CNS TRAUMA

DR Anwar Wardy W, dr.SpS, DFM

February 2012
anwar wardy FKK UMJ
anwar wardy FKK UMJ
TRAUMA
Concussion
Cerebral contusion
Epidural hematoma
Subdural hematoma/effusion
Intracerebral hematoma
Diffuse axonal injury
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EPIDURAL HEMATOMA
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SUBDURAL HEMATOMA
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DD:Metabolic Disorders
Hypoglycemia
Acidosis
Hyperammonemia
Uremia


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General Physical Exam
Vital signs
oTemperature -fever (may mean
infection)
oVery high temperature and dry skin
consider heat stroke
oHypothermia often seen in drug
intoxication

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Pupillary response
o pupillary constriction is controlled by the
parasympathetic system in the third nerve
o Dilation mediated by the sympathetic
system hypothalamus to spinal cord and
then the superior cervical ganglia
NEUROLOGIC EXAM
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Cranial Nerve Exam
I. olfactory-smell
II. Optic-Visual acuity, visual fields,
III. Oculomotor - eye movement
IV. Trochlear eye movement
V. Trigeminal Nerve - facial sensation, corneals,
VI. Abducens-eye movement
VII. Facial nerve - motor and sensory to face
VIII. Acoustic nerve - hearing
IX. Glossopharyngeal - gag reflex, elevate palate
X. Vagus - swallowing movement of the cords
XI. Accessory Nerve - sternocleidomastoid muscle ,
trapezius function
XII. Hypoglossal nerve - tongue movement, fasciculations
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Corneal reflex
Test the fifth nerve sensory and seventh
nerve motor
Cotton on cornea and look for a blink or
watch the lower eyelashes move toward
the midline
Good test for mid and low pontine
dysfunction
Swab the nose to test seventh nerve
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Respiratory Pattern
Injury location and type of breathing
o Post hyperventilation apnea -bilateral
hemispheric dysfunction
Cheyne-stokes breathing
o Central reflex hyperpnea- bilateral hemispheric
dysfunction injury to lower midbrain or upper
pons
o Apneustic respiration- pons
o Central Neurogenic Hyperventilation (formerly
known as Ondines curse) loss of involuntary
respiration- medulla
o Apnea-medulla to C4, neuromuscular junction
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UPPER MOTOR NEURON
LESIONS
Cerebrum
o Aphasia cortical sensory loss
o Gaze preference
o Nystagmus
o Visual field deficit
Internal capsule
o Equal paralysis of arm, legs, face
o Motor loss without sensory loss
o Motor loss with dense hemi sensory loss

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UPPER MOTOR NEURON
LESIONS
Midbrain-hemiplegia with contralateral 3rd nerve
palsy-Webers
Pons-Hemiplegia with contralateral 6th or 7th
palsy-Millard Gubler
Medulla-spastic weakness difficulty swallowing
Spinal cord -weakness of one with contralateral
loss of pain Brown-Sequard /or paraplegia

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INFRATENTORIAL LESIONS
Brainstem symptoms are often seen
initially
Sudden onset of coma
Cranial nerve abnormalities
Alteration of the respiratory pattern
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The ABCDEs of trauma care sequentially
identify life-threatening conditions
A. Airway maintenance with cervical spine
protection
B. Breathing and ventilation
C. Circulation with hemorrhage control
D. Disability: Neurologic status
E. Exposure: Completely undress but
prevent hypothermia
Life-threatening conditions are identified and
simultaneous management is instituted
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KEY TO DIAGNOSIS
A good history
A thorough physical exam
Knowledge of CNS anatomy
Neurologic Evaluation
Level of consciousness
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AVPU method:
A - Alert,
V - Responds to Vocal stimuli
P - Responds only to Painful stimuli
U - Unresponsive to all stimuli

Pupillary size and reaction.
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Pupillary response
Mid-position unreactive pupils
o both parasympathetic and sympathetic mid brain lesions
Pinpoint pupils parasympathetic
innervation is intact but sympathetic
nerve is involved-pontine lesions
Unilateral dilation uncal herniation
from compression of oculomotor nerve
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Pupillary reflex
Metabolic causes of coma
o Can give a variety of changes but pupils
usually remain reactive
Drugs:
o Narcotics-pinpoint but reactive
o Atropine-dilated and nonreactive

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Glasgow Coma Scale
Developed to define outcome in adult
patients with head injury
Coma: score of 8 or less
There is a modified scale used for infants
and children


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Glasgow Score
Eye opening Motor Response
o Spontaneous 4 obeys commands 6
o To command 3 localizes pain 5
o To pain 2 withdraws to pain 4
o None 1 abnormal flexion 3
Verbal abnormal extension 2
o Oriented 5 none 1
o Confused 4
o Inappropriate words 3 TOTAL 3-15
o Incomprehensible sounds 2
o None 1

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MODIFIED GLASGOW
COMA SCORE For Infants
Eye opening Motor
o spontaneous 4 normal 6
o To speech 3 withdraws to touch 5
o To pain 2 withdraws to pain 4
o None 1 abnormal flexion 3
Verbal abnormal extension 2
o Coos 4 none 1
o Irritable cries 4
o Cries to pain 3
o Moans to pain 2
o None 1
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Glasgow Coma Scale
A strong predictor of outcome
13: mild brain injury
9-12: Moderate brain injury
< 8: Severe brain injury (coma)
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Progression of Mass Lesions
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Herniation
Skull Fracture
This is a simple,
single line fracture
that has reached
the posterior midline
suture to open it.
There is an epidural
hematoma in the
occipital region at
the site of impact.
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Middle Meningeal Artery
This is a display of a
young (straight) middle
meningeal artery
serving the dura.
Pressure in the artery
creates a canal on the
inner table of the skull.
A fracture with shifting
bone plates severs the
artery for instantaneous
bleeding and rapid
expansion.

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Epidural Hematoma
This hematoma is
seen to be
between the dura
and skull.
The dura ordinarily
would be tight and
tamponade (stop)
the bleeding.
The fracture
loosened the dura
to allow easy and
fatal expansion
against a soft brain.
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Cerebral Edema
Swelling of tissue can
become severe to
flatten gyri against
the skull.
Sulci are obliterated
and major arteries
traversing the sulci
get compressed,
congested, and may
thrombose.
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Compression by
Hematomas
Both epidural and
subdural hematomas
become space
occupying and brain-
deforming phenomena.
All gyri are flattened and
vessels congested.
The hemisphere can only
go under the falx, down
to the posterior fossa
(uncal herniation) and
out the foramen
magnum (tonsillar
herniation.)
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Cerebral Contusions
Though from another
patient, the temporal
contusions are similar
Bleeding into the
cingular gyrus is likely
from hitting the falx.
In this case,
contusions are seen
in the opposite
temporal lobe as
well.
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Radical Surgical Decompression
When cerebral
edema is severe, one
or both sides of the
skull can be surgically
removed while
leaving a midline
basket handle for
later adhesion.
Our patient had one
side fractured so it
was stored for later.
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Reactions at the Cellular
Level
While all cells in the
center of the injury may
die, those at the edge
can show reversible
forms of injury.
This is an axonal
torpedo formed by
cytoplasmic jamming
at a node of Ranvier.
The silver is staining
neurotubules, fibrils,
mitochondria, and
endoplasmic reticulum.
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Uncal Herniation
Unilateral edema can
push the uncus of the
temporal lobe into the
posterior fossa (arrow).
This can compress the
posterior cerebral artery
against the midbrain for
an occipital infarct.
It can also push the
midbrain against the
opposite tentorium to
create Kernohans notch
and ipsilateral hemiplegia
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Tonsillar Herniation
The arrows point to
bilateral cerebellar
tonsils formed under
pressure from edema
above.
You can approximate
the size of the foramen
magnum by the tonsils.
Compression of the
basilar artery is a
potential fatal
complication.
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Acute Duret
Hemorrhages
Had the temporal lobe
not been removed, the
pons would have been
pushed away from the
basilar artery for
infarction followed by
hemorrhages.
Not how swollen,
round, and pale the
pons has become.
The midline ventral
trench for the basilar
artery no longer
suffices!
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Chronic Duret
Hemorrhage
This patient somehow
survived one year
after his secondary
Duret hemorrhages.
Note they still contain
hemosiderin stains
along the lining of the
cavities.
The aqueduct shows
hydrocephalus ex
vacuo.
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Old Contusion
The margin of temporal
lobe dissection and the
injured gyri have lost
their edema and most
tissue, but still have
hemosiderin
macrophages
providing a green hue
like a bruise.
Neighboring gray
matter may be intact a
short segment before
another injured spot
(on the right). These
islands can cause
seizures if axons
survived.
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Resolving Contusion
While most dead tissue
is gone, some
hemosiderin-laden
macrophages have yet
to return to the vessels.
No tissue remains under
the arachnoid on the
right (strokes leave
layer I).
Surviving vessels are
condensed and
markedly thickened.
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Critical Sites
A basal skull fracture
can lead to bleeding
and adhesions over the
foramina of Magendie
and Luschka and then
hydrocephalus.
The nucleus basalis of
Meynert and
hippocampus can be
damaged to cause
traumatic Alzheimers
disease, as in this
patient.
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Traumatic Alzheimers
Veterans and
athletes with head
injuries have a higher
incidence of senile
plaques and tangles.
They can be punch
drunk while young
and demented early
as an older adult.
The same applies to
auto accident
victims.
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15 vs 100 Year Old Brains
Note the open sulci and ventricles.
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REFERENCES
Robbins, 7
th
ed, 2005:1356-61
Townsend J, Klatt EC. Neuropathology Illustrated,
Dept Pathology, Univ Utah, Salt Lake, 2001
McArthur DL, Hovda DA. Symposium Traumatic
Brain Injury. Brain Pathology 2004;14:183-222
Whitelaw A, Love S. Symposium Hydrocephalus
(especially post-traumatic). Brain Pathology
2004;14:304-36
Jones NC et al. A detrimental role for nitric oxide
synthase-2 in the pathology resulting from acute
cerebral injury. J Neuropath Exp Neurol 2004;63:708-
20
All illustrations are from the first two references.
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Wassalam,.Terima kasih
DR Anwar Wardy W, dr.SpS, DFM(K)
Email: anwarwardy@gmail.com
Anwar_wardy@yahoo.com
Blogs and fb: anWARdyneurovision//
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