NEUROVASCULAR EMERGENCIES: MEDICAL AND SURGICAL MANAGEMENT OF STROKE

NEUROVASCULAR
EMERGENCIES: MEDICAL AND
SURGICAL MANAGEMENT OF
STROKE


by JAFRI MALIN DATOK HJ. ABDULLAH MD, Phd,
Diplomate Neurosurgery (Belgium) FICS,
Neurosurgical Division,
Hospital University Sciences Malaysia,
16150 Kubang Kerian,
Kelantan, Malaysia.

E-mail: amiruljafni@yahoo.com

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Introduction

In most states in Malaysia, strokes or better known as cerebrovascular accidents
(CVA) are the 3rd cause of mortality and the main cause of disability. Due to the
improvement of the treatment of ischeamic heart disease over ischaemic or haemorraghic
brain disease over the last 10 years, more and more patients can benefit from non surgical
and surgical intervention. The nineties have been called the decade of the brain in
developed countries where brain attack has been treated as aggresively as heart attacks.
Thus it is now the time for all developing countries to follow the same pathway.

Next to heart disease and cancer, cerebrovascular disease is the most frequent
cause of death in the western world and now in Malaysia. And at least one-half of all
neurologic patients in general has some type of cerebrovascular disease.

The term cerebrocvascular disease denotes any abnormality of the brain resulting
from a pathologic process of blood vessels, be they arteries, arterioles, capillaries, veins,
or sinuses. The pathologic change in the vessels takes the form of occlusion by thrombus
or embolus, or of rupture, and the resulting abnormalities in the brain are of two types:
ischemia, with and without infarction, and hemorrhage. Rarer forms of cerebrovascular
disease are those due to altered permeability of the vascular wall and increased viscosity
or other changes in the quality of blood. The latter changes underlie the strokes that
complicate diseases such as sickle-cell anemia and polycythemia and account for the
headache, brain edema, and convulsions of hypertensive encephalopathy. There are many
more types of cerebrovascular disease; these are listed in Table1, and the relative
frequency of the main types is indicated in Table 2


The stroke syndrome

The distinctive mode of presentation of cerebral vascular disease is the stroke,
defined as any sudden or acute nonconvulsion focal neurologic deficit. In its most severe
form the patient becomes hemiplegic or falls senseless, an event so dramatic that it is
given its own name-apoplexy, cerebrovascular accident, stroke, or shock. If death does
not follow within hours or days, there is nearly always some degree of recovery of

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function. This temporal profile of neurologic events, whether condensed into several
hours or days, is diagnostic. Variations in the temporal profile reflect the type of vascular
lesion. Embolic strokes characteristically begin with absolute suddenness, and they may
at times recede rapidly or they may last. Thrombotic strokes may have a similarly abrupt
onset, but often they evolve somewhat more slowly, over a period of minutes to hours or
even days. Cerebral hemorrhage from its onset causes a deficit that is steadily
progressive for hours or longer.

The major neurovascular thrombotic and embolic syndromes their symptoms and
signs, and the corresponding cerebral structures that are involved.

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Table ONE. Types of Cerebral Vascular Disease
1. Atherosclerotic
thrombosis
2.
Transient ischemic attacks
3.
Embolism
4
Primary (hypertensive) intracerebral hemorrhage
5
Ruptured or unruptured saccular aneurysm or AVM
6
Arteritis
a. Meningovascular syphilis, arteritis secondary to pyogenic and
tuberculous meningitis, rare infectivr types (typhus, schistosomiasis,
malaria, trichinosis, mucormycosis, etc.)
b. Connective tissue disease (polyarteritis nodosa, lupus erythematosus),
nectrozing arteritis, Wegener arteritis, temporal arteritis, Takayasu disease,
granulomatous of giant cell arteritis of the aorta, and giant cell
granulomatous angiitis of cerebral arteries.
7
Cerebral thrombophlebitis: secondary to infection of ear, paranasal sinus
face, etc.;with meningitis and subdural empyema; phlebothrombosis with
debilitating postpartum, postoperative states; prolonged immobility, cardiac
failure, hematologic disease (polycythema, sickle-cell disease); and of
undetermined cause
8
hematologic disorders: polycythemia, sickle-cell disease, thrombotic
thrombocytopenic purpura, thrombocytosis, etc.
9.
Trauma and dissection of carotid and vertebral arteries
10
Dissecting aortic aneurysm
11
Systemic hypotension with arterial stenoses: “simple faint,” acute blood
loss, myocardial infarction. Strokes-Adams syndrome, traumatid and
surgical shock, sensitive carotid sinus, severe postural hypotension
12
Systemic hypotension with arterial stenoses: “simple faint,” acute blood
loss, myocardial infarction. Strokes-Adams syndrome, traumatid and
surgical shock, sensitive carotid sinus, severe postural hypotension
13.
Neurologic migraine with persistent deficit
14.
With tentorial, foramen, magnum, and subfalcial herniations
15
Miscellaneous types: fibromuscular dysplasia, excessive x-irradiation,
unexplained middle cerebral artery territory infarction in closed
headinjury, pressure of unruptured saccular aneurysm, complication of oral
contraceptives
16
Undetermined caused in children and young adults: moyamoya; multiple,
progressive intracranial arterial occlusions (Taveras)




Table Two. Major Types of Cerebrovascular Disease and Their Frequency

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CVA
in
CVA resulting
alive
in death
patient
Atherosclerotic
32% 12%
thrombosis
Lacunes 18%
18.5%
Embolism 32%
32%
Hypertensive
11% 15.5%
hemorrhage
Ruptured aneurysms
7% 4.5%
and vascular
malformations
Indeterminate -
9.5%
Others -
8%

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Atherosclerotic-thrombotic infarction

The large intracranial arteries, like the aorta and coronary arteries, are predisposed
to atherosclerotic changes. Favored sites are the common and internal carotid, the
vertebral and basilar, and the stems of the major cerebral arteries. Factors enhancing this
atheromatous process are hypertension, diabetes mellitus, and hyperlipidemia, both
genetic and dietary.

More than one half of patients who develop a thrombotic stroke have one and
more brief warning episodes, called transient ischemic attacks (TIAs), the diagnosis and
treatment of which may prevent an oncoming stroke. The thrombotic stroke, whether or
no it is preceded by warning attacks, develops in one of the following ways: Most often
there is an abrupt onset of the neurologic deficit, evolving over a few minutes to a few
hours; or there may be a stuttering onset and intermittent progression over several hours
of a day or longer; or symptoms may regress for hours and then advance again. More
perplexing still is the rare stroke in which the deficit advances in a series of steps over a
period of weeks. Often the onset is during sleep; the patient awakens paralyzed.

The pattern of the neurologic deficit is determined by the site of arterial occlusion
and the available anastomotic arrangements.


Ancillary Examinations

Noninvasive blood flow procedures, such as carotid Doppler studies, may reveal a
stenotic or occluded artery. This can be verified by angiography, a procedure that carries a
small risk of worsening the neurologic deficit. Digital subtraction angiography (DSA),
preferably by the arterial route, more safety but less clearly visualizes the aorta and its
main cranial branches. All these methods will probably be replaced by MR angiography.
One can see by these several techniques both stenotic segments or occlusion of arteries
and sometimes mural thrombi that may become embolic (artery-to-artery embolism).

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Fig. ONE. Diagram of the left cerebral hemisphere, lateral aspect, showing the branches
and distribution of the middle cerebral artery and the principle regions of cerebral
localization. Following is a list of the clinical manifestations of infarction in the territory
of this artery and the corresponding regions of cerebral damage

Signs and symptoms
Structures involved
Paralysis of the contralateral face, arm, Somatic motor area for face and arm
and leg
and the fibers descending from the leg
area to enter the corona radiata

Sensory impairment over the
Somatic sensory area for face and arm
contralateral face, arm, and leg and thalamoparietal projections
(pinprick, cotton touch, vibration,
position, two-point discrimination,
stereognosis, tactile localization,
barognosis, cutaneographia)

Motor speech disorder
Broca’s area and frontal operculum of
the dominant hemisphere

“Central” aphasia, word deafness, Central language area and parieto-
anomia, jargon speech, alexia, agraphia, occipital cortex of the dominant
acalculia, finger agnosia, right-left hemisphere
confusion (the last four compose the
Gerstmann syndrome)

Apractagnosia (amorphosynthesis),
Usually nondominant parietal lobe. Loss
anosognosia, hemiasomatognosia,
of topographic memory is usually due to
unilateral neglect, agnosia for the left a nondominant lesion, occasionally to a
half of external space, “dressing dominant one
apraxia,” distortion of visual
coordinates, inaccurate localization in
the half field, impaired ability to judge
distance, upside-down reading, visual
illusions; inattention and confusion
usually associated

Homonymous hemianopia (often
Optic radiation deep to second temporal
superior homonymous quadrantanopia)
convolution

Paralysis of conjugate gaze to the Frontal contraversive field or fibers
opposite side
projecting therefrom

Avoidance reaction of opposite limbs
Parietal lobe

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FIG. ONE . (CONTINUED)

Signs and symptoms
Structures involved
Miscellaneous:
Ataxia of contralateral limbs (s)
Parietal lobe

So-called Bruns ataxia or apraxia of gait
Frontal lobes (bilateral)

Unilateral neglect of space and body
Parietal lobe , more often right
parts

Agitated delirium
Right temporal

Loss or impairment of optokinetic
Supramarginal or angular gyrus
nystagmus

Limb-kinetic apraxia
Premotor or parietal cortical damage

Mirror movements
Precise location of responsible lesions

not known
Cheyne-Stokes respiration, contralateral Precise location of responsible lesions
hyperhidrosis, mydriasis (occasionally)
not known

Pure motor hemiplegia
Upper portion of the posterior limb of

the internal capsule and the adjacent

corona radiata.

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Fig. Two. Diagram of a cerebral hemisphere, medial aspect, showing the branches and
distribution of the anterior cerebral artery and the principal regions of crebral localization.
Following is a list of the clinical manifestations of infarction in the territory of this artery
and the coreesponding regions of cerebral damage.

Signs and symptoms
Structures involved
Paralysis of opposite foot and leg
Motor leg area

Paresis of opposite arm
Involvement of arm area of cortex or
fibers descending therefrom to corona
radiata

“Cortical” sensory loss over toes, foot, and leg
Sensory area for foot and leg

Urinary incontinence
Posteromedial part of superior frontal
gyrus (bilateral)

Contralateral grasp reflex
Premotor and supplementary motor

areas
Abulia (akinetic mutism), slowness, delay, lack Uncertain localization-probably deep
of spontaneity, whispering, motor inaction, medial-orbital (usually bilateral)
reflex distraction to sights and sounds

Impairment of gait and stance (gait “apraxia”)
Inferomedial frontal-striatal

Mental impairment (preseveration and
Localization unknown
amnesia
Miscellaneous

Dyspraxia of left limbs
Corpus callosum
Cerebral paraplegia
Motor leg area bilaterally (due to
bilateral occlusion of anterior cerebral
arteries)

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What to do in the Emergency Room?


When a patient presents him or herself to the Emergency Room with the abrupt
onset of a focal cerebral deficit; 5% are seizure, tumor, or psychogenic, 95% are vascular
(i.e. stroke) of which I5% are hemorrhage such as intracerebral haemorraghe, subarchnoid
haemorraghe or subdural hemorraghe. 85% of these diagnosed strokes are ischemic
infarct and early cerebral angiography or computer spiral 3 Dimension angiogram of the
brain has show that arterial occlusion can be demonstrated in 80% of these, regardless of
subtype of infarcts. The ischeamic infarcts are there after clasified into various groups
according to their anatomopathology causes:
i) 41% unknown cause (this may decrease with the use of early




angiography)
ii) 21% lacune (small artery or arteriole cerebrovascular lesion)
iii) 16% cardiogenic embolus
iv) 11% large artery cerebrovascular lesion
v) 11% tandem arterial pathology


A recent study showed that atherosclerotic plaques in the aortic arch more than
4mm thick are a risk factor for the recurrent CVAs and other vascular events (myocardial
infarcts, peripheral embolism, and death from vascular causes)

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