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
23
CT Scan
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 formationhypoperfusion
– 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
• 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.
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)