphenoid (lost boundary of orbit): encephalocele
leading to pulsating exophthalmos d.t. transmission of cranial pulsations to orbital contents
called: "bare orbit" of neurofibromatosis on P.A view
8-Dermoids & epidermoids
- Dermoid is cystic (may contain fat, cholesterol & hair)
- Epidermoid is solid mass of desquamated cells with a capsule, site for both:
1)diploe of skull expanding both inner & outer table, sharply demarcated bone defect of skull
with well defined sclerotic margin
2)in orbit arise from supero-lateral quadrant (commonest), or from medial part of orbital roof
-CT: dermoid gives localised area of low attenuation of fat (-50 to -150 HU) superficially
located periorbital dermoids give shallow localised indentation on orbital rim.
9- Lacrimal gland tumors
a) Benign: pleomorphic ademona: local enlargement of lacrimal fossa without bone erosion
b) Carcinoma: in 50% may cause only local enlargement of lacrimal fossa without bone invasion
-CT show signs of malignancy: bony invasion & sclerosis of adjacent bones of lacrimal fossa,
calcification (diagnostic) in the tumor, extension of mass outside the fossa (intracranially)
c) Lymphoma: elderly, CT shows mild enlargement of the gland + no bone erosion.

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3- Inflammatory conditions of orbit:

a- Acute infection:
- Acute cellulitis of orbit 2ry to sinus infection esp. ethmoid & maxillary or 2ry to dental abscess
a) PXR: sinus infection - gas fluid level within orbital soft tissues (abscess)
b) CT:

1- Assoc. sinus infection + fluid level in sinus (to diff. preseptal cellulitis from orbital cellulitis)
2- Widening of extraconal space between ethmoid & orbite d.t. edema or abscess formation.
3- Local rectal muscle enlargement (extension of inflammatory process)
4- Soft tissue gas with or without fluid level
5- Ring enhancement after IV contrast suggest abscess formation.
b- Chronic infection ( Pseudo-tumors = Idiopathic orbital inflammation )2039:
- AD, unknown cause, most common cause of an orbital mass in adult
- Unilateral, resembling clinically orbital tumors & Grave's from w it is differentiated by
pathological examination and giving response to steroid therapy (very imp!).
-site: in order of frequency: lacrimal gland, extraoccular ms, sclera, optic nerve and fat
a) PXR: only clouding of nasal sinus d.t. infection or nasal polyp.
b)CT:
1- Loss of def with surrounding; infiltrative lesion e irregular ill defined edge of variable density
2- May show extraoccular ms enlargement; ant. portion (dd from Graves disease is by the fact
that IOI involves lacrimal gland, extraoccular ms tendinous insertions, sclera, optic nerve and
fat + usually on one side + normal thyroid fnc)
3- Markly enhancing enlarged optic nerve and sclera.
c)MRI:
- Like CT, low T1 & high T2 MRI signal intensities as Grave's (versus fat & muscle), thickened
sclera, enlarged optic nerve, sometimes simulating a mass.

Hyperostosis in orbit:
1. Meningioma.
2. Sclerosing metastasis eg neuroblastic reduced size of orbit.
3. Fibrous dysplasia: reduced size of orbit.
4. Pagets diseases.
5. Osteopetrosis.
6. Chronic osteomyelitis adjacent to ch. infected frontal sinus.
7. Tumor of lacrimal gland.
8. Radiotherapy.

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PARA NASAL SINUSES

* Radiological signs of sinus disease :a)soft tissue densities
-plain

usually appear as well defined margins (either scalloped or rounded) parallel to

edge of sinus
usually seen in antra

-CT

will show soft tissue as density attached to bone & replacing air in sinuses

b)loss of translucency
-vary from a minimal loss to complete opacification
-to estimate degree of opacification compare with that of opposite side or adjacent orbit
c)fluid level
-may be seen in any sinus (mostly in antrum) except ethmoid
d)deviation of nasal septum
-anterior deviations are clinically diagnosed
-posterior deviations will be demonstrated on O. M or CT
-associated soft tissue masses due to edema of nasal mucosa or nasal polyps
e)alteration of bony contours
-pressure from soft tissue mass
-interruption of a contour may be seen with a fracture
f)alteration of bony density
1.bone may be thin or destroyed by

pressure from benign lesion

infection & malignant lesions

2.absent bone

surgical

3.increased density

generalized disease

Pagets disease
fibrous dysplasia

localized disease

chronic infection
adjacent malignancy

g)increased translucency from

1.absent bone
2.air in an unusual site

orbit from a blow-out fracture

overlying soft tissues

3.normal variation
Inflammatory diseases of sinuses :-

-sinusitis is an inflammatory reaction of sinuses with hyperaemina & exudate in response to

infective, physical or chemical agents & it is either acute sinusitis or chronic sinusitis
-causes

accumulation of sero-purulent secretion

if ostium is blocked
when infection subside

empyema & extensive mucosal destruction

fibrosis & mucosal artrophy

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-acute sinusities is either

2ry bacterial infection following an upper respiratory tract infection

of viral origin
in maxillary sinus

infected tooth

-primary site of infection is mucosal lining of sinus & accompanying swelling of mucosa will show
as an opaque rim (due to out pouring of fluid into sinus cavity) around periphery of sinus
-opaque sinus on plain x-ray (differential diagnosis blood or new growth) & fluid level
NB :@ acute sinusites = thick mucosa + fluid level + osteomeatal complex
@ chronic sinusites = thick mucosa + obliteration of sinus cavity + bone density
-radiological signs (plain CT MR-T2)
fluid level
-an acute sinusits causes air-fluid level in sinus with pain, fever & localized tenderness
-fluid may be seropurulent, blood or CSF
-differential diagnosis

after trauma with or without treatment

after nasal packing
after dural tear (air-CSF level)

mucosal thickening
-it is measured as distance between medial edge of lateral soft tissue shadow & lateral wall
of antrum & if > 7mm thickness it is usually associated with purulent fluid
rounded densities in antrums
-well defined with rounded or scalloped margins
osteo-meatal complexes, nasal septum & conchae
loss of bone density
-commonly in ethmoid & the cause is
1.mucosal thickening contrast between soft tissue & bone
2.resorption of bone from hyperaemia of mucosa
increased density of bone
-seen with chronic sclerosing sinuisits
-complications of sinusites
I. obstructive (mucocoeles)

mucocoele = expansion with no destruction

mucocoele of frontal sinus :

-site

most common in frontal sinus (rare or never in antra)

-pathology
obstruction of ostium of sinus

trapping of mucous secretion

pressure effect on bony wall

causes of obstruction

previous inflammatory disease

osteoma
metastasis

distension of sinus

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-clinical picture

frontal headache & proptosis

-plain x-ray
soft tissue mass within one half of frontal sinus, bulging across the midline with a convex
outer margin, out lined against air in other half of sinus
erosion of upper medial half of orbital margin
expansion of sinus cavity characteristically causing loss of scalloped margin of the
normal sinus wall
forward bulging of anterior wall of sinus
thinning of walls of frontal sinus
sinus is more opaque than normal due to fluid in its cavity
-CT

(in axial & coronal cuts show full extent of expansion)

soft tissue mass with no enhancement

adjacent bony changes
+ displacement of globe
may shows obstruction cause

osteoma(well defined area of bone density within sinus)

bone destruction (carcinoma)

-MRI
optimum technique for demonstration of mucocoeles
low T1 & high T2 (the most usual)
total absence of enhancement confirms the fluid content
mucocoele of sphenoid sinus :
-clinical picture

sever intermittent frontal & orbital pain (headache)

occular signs

-plain x-ray
lesion expands sphenoid sinus resulting in elevation or destruction of floor of sella on
lateral skull film
progressive expansion

erosion of medial wall of optic canal

elevation of plannum sphenoidale

-CT

typical rounded or partially rounded expansion of sinus (differential diagnosis is the

malignancy which causes bone destruction)

mucocele of ethmoid sinus :
-clinical picture

(it involves anterior group)palpable mass at medial canthus

-radiologically (plain & CT findings)

opaque ethmoids with loss of their translucency & extension into orbit on plain films
expansion is best seen on CT

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II. orbital complications

-Infection following acute sinusitis (commonly follows ethmoidites as being near)
channels

via venous

inflammatory edema, orbital cellulites & abscess, subperiosteal abscess,

cavnernous sinus thrombosis

- Radiologically

loss of areation of affected sinus, bone destruction, soft tissue opacity

on affected side

CT demonstrate

abscess formation(soft tissue mass in medial or supero-medial orbit

sometimes accompanied by presence of gas or fluid level)
bone destruction

III. osteomyelitis & osteitis

-osteitis is an infection of compact bone & osteomyelitis is an infection of diploeic bone
-radiologically

usually follows an empyema which may rarely lead to bone involvement

with loss of outline of sinus wall followed by frank osteolysis & sometimes bone sequestration
-site

commonest are maxillary & frontal sinuses

IV. intracranial complications

meningitis - extradural abscess - brain abscess

Differential diagnosis of opaque maxillary sinus : imp

a) Technical

rotation of patient
under exposure

b) Outside antrum

overlying soft tissues swelling

Pagets & fibrous dysplasia (bones)

c) Congenital & developmental

fibrocystic disease (mucovisidosis)

Kartageners syndrome
cysts of dental origin
small antrum (hypoplasia)
+ chronic haemolytic anaemia

d) Inflammatory

acute & chronic sinusitis (infected mucocele)

allergic polypoidal mucosal thickenings & cysts
antro-choanal polyp
TB & aspergillosis

e) Trauma

orbital blow-out fracture

post operative washout
antral haematoma
fascial fracture

f) Neoplasm

Carcinoma of antrum, lymphoma, inverted papilloma, ivory osteoma,

plasmacytoma osteosarcoma & metastasis

g) Granulomatus

Sarcoid, Wagners granulomatsis (midline granulomas)

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Nasal polyps
-features

occurs with allergic rhinitis

nasal polys present in nasopharynx

choanal polyp

polyp originating from sinus & present in nasopharynx

antrochoanal polyp

-simple nasal polyps are pedunculated edematous respiratory tract mucosa & can arise from any
part of nasal mucosa & are often multiple & bilateral
-commonest site of origin is mucosa of ethmoid cells & less commonly they arise in maxillary
antrum & enter nasal cavity via osteum & pass backwards through posterior nares to form an
antro-choanal polyp
-radiological appearance

soft mass with a well defined edge (i.e. generalized opacity in

sinus) & outlined by air posteriorly & inferiorly (CT-plain)

accompanied by thinning sinus wall & nasal & ethmoid septa

-occipito-mental view
Tumors

soft tissue opacity in nostril & sinus of origin is opaque

benign

ivory osteoma
inverted papilloma (from middle meatusof nose to the antrum)
fibrous dysplasia (ground glass radiolucent area with islands of
calcified bone)
ossifying fibroma

malignant

squamous cell carcinoma (mostly arise from nose or maxillary antrum)

adenocarcinoma (principally naso-ethmoidal)

*Osteoma
-Features

common in frontal & rare in antrum &give symptoms when obstruct ostium

-Radiological appearance
-CT

well defined dense opacites within sinus with lobulated margin

lobulated mass denser than adjacent bone surrounded by air

*Carcinoma
-features

40-60 years male

medial wall of antrum is most commonly involved early
in most cases both ethmoids & antrum are involved

-plain x-ray changes

-early

ill defined opacification of sinus with loss of translucency

soft tissue mass may be seen in one side of nasal cavity
-tomography bone destruction in sinus wall (diagnostic)

-late

soft tissue mass outside sinus (i.e. in nasal cavity)

bowing of septum to the other side
wide spread bone destruction
invasion of other sinuses

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-CT & MRI changes

malignant sinus tumors are best assessed by CT & Gd-MRI where CT

shows sites of bone destruction while Gd-MRI shows soft tissue spread
soft tissue mass with bone destruction
extension through cribriform plate to anterior cranial fossa (best seen by Gd-MRI)
extension into orbit (best seen by CT & Gd-MRI)
. invasion of infra-temporal fossa (may be seen before trisums becomes clinically evident best
seen by Gd-MRI) & pterygopalatine (middle cranial) fossa (best seen by CT)
evaluation of progress & response after raadiotherapy
Osteosarcoma
-radiological appearance

sinus is opaque
periosteal new bone formation
marked displacement of teeth

Sarcoidosis
-opacification of one or more sinus
-destruction of bone
-chest (postero-antrerior view)

bilat hilar lymphadenopathy

Wegners granulomatosus
-generalised disease affects respiratory tract & kidney
-radiologically

mucosal thickening affecting all sinuses

later on destruction of nasal septum & antrum more than with carcinoma
chest shows nodular opacities or linear opacities

Kartageners syndrome
-triad of

aplasia of frontal sinus & opaque antrum

dextrocardia
bronchiectasis

Fibrocystic disease (mucovisidosis)

absent frontal sinus

mucocoele & nasal polyps
chest show bronchiectasis
multiple cysts of pancreas

Blow-out fractures
-plain

opaque maxillary antrum (due to blood)

-tomography
-CT

demonstrate blow out fracture

demonstrate fracture, bony fragments & herniation of orbital contents into the antrum

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EAR AND TEMPORAL BONE

*Acute infection of middle ear cleft :A)Acute otitis media and mastoiditis
- Def.

inflammation of mucoperiosteal lining of middle ear cleft = eustachian tube,

tympanic cavity, mastoid antrum & air cells

-mastoiditis is from otitis media with

break down of cell wall causing extensive cavity

loss of translucency & vague margin

which may cause brain abscess

-radiologically
1.exudate in mastoid air-cells

loss of radiographic contrast (air-cell opacity)

2.osteoporosis due to infection

difficult recognition of cell walls

-intracranial complications is temporal lobe or cerebellar abscess

B)Special forms of acute infection of middle ear
Petrositis
-with middle ear infection air cells of petrous bone are involved
-rarely abscess is formed in petrous apex

Grad Graderigo syndrome (5th nerve pain &

6th nerve paralysis with mastoiditis)

-radiologically

bone erosion in petrous apex

Acute mastoiditis with abscess formation (masked mastoiditis)

-cause is inadequate antibiotic therapy in child that obscure clinical & radiological picture
-pathology

air cells are often replaced by granulation tissue

-radiological appearance may be normal,there may be bone destruction &large abscess cavity.
*Chronic otitis media & mastoiditis :- (see figure beside)
-classification

chronic suppurative

tubo-tympanic

chronic non suppurative

tuberculosis
others

labrynthitis obliterans

attico-antral

cholesteatoma

chronic adhesive (tympanic sclerosis)

chronic secretory otitis media

A)Chronic supprative otitis media

Tubo-tympanic (benign or safe type)
-it is usually a mucosal type of infection which mainly affect epithelium of eustachian tube &
middle ear & mastoid is usually cellular & rarely give rise to complication
-radiology is of limited use (see figure beside)
Attico-antral (dangerous or unsafe)
-it is usually bony type of infection & lesion is mainly in attic and antrum with mastoid air
cells few or absent (see figure beside)
-it is more dangerous due to acquired form of cholesteatoma which because of its erosive

Neuroradiology 95
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nature carries a significant risk of complications & bone erosion in association with
cholesteatoma.
B)Chronic non supprative otitis media
Tuberculous otitis media

produces extensive ragged bone destruction

Adhesive otitis media (tympanosclerosis)

-tough adhesion result from fluid of secretory otitis media undergo hyaline degeneration &
subsequent calcification (produce calcified plaques as end result of suppurative ear disease)
-if suppurative process involves labyrinth a dead ear results & granulation tissue within
labrynth may ossify
-CT

labyrinthites obliterans

parts of lumen of bony labyrinth have disappeared

Complications of chronic otitis media

a)labyrinthitis

otitis media with attacks of vertigo

-radiologically Stenvers view will show erosion of arch of lateral semicircular canal
by cholestestoma
b)venous sinus thrombophlebitis
-late phase of carotid angiogram may demonstrate obstruction of affected sinus
c)intracranial complications demonestrated by CT
-extradural & subdural abscess
-brain abscess which is usually in temporal lobe but may occur in cerebellum
-hydrocephalus
* Cholesteatoma :- definition the accumulation of keratin in a confined narrow space(skin bag in wrong lace
?epidermoid cyst ? bone infection)
- pathology the pesence of keratinzing stratified squamous epithelium in middle ear cleft with
desquamation of sheet of keratin & 2ry infection
enzymes

discharge of scanty pus & formation of

erosion of bone (medial attic wall & lateral spur & lateral attic wall as well)
destruction of ossicles
facial nerve paralysis
+

effect on labryinth (semicircular canals)

brain complications
soft tissue

-etiology

the etiology of characteristic epidermoid cyst containing keratin is not fully

understood but two types - which dont differ histologically - occur

Congenital cholesteatoma (epidermoid)
-arises from ectodermal cell nests
-may arise in any cranial bone, commonly middle ear cleft & apex of petrous temporal

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bone is the most commonly affected

-in petrous apex it produces clearly defined punched out area of bone destruction
(differential diagnosis of such lesion is cholesterol granuloma which give strong signal in all MRI
protocoles whereas cholesteatoma appear on T2 weighted signal)

-associated features
-radiologically

may be congenital atresia of external auditory canal

extensive destruction with no bony sclerosis

-tomographic cuts

clearly defined punched out area of bone destruction at petrous

apex (comparison of both sides is important fordiagnosis)

Acquired (attico-antral) cholesteatoma

-associated with disorder of middle ear cleft involving attic with or without preceding
infection & arise in postero-superior part of middle ear & then extends to other parts of
middle ear cleft mastoid air cells & labyrinth
-associated erosion of wall of cleft & typically there is marginal perforation in posterosuperior aspect of ear drum
-plain (lateral oblique mastoid 30 caudal angulation)

view is important to show

extent of pneumatization & position of sigmoid sinus & dural plates & signs may be :
1.an area of extensive bone erosion or destruction in attic or mastoid artrum associated
with smooth clear cut outline and little sclerosis around destructed bone.
2.mastoid process is usually sclerotic due to associated chronic infection (v.imp.)
3.with cellular mastoid there is extensive destruction of all walls however cholesteatoma
occurs mostly inpoorly or unpneumatised mastoid
- Tomographic changes
1.those affecting antrum

characterized by cavity formation which is usually smooth

walled, when irregular it is due to chronic osteitis(differential diagnosis from giant

mastoid air cell)
2.those affecting attic & ossicles
@destruction of lateral spur of bone (formed by junction of lateral boundary of attic &
roof of external auditory canal)
@bone destruction in lateral attic wall
@destruction of ossicles & drum
@erosion of medial attic wall
@loss of normal bridge appearance of external auditory meatus
-CT(high resolution coronal cuts)
1.Optimum method for demonstrating small cholesteatomas in attic & antrum & presence
of soft tissue mass in that part (upper) of middle ear is characteristic.
2.Demonstration of attico-antral bone erosion or destruction in particular blunting of spur
or outer attic wall

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3.ossicles may be destructed, eroded or slightly displaced

4.Extension of infection medially erodes labyrinth (labyrinthine fistula) & lateral
semicircular canal is the first to be affected
5.Complications

brain & subdural abscesses & involvement of facial canal with

subsequent facial nerve paralysis

*summary

keratin bag
CT

congenital(anywhere specially apex destruction punched out)

acquired (middle ear cleft

destruction & sclerosis)

(destruction soft tissue brain complications)

-destruction occur in

medial attic wall - lateral attic wall - bony spur (bridge) of

external auditory canal - ossicles & drum - semicircular canal & labyrinth
-Ct appearance of congenital & acquired cholesteatoma differs greatly from ragged
infiltrative lesions produced by other infective & neoplastic processes which tend to
affect labyrinth capsule at a very late stage
differential diagnosisd of cholesteatoma = differential diagnosis of destruction of petrous apex
1.Acoustic neuroma

2.congenital cholesteatoma

3.Naso-pharyngeal carcinoma

4.meningioma

5.Metastases particularly from breast, lung & kidney with irregular lytic defects + pain,
bleeding & nerve palsy
7.5th nerve neuroma (see figure beside)
8.Apical petrositis (Gradingo syndrome)

6.chordoma
trigeminal pain
6th nerve paralysis
mastoiditis

differential diagnosis of lucent area in mastoid process

1.cholesteatoma

2.mostoid abscess

3.gaint mastoid air cells

4.post operative

differential diagnosis of destruction of petrous bone

1.acquired cholesteatoma

2.glomus jugular

3.metastases

4.tuberculosis

5.rhabdomyosarcoma (in children) & middle ear carcinoma

Groups of mastoid air cells (see figure beside)
1.zygomatic

2.subdural

3.periantral

5.perisinus

6.tip

7.retro facial

4.sinodural

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Neoplasms of ear & temporal bone :A) Osteoma

-compact osteoma, well defined usually single + lobulated mass of bone density
-patient has conductive deafness (blocking of external auditory canal & middle ear)
B) Glomus tumors

(= chemodectomas = paragangliomas)

- Arise from glomus bodies (lies in top of jugular bulb & in middle ear) & include
glomus jugular, tympanicum from post ganglia of 8th nerve & vagal, carotid body tumor.
Glomus jugular
-Arises in roof of jugular fossa (floor of middle ear) to fill it & extends to middle ear &
posterior fossa & downwards to the neck
-clinical picture

conductive deafness
pulsating tinnitus
paralysis of cranial nerves (facial)

-on examination haemorrahgic polyp in external auditory canal or by otoscope

red tissue behind middle ear drum
-plain

erosion of margins of jugular foramen

asymmetry of both foramina due to enlargement of vein
erosion of septum (spur) between jugular & carcotid canals intracranially

-CT

soft tissue enhancing mass

destruction of jugular foramen & spur
soft tissue mass in the neck (para pharyngeal space)

-MRI

show extents of tumor intracranially & in neck (characteristic picture)

-Angiography by CCA & selective ECA angiography

1.arterial phase

vascular tumor (blood supply from ascending pharyngeal artery

via external carotid artery)
A-V communication

2.venous phase

early filling of jugular vein

shows the full extent of tumor inferiorly

- Vertebral angiography may be needed to detect other collaterals

C) Neuromas

arise from schwann cells in V, VII, VIII, IX, X, XI cranial nerves

See before

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Diffusion & Perfusion MR:

Stroke has a major social & economic impact on our society. Current CNS imaging modalities as CT
& MRI can miss early ischemic changes until permanent damage has occurred. MCA is the largest and most
direct branch of ICA & therefore the most subjected to embolism.
Stroke remains the major cause of disability among adults and the 3rd leading cause of death after noncerebral cardiovascular stroke disease and cancer.
Spectrum of pathological entities responsible for cerebral hypoperfusion:
1- Atherosclerosis (being one of the most important causes).
2- Cardiogenic brain embolism.
3- Arteriosclerosis
4- Arteriopathy
5- Arteritis
6- Arterial dissection
7- Venous and dural sinus thrombosis.

123-

Type of cerebral stroke:

Cerebral infarction (80%). Being by far m/c cause of cerebral stroke.
Primary intracranial hemorrhage (15%)
Non-traumatic subarachnoid hemorrhage ( 5%)

Diffusion MR
Diffusion is defined as the manner by which nutrients diffuse through capillary wall of cerebral
tissues. MRI was found to be an ideal method for investigating the diffusion of H2O by the possibility of
labeling its molecules by manipulating the magnetization of H+ proton.
Free diffusion is a process by which molecules move in a random fashion (incoherent intracellular
movement). In biological systems, totally free diffusion doesn't exist, instead we have restricted diffusion,
that is attributed to the presence of cell membranes and intracellular macromolecules. Therefore, water
motion is measured with a constant known as apparent diffusion coefficient (ADC) as opposed to a measure
of free diffusion.
In an ischemic cell, there is failure of the Na/K pump leading to intracellular influx of H 20. So the
net result is an in the intracellular content of H20 with a consequent in the sum of regional diffusional
movement of molecules.
So, in a normal cell, to obtain a DW Image:
If we have in a cell intracellular incoherent motion rephasing errors signal loss w is base of
a DWI. In normal situation: In DWI areas of the brain with less restricted diffusion of H 2O protons appears
dark and areas where diffusion is highly restricted appear bright.
However, on ADC images (calculated from DWI), the trend is reversed; areas of less restricted
diffusion appear bright & areas of restricted diffusion appear dark. In ischemic cells, we have increase in
intracellular H2O and decrease in sum of regional diffusion movement i.e. (which means) restricted
diffusion.
As a reflection of this restricted intracellular diffusion, in an ischemic cell, we have 33-66% decrease
in ADC within 1st hours, and as normally diffusion motion leads to signal loss, the ischemic areas having
less diffusion and consequently less signal loss, will have less signal loss than normal areas giving us higher
signal intensity on DWI as opposed to normal tissue (bright image).
In T2w image no differentiation can be made between restricted diffusion and highly restricted
diffusion areas. On the other hand, DW image and ADW image can help us in differentiation between acute
& chronic infarcts and in diagnosis of hyperacute stroke. Region of acute stroke is much better delineated in
DW image appearing as a hyperintense area and iIn ADW ischemic area are of low signal intensity.
Contribution of T2W versus DWI to final image contrast is determined by b value. We can have low
and high "b" value. To obtain a large b value we need MR machine with very high amplitude.

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Pefusion MR:
Perfusion is defined as the vascular process by which nutrients are delivered to the brain.
1st)
So far, most experiences have been gained with dynamic bolus studies using intravascular contrast.
2nd) In arterial spin techniques, blood is labeled by changing the state of its longitudinal magnetization e
RF
prepulses incorporated in imaging sequence. We use spin properties of H2O molecules, as an
endogenous indicator capable of passing blood brain barrier. These methods show the rCBV and provide
qualitative information on rCBF.
In dynamic bolus studies, 0.15-0.2 mmol/kg of Gd-DTPA I.V. (which is almost the standard dose) is
administered as quickly as possible (5-6 ml/s). Arterial spin labeling is a non-invasive technique, it allows
direct observation of rCBF. However, it necessitates a long acquisition time.
Used Pulse sequences for Diffusion Perfusion: the main drawback of old techniques, is their long acquisition
time increasing the chance of patient motion to which DWI is very sensitive. EPI is ccc by short acquisition
time of 30-100 ms by comparison for e.g. to larger turbo gradient acquisition time of 300 ms. So EPI can be
used in both diffusion perfusion imaging technique.
So less remember that infarcted area in DWI is bright and in ADW image it is dark.