Anda di halaman 1dari 69

Radiology Interactive Case

9
Neurology A
Section C
Macadangdang, Panganiban, A.,
Panganiban, J., Paredes, Pasana,
Pau, Paulino, Payuyo, Pelino,
Perez
78 yo right handed
female
from Cavite
Chief Complaint:
Alteration in level of
sensorium
History of Present Illness
Past Medical History
• (+) Hypertension Stage 2 with Atrial
Fibrillation
– poor compliance with her medication
• (+) DM Type 2, uncontrolled
Personal and Social History
• Non smoker
• Non alcoholic beverage drinker
Pertinent Physical
Examination
• BP 140/100 mm Hg
CR/PR 80s irregularly irregular
RR 24
• No carotid bruit
• Symmetrical chest expansion, clear
breath sounds
• Adynamic precordium, AB 6th LICS
MCL, (+) holosystolic murmurs at the
apex
Neurologic Examination
• Eye opening to name calling but with difficulty in
maintaining wakefulness, incomprehensible
words, can follow simple commands
• Pupils isocoric 2-3 mm ERTL
• EOMs: conjugate; no preferential gaze
• (+) corneal reflex, bilateral
• Can raise eyebrows equally, shallow left
nasolabial fold
• Tongue deviated to the left
• Motor Exam: unable to move her left extremities
(0/5)
• Numbness on the left extremities
• Cerebellum: difficult to assess at this time
• Babinski, left
• No nuchal rigidity
Glasgow Coma Scale
• Eye opening
4 – spontaneous eye opening
3 – eyes open to speech
2 – eyes open to pain
GCS

1 – no eye opening
Verbal response
Score: 11
5 – alert and oriented
4 – confused, yet coherent; can speak coherently
3 – garbled phrases; inappropriate words
2 – incomprehensible sounds
1 – no sounds
• Motor response
6 – full obeys commands
5 – responds to painful stimuli
4 – withdraws from noxious stimuli or pain; not as purposeful as in 5
3 – abnormal reaction to stimuli
2 – unnatural posturing; head arched back, arms bend in toward chest,
fists clenched, legs extended
1 – no response
Salient Features – Pertinent
Positive
Subjective Objective
• 78 yo • (+) Hypertension Stage 2
with Atrial Fibrillation, poor
• Slurring of speech compliance
• (+) DM Type 2, uncontrolled
• Left-sided weakness • BP 140/100 mm Hg
• Vomiting • CR/PR 80s irregularly
irregular
• Drowsy • AB 6th LICS MCL, (+)
holosystolic murmurs at the
apex
• GCS score: 11
• shallow left nasolabial fold
• Tongue deviated to the left
• left extremities – MMT: 0/5,
numbness
• (+) left Babinski
Salient Features – Pertinent
Negative
Subjective Objective
• Non smoker • No nuchal rigidity
• Non alcoholic
beverage drinker
Lesion

LEVELIZE:
cerebral cortex
LATERALIZE:
right side
LOCALIZE:
CT and MRI findings
Working Diagnosis:
Stroke
Stroke
a.k.a. cerebrovascular accident

A symptom complex resulting from


cerebral hemorrhage or from
embolism or thrombosis of the
cerebral vessels, characterized by
alterations in consciousness,
seizures, and development of focal
neurologic deficit
Blakinston’s Pocket Medical Dictionary, 4th edition
Risk Factors
Modifiable Non-Modifiable
• High blood pressure • Age
• Cigarette smoking • Family history
• Diabetes mellitus • Race
• Carotid or other artery • Sex
disease • Prior stroke, TIA or heart
• Atrial fibrillation attack
• Other heart disease
• Sickle cell disease
• High blood cholesterol
• Poor diet
• Physical inactivity and
obesity American Heart Association
14
http://www.americanheart.org/presenter.jhtml?identifier=4716
Types of Stroke
Type % of Onset Precedi Altered MRI or CT Other
all ng TIAs Mental Scan Features
stroke (%) Status
Thrombotic s
40 May be 50 (%)
5 Ischemic Carotid bruit,
gradua infarction stroke during
l sleep
Embolic 30 Sudden 10 1 Superficial Underlying
(cortical) heart disease,
infarction peripheral
emboli or
strokes in
different
Lacunar 20 May be 30 0 Small, deep vascular
Pure motor or
gradua infarction territories
pure sensory
l stroke
Hemorrhagi 10 Sudden 5 25 Hyperdense Nausea and
c mass vomiting,
decreased
mental status
Medical Secrets by Anthony Zollo, Jr.
16
Embolic Stroke
• Most often diagnosed in patients with an
underlying cardiac disease

• Abrupt in onset, with more rapid resolution,


and tend to cause smaller neurologic deficits than
thrombotic stroke

• Embolus travel in the arterial stream until it


reaches a blood vessel to occlude it

• Cortical deficits, such as aphasia


17
Radiology
• CT scan
• Magnetic Resonance Imaging (MRI)
– Magnetic Resonance Angiograph
Computed Tomography (CT)
• method of choice for the
assessment of acute ischemic injury
• recommended imaging modality for
initial evaluation of patients
suspected of having a stroke
• Sensitive for detection of
calcifications and acute hemorrhage
• Rapid, widely available, low cost,
non-invasive, short study time
GILMAN, C., 1998. Imaging the Brain. The New
England Journal of Medicine. 332: 812-820 19
Computed Tomography (CT)
• Can not detect an infarction in the
first three hours after the onset of
symptoms
• Hyperdensity of a major cerebral
vessel-important sign of vessel
thrombosis
• Limited capacity to show vascular
lesions in the brainstem, cerebellum
and small deep ischemic infarctions
GILMAN, C., 1998. Imaging the Brain. The New
England Journal of Medicine. 332: 812-820 20
Normal CT Scan
CT Scan
Early CT Changes in Ischemic
Stroke
• Hypodensity
• Obscured insular
ribbon
• Dense MCA sign
• Loss of gray-white
interface
• Loss of sulci
• Mass effect

23
CT Scan

*HEWKO, C., 2004. Acute ischemic stroke--swift


assessment 24
& quick action produce optimal outcomes. JAAPA,
Non-hemorrhagic Hemorrhagic

GILMAN, C., 1998. Imaging the Brain. The New England


Journal of Medicine. 332: 812-820
Computed Tomography (CT)
• Loss of Insular Ribbon Sign
– insular ribbon
• is an area of extreme gray-white
differentiation that is readily examined on
the CT scan
• between the Sylvian fissure and the basal
ganglia
• supplied by small perforating branches of
the MCA
• appears as a thin white line (gray-matter)
adjacent to a darker gray subcortical area
(white-matter)
Loss of Insular Ribbon

FLACKE, S. et al. 1999. Middle Cerebral Artery (MCA) Susceptibility Sign at Susceptibility-based Perfusion MR
Imaging: Clinical Importance and Comparison with Hyperdense MCA Sign at CT. Radiology. 2000; 215:476-482.
Computed Tomography (CT)
• Hyperdense MCA sign:
– major occlusion of the vessel with
thrombus formationhypoperfusion
– 98 % specificity, 50% sensitivity
– also correlates with final stroke severity
Hyperdense MCA Sign

FLACKE, S. et al. 1999. Middle Cerebral Artery (MCA) Susceptibility Sign at Susceptibility-based Perfusion MR
Imaging: Clinical Importance and Comparison with Hyperdense MCA Sign at CT. Radiology. 2000; 215:476-482.
Hyperdense MCA Sign
Computed Tomography (CT)
• The earliest signs of infarction are
usually subtle and include:
– loss of gray-white differentiation at
the cortical-subcortical junction
– basal ganglia and sulcal effacement
• These signs appear within 6 hours
of onset in over 80% of patients
with MCA infarctions, but are often
less obvious when infarcts affect
other territories
Loss of Gray-White
Interface

American College of Physicians, Inc. 2006. Internal Medicine Essentials for


Clerkship Students. Accessed from: acponline.org/essentials
Computed Tomography (CT)
• Hypodensity (edema) and mass
effect develop next
– if present in more than 50% of the MCA
territory within 24 hours of onset
correlate with early neurologic
deterioration and death
Computed Tomography (CT)
• Mass effect
– Compression of CSF spaces and
asymmetry of cortical sulci
Mass Effect

American College of Physicians, Inc. 2006. Internal Medicine Essentials for


35
Clerkship Students. Accessed from: acponline.org/essentials
CT scan of
patient
9 hours after
the onset of
symptoms
CT Scan of Patient
Contrast-
enhanced
CT scan of
patient
9 hours after the
initial non-
contrast CT scan
Contrast-enhanced CT of
Patient
Contrast-enhanced CT of
Patient
Early CT Changes in Ischemic
Stroke

• Hypodensity
• Obscured insular
ribbon
• Dense MCA sign
• Loss of gray-white
interface
• Loss of sulci
• Mass effect
41
CT Scan of Patient
CT Scan of Patient
• Hypodensity
• Loss of gray-white
interface
• Loss of sulci
• Mass effect

43
Obscured Insular Ribbon
Contrast-enhanced CT of
Patient
Hyperdense MCA Sign
Magnetic Resonance
Imaging (MRI)
• More sensitive than CT to the early pathologic
changes of ischemic infarction
• Relatively insensitive for detecting early signs
of cerebral ischemia
• Superior in detecting brain edema, small cortical
and subcortical infarcts, as well as those in the
brainstem and cerebellum
• more sensitive and specific than CT for
identifying infarct location, size, and age
• Longer time to perform
• More expensive than CT
GILMAN, C., 1998. Imaging the Brain. The New
England Journal of Medicine. 332: 812-820 47
Magnetic Resonance
Imaging (MRI)
• Diffusion-weighted imaging
(DWI)
– detects subtle changes in the diffusion
of water molecules within ischemic
tissue and can accurately identify areas
of ischemia
– within minutes of onset and may persist
for weeks
– for acute ischemia, sensitivity: >90%
and specificity: >95%
Magnetic Resonance
Imaging (MRI)
• Perfusion-weighted imaging
(MRI)
– Tracks a gadolinium bolus into the brain
parenchyma
– PWI detects areas of hypoperfusion or
“at risk” tissue that is still viable
DWI/PWI Mismatch
• Subtract DWI signal (infarct core)
from PWI signal
• DWI/PWI mismatch is the
hypoperfused area that may still be
viable (ISCHEMIC PENUMBRA)
– Large mismatch: reperfusion may
benefit even beyond the 3-hour t-PA
window
– No mismatch: there may be little benefit
to thrombolytic therapy, even within 3-
hour period
DWI MRI 35 minutes after
symptom onset
Magnetic Resonance Angiography
(MRA)
• a sequence which enables the
evaluation of cervical and cerebral
arteries
• a noninvasive test that can be
performed without contrast injection
and provides 3D images of the
vascular system
Catheter Angiography
• best parameter to document stroke
• invasive, potentially high-risk procedure 
• although this test has largely been
supplanted by MR angiography and CT
angiography, it remains the gold standard in
the evaluation of intracranial, extracranial,
and spinal vascular lesions.
• performed routinely in patients with
subarachnoid hemorrhage or
unexplained intracranial hemorrhage.
• occasionally performed to evaluate the
intracranial blood vessels for vasculitis
Catheter Angiography
• Major complications:
– Bleeding and thrombosis at the puncture site
– Vascular dissections at any level
– Small plaques dislodged by the catheter and
small clots forming around the catheter tip
may embolize, leading to cerebral or spinal
infarction
• Major risk factors for complications:
– Age − Hypertension
– Diabetes − Peripheral vascular
disease
– Coronary artery disease 
Catheter Angiography
• Advantages:
– extremely high spatial resolution
– remains the gold standard in the evaluation
of the vascular system. 
• Disadvantages:
– procedure is long and often requires
serious sedation

• When to Order:
– Subarachnoid or parenchymal hemorrhage
– Vasculitis
– Spinal vascular malformation
Diagnosis:
Thromboembolic Stroke
Pathophysiology
Cerebral ischemia is caused by a
reduction in blood flow that lasts
longer than several seconds.

A stroke, or cerebrovascular accident, is


defined by this abrupt onset of a
neurologic deficit that is attributable to a
focal vascular cause.

Most cerebrovascular diseases are manifest


by the abrupt onset of a focal neurologic
deficit, as if the patient was “struck by the
hand of God”.
Harrison’s Principles of Internal Medicine, 16th Ed. 59
Blood Flow
• 0 = death of brain within 4 to 10 minutes

• <16-18 ml/100g tissue/min = infarction


within an hour

• <20 mL/100g tissue/min = ischemia w/o


infarction (unless prolonged for hours or
days)

*If blood flow is restored prior to a significant amount of cell


death, the patient may experience only transient
symptoms, i.e. TIA
Harrison’s Principles of Internal Medicine, 16th Ed.
60
Penumbra
• Heterogeneity in brain injury has
been documented in an infarcted
zone.
• Blood flow to an infarcted zone is
said to have:

– A. a central region or core of very low


flow that results in rapid cell demise and
– B. a peripheral penumbra where decline
in flow is more moderate and cell death
Penumbra
• The penumbra is thought to
represent salvageable tissues that
may go on to infarction.

• If blood flow is normalized at an


adequate time, the brain cells will
normalize.
63
Cell Death Pathways
1. Necrotic pathway
– Rapid cellular cytoskeleton breakdown

2. Apoptotic pathway
– Cells become programmed to die

64
Harrison’s Principles of Internal Medicine, 16th Ed. 65
Thank you!!!
Necrotic Pathway
↓ glucose in ↓ ATP
ischemia production
neurons
by
mitochondria
agonize glutamate
postsynaptic release from
glutamate synaptic
receptors terminals

membrane
↑ depolarization ion pumps
intracellular of neurons stop
calcium functioning

proteolysis necrosis
67
Management
PHARMACOLOGIC
• by optimizing cerebral perfusion in
1. Reverse or the surrounding ischemic
lessen the penumbra
amount of 1. Reperfuse the tissues
(thrombolytics and
tissue
vasodilators)
infarction
2. Prevent further thrombotic
(initial events (antiplatelets and
management) anticoagulation)
3. Maintain blood pressure
1. Reduce the
risk of further
• plan for secondary prophylaxis
strokes and
other vascular (drugs)
problems
Management
NON- PHARMACOLOGIC
1. Reduce the patient’s disability and
handicap through rehabilitation (physical,
occupational, and speech therapy
consultation)

2. Plan for secondary prophylaxis (risk


factor modifications)

3. Prevent the common complication of


bedridden patients

Anda mungkin juga menyukai