CEREBRALVASCULAR DISEASE
Dr,LU,QINCHI
DEPARTMENT OF NEUROLOGY
REN JI HOSPITAL
SHANGHAI JIAO TONG UNIVERSITY
SCHOOL OF MEDICINE
Tel,58752345-3094
Email,qinchilu@hotmail.com
Cerebral vascular Disease
?Definition of term,
?The term cerebrovascular disease designates any
abnormality of the brain resulting from a pathologic
process of the blood vessels,Sudden loss of neurological
function is the hallmark of cerebrovascular disease,
?Cerebrovascular disease is the third most common cause
of death and the most common disabling neurologic
disorder in western civilized countries where an increasing
proportion of people survive to old age,Shanghai is
entering the aging society
?Its incidence increases with age and is somewhat higher in
men than in women,
Risk factors for stroke
?Systolic or diastolic hypertension
?Diabetics
?Hypercholesterolemia
?Heart disease (afib)
?Cigarette smoking
?Heavy alcohol consumption
?High homocystine
?Oral contraceptive use
The major types of
cerebrovascular disease
?Cerebral ischaemia and infarction
?Transient Ischemic Attacks
?Atherosclerotic thrombosis
?Lacunes
?Embolism
?Hemorrhage
?Hypertensive hemorrhage
?Ruptured aneurysms and vascular malformations
?Other
I,Cerebral ischaemia and
infarction
?Anatomy and pathology
?The principal pathological process under consideration here is
the occlusion of arteries supplying the brain,The two internal
carotid arteries and the basilar artery form the Circle of Willis
at the base of the brain,which acts as an efficient anatomotic
device in the event of occlusion of arteries proximal to it,
?Anatomy and pathology
?Occlusion leads to sudden severe ischaemia in the area of
brain tissue supplied by the occluded artery,and recovery
depends upon rapid lysis or fragmentation of the occluding
material,
Reversal of neurological function within minutes or hours
gives rise to the clinical picture of a transient ischaemic
attack,
?Anatomy and pathology
?When the neurological deficit lasts longer than 24 hours,it
may be called a reversible ischaemic neurological deficit
( RIND ) if it recovers completely in a few days,
or a completed stroke if there is a persistent deficit,
Sometimes recovery is very slow and incomplete,
Neurological symptoms and
signs
?The loss of function that the patient notices,
and which may be apparent on examination,
entirely depends on the area of brain tissue
involved in the ischaemic process,
Neurological symptoms and
signs
?The following suggest middle cerebral
territory,
?Dysphasia;
Dyslexia,dysgraphia,dyscalculia;
Loss of use of contralateral face and arm;
Loss of feeling in contralateral face and arm,
Neurological symptoms and
signs
?The following suggests anterior cerebral
territory,
Loss of use and/ or feeling in the
contralateral leg,
?The following suggests posterior cerebral
territory,
Development of a contralateral
homonymous hemianopia,
Neurological symptoms and
signs
?The following suggests a deep-seated lesion
affecting the internal capsule which is
supplied by small perforating branches of the
middle and posterior cerebral arteries close
to their origins,
Complete loss of motor and sensory
function throughout the whole of the
contralateral side of the body with a
homonymous hemianopia,
Neurological symptoms and
signs
?The following suggests ophthalmic artery
territory (the ophthalmic artery arises from
the internal carotid artery just below the
Circle of Willis),
Monocular loss of vision,
Neurological symptoms and
signs
?The following suggest vertebro-basilar territory,
double vision( 3,4,6);
facial numbness(5);
facial weakness(7);
vertigo (8);
dysphagia (9,10);
dysarthria ( 9,10,12);
ataxia;
drop attacks;
motor or sensory loss in both arms or legs,
1,Transient Ischemic
Attacks(TIA)
?Definition of term
?Current opinion holds that TIAs are brief,
reversible episodes of focal,nonconvulsive
ischaemic neurologic disturbance,Consensus has
been that their duration should be less than 24 h,
Clinical picture
?Transient Ischaemic Attacks can reflect the
involvement of any cerebral artery,The loss of
function entirely depends on the influenced
artery,
It may last a few seconds or up to 12 to 24 h,
Most of them last 2 to 15 min,
There are only a few attacks or several hundred,
Between attacks,the neurologic examination may
disclose no abnormalities,
A stroke may occur after numerous attacks have
occurred over a period of weeks or months,
Differential diagnosis of TIAs
?Transient episodes,indistinguishable from TIAs,
are known to occur in patients with
Seizure,Migraine,Transient global amnesia,and
occasionally in patients with multiple sclerosis,
meningioma,glioblastoma,metastatic brain
tumors situated in or near the cortex,and even
with subdural hematoma,
2,Cerebral thrombosis
?Most cerebrovascular disease can be
attributed to atheroscleroses and chronic
hypertension; until ways are found to prevent
or control them,vascular disease of the brain
will continue to be a major cause of morbidity,
Pathogenesis
?Pathogenesis of Ischemic neuronal death
Ischemia
↓
Excitatory amino acid receptors
↓
Borderzone or penumbra
↓
Programmed cell death
Clinical picture
?In general,evolution of the clinical
phenomena in relation to cerebral
thrombosis is more variable than that of
embolism and hemorrhage,The loss of
function that the patient notices,and which
may be apparent on examination,entirely
depends on the area of brain tissue
involved in the ischaemic process.(above)
Clinical picture
?In more than half of patients,the main part of
the stroke is preceded by minor signs or one or
more transient attacks of focal neurologic
dysfunction,The final stroke may be preceded by
one or two attacks or a hundred or more brief
TIAs,and stroke may follow the onset of the
attacks by hours,weeks,or,rarely,months,
?The most occurrence of the thrombotic stroke is
during sleep.The patient awakens paralyzed,
Either during the night or in the morning,
?Unaware of any difficulty,he may arise and fall
helplessly to the floor with the first step,
Clinical picture
?Associated symptoms
?Seizures accompany the onset of stroke in a small
number of cases (10-50%); in other instances,
they follow the stroke by weeks to years,The
presence of seizures does not definitively
distinguish embolic from thrombotic strokes,but
seizure at the onset of stroke may be more
common with embolus,
Clinical picture
?Associated symptoms
?Headache occurs in about 25% of patients with
ischaemic stroke,possibly because of the acute
dilation of collateral vessels,
Laboratory Findings
?CT Scan or MRI,A CT scan or MRI should be
obtained routinely to distinguish between
infarction and hemorrhage as the cause of stroke,
to exclude other lesions (eg,tumor,abscess) that
can mimic stroke,and to localize the lesion,CT is
usually preferred for initial diagnosis because it is
widely available and rapid and can readily make
the critical distinction between ischaemia and
hemorrhage,
?Lumbar Puncture,This should be performed in
selected cases to exclude subarachnoid
hemorrhage,
Laboratory Findings
?Cerebral Angiography,
Intra-arterial angiography is used to identify
operable extracranial carotid lesions in patients
with anterior circulation TIAs who are good
surgical candidates,It also can be used for intra-
arterial thrombolysis ( r-tPA)
?Magnetic resonance angiography (MRA) may
detect stenosis of large cerebral arteries,
aneurysms,and other vascular lesion,but its
sensitivity is generally inferior to that of
conventional angiography,
Differential Diagnosis
?Vascular disorders are mistaken for ischaemic stroke
include intracerebral hemorrhage,subdural or
epidural hematoma,and subarachnoid hemorrhage
from rupture of an aneurysm or vascular
malformation,These condition can often be
distinguished by a history of trauma or of
excruciating headache at onset,a more marked
depression of consciousness,or by the presence of
neck stiffness on examination,They can be excluded
by CT scan or MRI,
Differential Diagnosis
?Differential Diagnosis,Other structural brain lesion
such as tumor or abscess can also produce focal
cerebral symptoms of acute onset,Brain abscess is
suggested by concurrent fever,and both abscess and
tumor can usually be diagnosed by CT scan or MRI,
Metabolic disturbances,particularly hypoglycemia
and hyperosmolar nonketotic hyperglycemia,may
present in stroke like fashion,The serum glucose
level should therefore be determined in all patients
with apparent stroke,
Treatment of Cerebral
Thrombosis and Transient
Ischemic Attacks
? The current treatment of it may be divided into four parts,Management in the acute phase
Measures to restore the circulation and arrest the pathologic process
1,Thrombolytic agents ( t-PA only for completed stroke,w/in 3~6hrs )
2.Anticoagulant drugs ( Heparin,LMWH & warfarin)
3,Antiplatelet drugs ( Aspirin or Clopidogrel,Dipyridamole or
Ticlopidine )
4.Difibrase
5,Neuroprotective agents,barbiturates,opioid antagonist
naloxone,Manitol
Treatment
Treatment of cerebral edema and raised intracranial
pressure
Acute surgical revascularization
Surgery for symptomatic carotid stenosis
Carotid endarterectomy,intralumenal stents,
extracranial-intracranial bypass
Physical therapy and rehabilitation
Measures to prevent further strokes and progression
of vascular disease,
Treatment
Since the primary objective in the treatment of
atherothrombotic disease is prevention,efforts to
control the risk factors must continue,
Aspirin
Hypotensive agents
Oversedation should be avoided
Systemic hypotension,severe anemia should be
treated promptly
Particular care should be taken to maintain the
systemic blood pressure,oxygenation and
intracranial blood flow during surgical
procedures,especially in elderly patient,
Course and Prognosis
?When the patient is seen early in the cerebral
thrombosis,it is difficult to give an accurate
prognosis,
?As for the eventual or long-term prognosis of the
neurologic deficit,there are many possibilities,
?It must be mentioned that having had one
thrombotic stroke,the patient is at risk in the
ensuing months and years of having a stroke at
the same or another site,especially if there is
hypertension or diabetes mellitus,
3.Embolic infarction
?This is one of the most common cause of stroke,
In most cases of cerebral embolism,the embolic
material consists of a fragment that has broken
away from a thrombus within the heart,
Embolism due to fat,tumor cells,fibrocartilage,
amniotic fluid,or air is a rare occurrence and
seldom enters into the differential diagnosis of
stroke,
Clinical Picture
?Of all strokes,those due to cerebral
embolism develop most rapidly,
The embolus strikes at any time of the day
or night,Getting up to go to the bathroom
is a time of danger,
The neurologic picture will depend on the
artery involved and the site of obstruction,
Clinical Picture
?It is important to repeat that an embolus may
produce a severe neurologic deficit that is only
temporary; symptoms disappear as the embolus
fragments,In other words,embolism is a
common cause of a single evanescent stroke that
may reasonably be called a prolonged TIA,Also
as already pointed out,several emboli can give
rise to two or three transient attacks of differing
pattern or,rarely,of almost identical pattern,
Causes of cerebral embolism,
?Cardiac origin
Noncardiac origin
Undetermined origin
Laboratory Findings
?Not infrequently the first sign of
myocardial infarction is the occurrence of
embolism; therefore it is advisable that an
ECG and echocardiogram be obtained in
all patients with stroke of uncertain origin,
Prolonged study of heart rhythm with
Holter monitoring should be undertaken,
Laboratory Findings
?In some 30 percent of cases,cerebral
embolism produces a hemorrhagic
infarction,CT scanning or MRI may be
helpful in showing the more intense
hemorrhagic infarcts,particularly if the
scan is repeated on the second or third day,
Course and prognosis
?Most patients survive the initial insult,and in
many the neurologic deficit may recede relatively
rapidly,as indicated above,
The eventual prognosis is determined by the
occurrence of further emboli and the gravity of
the underlying illness- cardiac failure myocardial
infarction,bacterial endocarditis and so on,
Treatment and prevention
?Three phases of therapy,
General medical management in the acute phase,
Measures directed to restoring the circulation
Physical therapy and rehabilitation
These are much the same as described above the
prevention of atherothrombotic infarction,
4,Lacunar infarct
?As one might surmise,small penetrating
branches of the cerebral arteries may
become occluded,and the resulting infarcts
may be so small or so situated as to cause
no symptoms whatever,As the softened
tissue is removed,it leaves a small cavity,
or lacune,
Lacunar infarct
?In our clinical and pathologic material,
there has always been a strong correlation
of the lacunar state with a combination of
hypertension and atherosclerosis and,to a
lesser degree,with diabetes,
In all the cases of lacunar infarction,the
diagnosis depends essentially on the
occurrence of the certain unique stroke
syndromes of limited proportions,
Lacunar infarct
?As mentioned above,CT scanning is less
reliable than MRI in demonstrating the
lacunes,The EEG may be helpful in a
negative sense; in the case of lacunes in the
pons or the internal capsule,there is a
notable discrepancy between the unilateral
paralysis or sensory loss and the negligible
electrical changes over the affected
hemisphere,
Lacunar infarct
?Recognition of lacunar stroke is important
?Future lacunar stroke can be reduced by
treating HTN
Anticoagulation is not indicated ( No
evidence)
Aspirin is also of uncertanty
II,Intracranial Hemorrhage
?This is the common,well-known,spontaneous”
brain hemorrhage,It is due predominantly to
chronic hypertension and degenerative changes in
cerebral arteries.Hemorrhage may interfere with
cerebral function through a variety of
mechanisms,including destruction or
compression of brain tissue and compression of
vascular structures,leading to secondary
ischaemia and edema,
Intracranial Hemorrhage
?Intracranial hemorrhage is classified by its
location as intracerebral,subarachnoid,
subdural,or epidural,all of which- except
subdural hemorrhage- are usually caused
by arterial bleeding,
Intracranial Hemorrhage
?The bleeding occurs within brain tissue,and
rupture of arteries lying in the subarachnoid
space is practically unknown apart from
aneurysms,The extravasation forms a roughly
circular or oval mass that disrupts the tissue and
grows in volume as the bleeding continues,
Adjacent brain tissue is distorted and compressed,
If the hemorrhage is large,midline structures are
displaced to the opposite side and reticular
activating and respiratory centers are
compromised,leading to coma and death,
1,Intracerebral Hemorrhage
Of all the cerebrovascular diseases,brain
hemorrhage is the most dramatic.It has been given
its own name,“apoplexy”,
Clinical Picture
?With smaller hemorrhages,the clinical picture
conforms more closely to the usual temporal
profile of a stroke,i.e,an abrupt onset of
symptoms that evolve gradually and steadily over
minutes,hours,or a day or two,depending on the
size of the ruptured artery and the speed of
bleeding,
?Headache and vomiting are cardinal
features.Very small hemorrhages in,silent”
regions of the brain may escape clinical detection,
Clinical Picture
?Clinical features vary with the site of hemorrhage,
?Deep cerebral hemorrhage The two most common
sites of hypertensive hemorrhage are the putamen
and the thalamus,which are separated by the
posterior limb of the internal capsule,This
segment of the internal capsule is traversed by
descending motor fibers and ascending sensory
fibers,including the optic radiations,
Clinical Picture
?Lobar hemorrhage Hypertensive
hemorrhages also occur in subcortical
white matter underlying the frontal,
parietal,temporal,and occipital lobes,
Symptoms and signs vary according to the
location,
Clinical Picture
?Pontine hemorrhage With bleeding into the pons,
coma occurs within seconds to minutes and
usually leads to death within 48 hours,Ocular
findings typically include pinpoint pupils,
Horizontal eye movements are absent or
impaired,but vertical eye movements may be
preserved,
?Cerebellar hemorrhage The distinctive symptoms
of cerebellar hemorrhage (headache,dizziness,
vomiting,and the inability to stand or walk)
begin suddenly,within minutes after onset of
bleeding,
Laboratory Findings
?Among laboratory methods for the diagnosis of
intracerebral hemorrhage,the CT scan occupies
the foremost position,In CT scans,fresh blood is
visualized as a white mass as soon as it is shed,
The mass effect and the surrounding extruded
serum and edema are hypodense,
?By MRI,either in T1-or-T2 weighted images,the
hemorrhage is not easily visible in the 2 or 3 days
after bleeding,
Laboratory Findings
?In general,lumbar puncture is ill advised,
for it may precipitate or aggravate an
impending shift of central structures and
herniation,The white cell count in the
peripheral blood may rise transiently to
15,000 per cubic millimeter,a higher figure
than in thrombosis,
Differential Diagnosis,
?Putaminal,thalamic,and lobar hypertensive
hemorrhages may be difficult to distinguish from
cerebral infarctions,To some extent,the presence
of severe headache,nausea and vomiting,and
impairment of consciousness are useful clues that
a hemorrhage may have occurred; the CT scan
identifies the underlying disorder definitively,
?CT scan or MRI is the most useful diagnostic
procedure,since hematomas can be quickly and
accurately localized,
Treatment
?The management of patients with large
intracerebral hemorrhages and coma includes the
maintenance of adequate ventilation,use of
controlled hyperventilation to a Pco2 of 25 to 30
mmHg,monitoring of intracranial pressure (ICP)
in some cases and its control by the use of tissue-
dehydrating agents such as mannitol (osmolality
kept at 295 to 305 mosmol/L and Na at 145 to 150
meq),and limiting intravenous infusions to
normal saline,
Treatment
?Rapid reduction in blood pressure,in the hope of
reducing further bleeding,is not recommended,
since it risks compromising cerebral perfusion in
cases of raised intracranial pressure,On the
other hand,sustained mean blood pressure of
greater than 110mmHg may exaggerate cerebral
edema and risk extension of the clot,It is at
approximately this level of acute hypertension
that the use of beta-blocking drugs(esmolol,
labetalol) or angiotensin-converting enzyme
inhibitory drugs is recommended,
Treatment
?In contrast to cerebral hemorrhage,the
surgical evacuation of cerebellar
hematomas is a generally accepted
treatment and is a more urgent matter
because of the proximity of the mass to
brainstem and the risk of abrupt
progression to coma and respiratory failure,
Course and Prognosis
?The immediate prognosis for large and medium-
size cerebral clots is grave; some 30 to 35 percent
of patients die in 1 to 30 days,
?Either the hemorrhage extends into the
ventricular system or intracranial pressure is
elevated to levels that preclude normal perfusion
of the brain,
?Sometimes the hemorrhage itself seeps into vital
centers such as the hypothalamus or midbrain,
Course and Prognosis
?A volume of 30 ml or less,calculated from
the CT scan,predicted a generally
favorable outcome,
?In patients with clots of 60 ml or larger and
an initial Glasgow Coma Scale score of 8 or
less,the mortality was 90 percent,As
remarked earlier,it is the location of the
clinical effects,
2.Spontaneous Subarachnoid
Hemorrhage
?This is the fourth most frequent cerebrovascular
disorder following atherothrombosis,embolism,
and primary intracerebral hemorrhage,Saccular
aneurysms are also called berry” aneurysms;
actually they take the form of small,thin-walled
blisters protruding from arteries of the circle of
Willis or its major branches,Their rupture
causes a flooding of the subarachnoid space with
blood under high pressure,
?Aneurysms are multiple in 20 percent of patients
Spontaneous Subarachnoid
Hemorrhage
?In childhood,rupture of saccular aneurysms is
rare,and they are seldom found at routine
postmortem examination; beyond childhood,they
gradually increase in frequency to reach their
peak incidence between 35 and 65 years of age,
?Approximately 90 to 95 percent of saccular
aneurysms lie on the anterior part of the circle of
Willis,
Clinical picture
?Prior to rupture,saccular aneurysms are usually
asymptomatic,Exceptionally,if sufficiently large
to compress pain-sensitive structures,they may
cause localized cranial pain,
?The presence of a partial oculomotor palsy with
dilated pupil may be indicative of an aneurysm of
the posterior communicating-- internal carotid
junction,
?With rupture of the aneurysm,blood under high
pressure is forced into the subarachnoid
space(where the circle of Willis lies),
Clinical picture
?Rupture of the aneurysm usually occurs while the
patient is active rather than during sleep,and in
some instances sexual intercourse,straining at
stool,lifting heavy objects,or other sustaining
exertion precipitates the ictus,In patients who
survive the initial rupture,the most feared
complication is rerupture,an event that may
occur at any time from minutes up to 2 or 3
weeks later,
?In less severe cases,consciousness,if lost,may be
regained within a few minutes or hours,but a
residual of drowsiness,confusion,and amnesia
accompanied by severe headache and stiff neck
persists for several days,
Clinical picture
?Since the hemorrhage is confined to the
subarachnoid space,there are few or no
focal neurologic signs,
?AVM is another most common cause for
SAH
?Convulsive seizures,usually brief and
generalized,
Clinical picture
?Vasospasm Delayed hemiplegia or other focal
deficit usually appears 3 to 12 days after rupture
and rarely before or after this period,These
delayed accidents and the focal narrowing of a
large artery or arteries,seen on angiography,are
refered to as vasospasm,
?Hydrocephalus If a large amount of blood
ruptures into the ventricular system or floods the
basal subarachnoid space,The patient then may
become confused or unconscious as a result of
acute hydrocephalus,A subacute hydrocephalus
due to blockage of the CSF pathways by blood
may appear after 2 to 4 weeks,
Laboratory Findings
?A CT scan will detect blood locally or diffusely in
the subarachnoid spaces or within the brain or
ventricular system in more than 90 percent of
cases and in practically all cases in which the
hemorrhage has been severe enough to cause
momentary or persistent loss of consciousness,
?In all other cases a lumbar puncture should be
undertaken when the clinical features suggest a
subarachnoid hemorrhage,Usually the CSF is
grossly bloody within 30 min of the hemorrhage,
with RBC counts up to 1 million per cubic
millimeter or even higher,
Laboratory Findings
?Carotid and vertebral angiography is the only
certain means of demonstrating an aneurysm and
does so in some 85 percent of patients in whom
the correct diagnosis of spontaneous
subarachnoid hemorrhage is made on clinical
grounds,
?MRI and MRA detect most aneurysms of the
basal vessels but are as yet of insufficient
sensitivity to replace conventional angiography,
Even when MRA or, CT angiography
,demonstrates the aneurysm,the surgeon usually
requires the kind of anatomic definition that can
only be obtained by conventional angiography,
Establish the diagnosis
?If there is a typical history,marked neck
stiffness and no focal neurological deficit,
lumbar puncture is still the best way to
make the diagnosis,revealing uniformly
blood-stained CSF,
Establish the diagnosis
?If the history is typical with marked neck stiffness,
but the patient remains in coma or shows a
marked focal neurological deficit,a CT scan is a
safer way to establish the diagnosis (revealing
blood in the subarachnoid space),since lumbar
puncture may lead to worse condition in this
group of patients (whose coma or focal
neurological deficit may indicate the presence of
an associated intracerebral blood clot),
Treatment
?This is influenced by the neurologic and general
medical state of the patient as well as by the
location and morphology of the aneurysm,
?The general medical management in the acute
stage includes the following,in all or part,
?bed rest
?fluid administration to maintain above-normal
circulating volume and central venous – pressure
?use of elastic stockings and stool softeners
?administration of beta-blockers
?calcium channel blockers
Treatment
?intravenous nitroprusside
?or other medication to reduce greatly elevated
blood pressure and then maintain systolic blood
pressure at 150 mmHg or less;
?and pain-relieving medication for headache ( this
alone will often reduce the hypertension ),
?The prevention of systemic venous thrombosis is
critical,usually accomplished by the use of
cyclically inflated whole-leg compression boots,
Treatment
?The use of anticonvulsants is controversial;
many neurosurgeons administer them early,
with a view of preventing a seizure-induced
risk of rebleeding,
?Calcium channel blockers are being used
extensively to reduce the incidence of
stroke from vasospasm,Nimodipine 50 mg,
administered intravenus,is currently
favored,
Treatment
?Notable advances in the techniques for the
obliteration of aneurysms,particularly the
operating microscope,and the management of
circulatory volume have significantly improved
the outcome of patients with ruptured aneurysms,
?Both the risk of rerupture of the aneurysm and
some of the secondary problems that arise
because of the massive amount of blood in the
subarachnoid space can be obviated by early
obliteration of the aneurysm,
?
Treatment
? lumbar puncture is carried out for
diagnostic purposes if the CT scan is
inconclusive; thereafter this procedure is
performed only for the relief of intractable
headache,to detect recurrence of bleeding,
or to measure the intracranial pressure
prior to surgery,
Treatment
?Advice from specialist neurosurgical units should
be sought,Patients who have withstood their first
bleed well are submitted to carotid and vertebral
angiography within a few days to establish
whether or not an operable aneurysm is present,
Patients who do not recover from their first bleed
well,patients with inoperable aneurysms should
be nursed in bed for a few weeks and then
mobilized over a further few weeks,being
encouraged to return to full normal activities at
about 3-4 months,
?Prevent re-bleeding
Rehabilition
?Since the incidence of significant damage
to the brain is high in patients surviving
subarachnoid haemorrhage,many will not
be able to return to normal activities,
?They will need support from relatives,
nurses,physiotherapists,speech therapists,
occupational therapists,social workers and
specialist units in rehabilitation,
Course and prognosis
? Patients with the typical clinical picture of
spontaneous subarachnoid hemorrhage in whom
an aneurysm or arteriorvenous malformation
cannot be demonstrated angiographically have a
distinctly better prognosis than those in whom
the lesion is visualized,
? Vasospasm and rebleeding were the leasing
causes of morbidity and mortality in addition to
the initial bleed,In respect to rebleeding,Aoyagi
and Hayakawa found that this occurred within 2
weeks in 20 percent of patients,with a peak
incidence in the 24 h after the initial bleed,
THANKS!
Dr,LU,QINCHI
DEPARTMENT OF NEUROLOGY
REN JI HOSPITAL
SHANGHAI JIAO TONG UNIVERSITY
SCHOOL OF MEDICINE
Tel,58752345-3094
Email,qinchilu@hotmail.com
Cerebral vascular Disease
?Definition of term,
?The term cerebrovascular disease designates any
abnormality of the brain resulting from a pathologic
process of the blood vessels,Sudden loss of neurological
function is the hallmark of cerebrovascular disease,
?Cerebrovascular disease is the third most common cause
of death and the most common disabling neurologic
disorder in western civilized countries where an increasing
proportion of people survive to old age,Shanghai is
entering the aging society
?Its incidence increases with age and is somewhat higher in
men than in women,
Risk factors for stroke
?Systolic or diastolic hypertension
?Diabetics
?Hypercholesterolemia
?Heart disease (afib)
?Cigarette smoking
?Heavy alcohol consumption
?High homocystine
?Oral contraceptive use
The major types of
cerebrovascular disease
?Cerebral ischaemia and infarction
?Transient Ischemic Attacks
?Atherosclerotic thrombosis
?Lacunes
?Embolism
?Hemorrhage
?Hypertensive hemorrhage
?Ruptured aneurysms and vascular malformations
?Other
I,Cerebral ischaemia and
infarction
?Anatomy and pathology
?The principal pathological process under consideration here is
the occlusion of arteries supplying the brain,The two internal
carotid arteries and the basilar artery form the Circle of Willis
at the base of the brain,which acts as an efficient anatomotic
device in the event of occlusion of arteries proximal to it,
?Anatomy and pathology
?Occlusion leads to sudden severe ischaemia in the area of
brain tissue supplied by the occluded artery,and recovery
depends upon rapid lysis or fragmentation of the occluding
material,
Reversal of neurological function within minutes or hours
gives rise to the clinical picture of a transient ischaemic
attack,
?Anatomy and pathology
?When the neurological deficit lasts longer than 24 hours,it
may be called a reversible ischaemic neurological deficit
( RIND ) if it recovers completely in a few days,
or a completed stroke if there is a persistent deficit,
Sometimes recovery is very slow and incomplete,
Neurological symptoms and
signs
?The loss of function that the patient notices,
and which may be apparent on examination,
entirely depends on the area of brain tissue
involved in the ischaemic process,
Neurological symptoms and
signs
?The following suggest middle cerebral
territory,
?Dysphasia;
Dyslexia,dysgraphia,dyscalculia;
Loss of use of contralateral face and arm;
Loss of feeling in contralateral face and arm,
Neurological symptoms and
signs
?The following suggests anterior cerebral
territory,
Loss of use and/ or feeling in the
contralateral leg,
?The following suggests posterior cerebral
territory,
Development of a contralateral
homonymous hemianopia,
Neurological symptoms and
signs
?The following suggests a deep-seated lesion
affecting the internal capsule which is
supplied by small perforating branches of the
middle and posterior cerebral arteries close
to their origins,
Complete loss of motor and sensory
function throughout the whole of the
contralateral side of the body with a
homonymous hemianopia,
Neurological symptoms and
signs
?The following suggests ophthalmic artery
territory (the ophthalmic artery arises from
the internal carotid artery just below the
Circle of Willis),
Monocular loss of vision,
Neurological symptoms and
signs
?The following suggest vertebro-basilar territory,
double vision( 3,4,6);
facial numbness(5);
facial weakness(7);
vertigo (8);
dysphagia (9,10);
dysarthria ( 9,10,12);
ataxia;
drop attacks;
motor or sensory loss in both arms or legs,
1,Transient Ischemic
Attacks(TIA)
?Definition of term
?Current opinion holds that TIAs are brief,
reversible episodes of focal,nonconvulsive
ischaemic neurologic disturbance,Consensus has
been that their duration should be less than 24 h,
Clinical picture
?Transient Ischaemic Attacks can reflect the
involvement of any cerebral artery,The loss of
function entirely depends on the influenced
artery,
It may last a few seconds or up to 12 to 24 h,
Most of them last 2 to 15 min,
There are only a few attacks or several hundred,
Between attacks,the neurologic examination may
disclose no abnormalities,
A stroke may occur after numerous attacks have
occurred over a period of weeks or months,
Differential diagnosis of TIAs
?Transient episodes,indistinguishable from TIAs,
are known to occur in patients with
Seizure,Migraine,Transient global amnesia,and
occasionally in patients with multiple sclerosis,
meningioma,glioblastoma,metastatic brain
tumors situated in or near the cortex,and even
with subdural hematoma,
2,Cerebral thrombosis
?Most cerebrovascular disease can be
attributed to atheroscleroses and chronic
hypertension; until ways are found to prevent
or control them,vascular disease of the brain
will continue to be a major cause of morbidity,
Pathogenesis
?Pathogenesis of Ischemic neuronal death
Ischemia
↓
Excitatory amino acid receptors
↓
Borderzone or penumbra
↓
Programmed cell death
Clinical picture
?In general,evolution of the clinical
phenomena in relation to cerebral
thrombosis is more variable than that of
embolism and hemorrhage,The loss of
function that the patient notices,and which
may be apparent on examination,entirely
depends on the area of brain tissue
involved in the ischaemic process.(above)
Clinical picture
?In more than half of patients,the main part of
the stroke is preceded by minor signs or one or
more transient attacks of focal neurologic
dysfunction,The final stroke may be preceded by
one or two attacks or a hundred or more brief
TIAs,and stroke may follow the onset of the
attacks by hours,weeks,or,rarely,months,
?The most occurrence of the thrombotic stroke is
during sleep.The patient awakens paralyzed,
Either during the night or in the morning,
?Unaware of any difficulty,he may arise and fall
helplessly to the floor with the first step,
Clinical picture
?Associated symptoms
?Seizures accompany the onset of stroke in a small
number of cases (10-50%); in other instances,
they follow the stroke by weeks to years,The
presence of seizures does not definitively
distinguish embolic from thrombotic strokes,but
seizure at the onset of stroke may be more
common with embolus,
Clinical picture
?Associated symptoms
?Headache occurs in about 25% of patients with
ischaemic stroke,possibly because of the acute
dilation of collateral vessels,
Laboratory Findings
?CT Scan or MRI,A CT scan or MRI should be
obtained routinely to distinguish between
infarction and hemorrhage as the cause of stroke,
to exclude other lesions (eg,tumor,abscess) that
can mimic stroke,and to localize the lesion,CT is
usually preferred for initial diagnosis because it is
widely available and rapid and can readily make
the critical distinction between ischaemia and
hemorrhage,
?Lumbar Puncture,This should be performed in
selected cases to exclude subarachnoid
hemorrhage,
Laboratory Findings
?Cerebral Angiography,
Intra-arterial angiography is used to identify
operable extracranial carotid lesions in patients
with anterior circulation TIAs who are good
surgical candidates,It also can be used for intra-
arterial thrombolysis ( r-tPA)
?Magnetic resonance angiography (MRA) may
detect stenosis of large cerebral arteries,
aneurysms,and other vascular lesion,but its
sensitivity is generally inferior to that of
conventional angiography,
Differential Diagnosis
?Vascular disorders are mistaken for ischaemic stroke
include intracerebral hemorrhage,subdural or
epidural hematoma,and subarachnoid hemorrhage
from rupture of an aneurysm or vascular
malformation,These condition can often be
distinguished by a history of trauma or of
excruciating headache at onset,a more marked
depression of consciousness,or by the presence of
neck stiffness on examination,They can be excluded
by CT scan or MRI,
Differential Diagnosis
?Differential Diagnosis,Other structural brain lesion
such as tumor or abscess can also produce focal
cerebral symptoms of acute onset,Brain abscess is
suggested by concurrent fever,and both abscess and
tumor can usually be diagnosed by CT scan or MRI,
Metabolic disturbances,particularly hypoglycemia
and hyperosmolar nonketotic hyperglycemia,may
present in stroke like fashion,The serum glucose
level should therefore be determined in all patients
with apparent stroke,
Treatment of Cerebral
Thrombosis and Transient
Ischemic Attacks
? The current treatment of it may be divided into four parts,Management in the acute phase
Measures to restore the circulation and arrest the pathologic process
1,Thrombolytic agents ( t-PA only for completed stroke,w/in 3~6hrs )
2.Anticoagulant drugs ( Heparin,LMWH & warfarin)
3,Antiplatelet drugs ( Aspirin or Clopidogrel,Dipyridamole or
Ticlopidine )
4.Difibrase
5,Neuroprotective agents,barbiturates,opioid antagonist
naloxone,Manitol
Treatment
Treatment of cerebral edema and raised intracranial
pressure
Acute surgical revascularization
Surgery for symptomatic carotid stenosis
Carotid endarterectomy,intralumenal stents,
extracranial-intracranial bypass
Physical therapy and rehabilitation
Measures to prevent further strokes and progression
of vascular disease,
Treatment
Since the primary objective in the treatment of
atherothrombotic disease is prevention,efforts to
control the risk factors must continue,
Aspirin
Hypotensive agents
Oversedation should be avoided
Systemic hypotension,severe anemia should be
treated promptly
Particular care should be taken to maintain the
systemic blood pressure,oxygenation and
intracranial blood flow during surgical
procedures,especially in elderly patient,
Course and Prognosis
?When the patient is seen early in the cerebral
thrombosis,it is difficult to give an accurate
prognosis,
?As for the eventual or long-term prognosis of the
neurologic deficit,there are many possibilities,
?It must be mentioned that having had one
thrombotic stroke,the patient is at risk in the
ensuing months and years of having a stroke at
the same or another site,especially if there is
hypertension or diabetes mellitus,
3.Embolic infarction
?This is one of the most common cause of stroke,
In most cases of cerebral embolism,the embolic
material consists of a fragment that has broken
away from a thrombus within the heart,
Embolism due to fat,tumor cells,fibrocartilage,
amniotic fluid,or air is a rare occurrence and
seldom enters into the differential diagnosis of
stroke,
Clinical Picture
?Of all strokes,those due to cerebral
embolism develop most rapidly,
The embolus strikes at any time of the day
or night,Getting up to go to the bathroom
is a time of danger,
The neurologic picture will depend on the
artery involved and the site of obstruction,
Clinical Picture
?It is important to repeat that an embolus may
produce a severe neurologic deficit that is only
temporary; symptoms disappear as the embolus
fragments,In other words,embolism is a
common cause of a single evanescent stroke that
may reasonably be called a prolonged TIA,Also
as already pointed out,several emboli can give
rise to two or three transient attacks of differing
pattern or,rarely,of almost identical pattern,
Causes of cerebral embolism,
?Cardiac origin
Noncardiac origin
Undetermined origin
Laboratory Findings
?Not infrequently the first sign of
myocardial infarction is the occurrence of
embolism; therefore it is advisable that an
ECG and echocardiogram be obtained in
all patients with stroke of uncertain origin,
Prolonged study of heart rhythm with
Holter monitoring should be undertaken,
Laboratory Findings
?In some 30 percent of cases,cerebral
embolism produces a hemorrhagic
infarction,CT scanning or MRI may be
helpful in showing the more intense
hemorrhagic infarcts,particularly if the
scan is repeated on the second or third day,
Course and prognosis
?Most patients survive the initial insult,and in
many the neurologic deficit may recede relatively
rapidly,as indicated above,
The eventual prognosis is determined by the
occurrence of further emboli and the gravity of
the underlying illness- cardiac failure myocardial
infarction,bacterial endocarditis and so on,
Treatment and prevention
?Three phases of therapy,
General medical management in the acute phase,
Measures directed to restoring the circulation
Physical therapy and rehabilitation
These are much the same as described above the
prevention of atherothrombotic infarction,
4,Lacunar infarct
?As one might surmise,small penetrating
branches of the cerebral arteries may
become occluded,and the resulting infarcts
may be so small or so situated as to cause
no symptoms whatever,As the softened
tissue is removed,it leaves a small cavity,
or lacune,
Lacunar infarct
?In our clinical and pathologic material,
there has always been a strong correlation
of the lacunar state with a combination of
hypertension and atherosclerosis and,to a
lesser degree,with diabetes,
In all the cases of lacunar infarction,the
diagnosis depends essentially on the
occurrence of the certain unique stroke
syndromes of limited proportions,
Lacunar infarct
?As mentioned above,CT scanning is less
reliable than MRI in demonstrating the
lacunes,The EEG may be helpful in a
negative sense; in the case of lacunes in the
pons or the internal capsule,there is a
notable discrepancy between the unilateral
paralysis or sensory loss and the negligible
electrical changes over the affected
hemisphere,
Lacunar infarct
?Recognition of lacunar stroke is important
?Future lacunar stroke can be reduced by
treating HTN
Anticoagulation is not indicated ( No
evidence)
Aspirin is also of uncertanty
II,Intracranial Hemorrhage
?This is the common,well-known,spontaneous”
brain hemorrhage,It is due predominantly to
chronic hypertension and degenerative changes in
cerebral arteries.Hemorrhage may interfere with
cerebral function through a variety of
mechanisms,including destruction or
compression of brain tissue and compression of
vascular structures,leading to secondary
ischaemia and edema,
Intracranial Hemorrhage
?Intracranial hemorrhage is classified by its
location as intracerebral,subarachnoid,
subdural,or epidural,all of which- except
subdural hemorrhage- are usually caused
by arterial bleeding,
Intracranial Hemorrhage
?The bleeding occurs within brain tissue,and
rupture of arteries lying in the subarachnoid
space is practically unknown apart from
aneurysms,The extravasation forms a roughly
circular or oval mass that disrupts the tissue and
grows in volume as the bleeding continues,
Adjacent brain tissue is distorted and compressed,
If the hemorrhage is large,midline structures are
displaced to the opposite side and reticular
activating and respiratory centers are
compromised,leading to coma and death,
1,Intracerebral Hemorrhage
Of all the cerebrovascular diseases,brain
hemorrhage is the most dramatic.It has been given
its own name,“apoplexy”,
Clinical Picture
?With smaller hemorrhages,the clinical picture
conforms more closely to the usual temporal
profile of a stroke,i.e,an abrupt onset of
symptoms that evolve gradually and steadily over
minutes,hours,or a day or two,depending on the
size of the ruptured artery and the speed of
bleeding,
?Headache and vomiting are cardinal
features.Very small hemorrhages in,silent”
regions of the brain may escape clinical detection,
Clinical Picture
?Clinical features vary with the site of hemorrhage,
?Deep cerebral hemorrhage The two most common
sites of hypertensive hemorrhage are the putamen
and the thalamus,which are separated by the
posterior limb of the internal capsule,This
segment of the internal capsule is traversed by
descending motor fibers and ascending sensory
fibers,including the optic radiations,
Clinical Picture
?Lobar hemorrhage Hypertensive
hemorrhages also occur in subcortical
white matter underlying the frontal,
parietal,temporal,and occipital lobes,
Symptoms and signs vary according to the
location,
Clinical Picture
?Pontine hemorrhage With bleeding into the pons,
coma occurs within seconds to minutes and
usually leads to death within 48 hours,Ocular
findings typically include pinpoint pupils,
Horizontal eye movements are absent or
impaired,but vertical eye movements may be
preserved,
?Cerebellar hemorrhage The distinctive symptoms
of cerebellar hemorrhage (headache,dizziness,
vomiting,and the inability to stand or walk)
begin suddenly,within minutes after onset of
bleeding,
Laboratory Findings
?Among laboratory methods for the diagnosis of
intracerebral hemorrhage,the CT scan occupies
the foremost position,In CT scans,fresh blood is
visualized as a white mass as soon as it is shed,
The mass effect and the surrounding extruded
serum and edema are hypodense,
?By MRI,either in T1-or-T2 weighted images,the
hemorrhage is not easily visible in the 2 or 3 days
after bleeding,
Laboratory Findings
?In general,lumbar puncture is ill advised,
for it may precipitate or aggravate an
impending shift of central structures and
herniation,The white cell count in the
peripheral blood may rise transiently to
15,000 per cubic millimeter,a higher figure
than in thrombosis,
Differential Diagnosis,
?Putaminal,thalamic,and lobar hypertensive
hemorrhages may be difficult to distinguish from
cerebral infarctions,To some extent,the presence
of severe headache,nausea and vomiting,and
impairment of consciousness are useful clues that
a hemorrhage may have occurred; the CT scan
identifies the underlying disorder definitively,
?CT scan or MRI is the most useful diagnostic
procedure,since hematomas can be quickly and
accurately localized,
Treatment
?The management of patients with large
intracerebral hemorrhages and coma includes the
maintenance of adequate ventilation,use of
controlled hyperventilation to a Pco2 of 25 to 30
mmHg,monitoring of intracranial pressure (ICP)
in some cases and its control by the use of tissue-
dehydrating agents such as mannitol (osmolality
kept at 295 to 305 mosmol/L and Na at 145 to 150
meq),and limiting intravenous infusions to
normal saline,
Treatment
?Rapid reduction in blood pressure,in the hope of
reducing further bleeding,is not recommended,
since it risks compromising cerebral perfusion in
cases of raised intracranial pressure,On the
other hand,sustained mean blood pressure of
greater than 110mmHg may exaggerate cerebral
edema and risk extension of the clot,It is at
approximately this level of acute hypertension
that the use of beta-blocking drugs(esmolol,
labetalol) or angiotensin-converting enzyme
inhibitory drugs is recommended,
Treatment
?In contrast to cerebral hemorrhage,the
surgical evacuation of cerebellar
hematomas is a generally accepted
treatment and is a more urgent matter
because of the proximity of the mass to
brainstem and the risk of abrupt
progression to coma and respiratory failure,
Course and Prognosis
?The immediate prognosis for large and medium-
size cerebral clots is grave; some 30 to 35 percent
of patients die in 1 to 30 days,
?Either the hemorrhage extends into the
ventricular system or intracranial pressure is
elevated to levels that preclude normal perfusion
of the brain,
?Sometimes the hemorrhage itself seeps into vital
centers such as the hypothalamus or midbrain,
Course and Prognosis
?A volume of 30 ml or less,calculated from
the CT scan,predicted a generally
favorable outcome,
?In patients with clots of 60 ml or larger and
an initial Glasgow Coma Scale score of 8 or
less,the mortality was 90 percent,As
remarked earlier,it is the location of the
clinical effects,
2.Spontaneous Subarachnoid
Hemorrhage
?This is the fourth most frequent cerebrovascular
disorder following atherothrombosis,embolism,
and primary intracerebral hemorrhage,Saccular
aneurysms are also called berry” aneurysms;
actually they take the form of small,thin-walled
blisters protruding from arteries of the circle of
Willis or its major branches,Their rupture
causes a flooding of the subarachnoid space with
blood under high pressure,
?Aneurysms are multiple in 20 percent of patients
Spontaneous Subarachnoid
Hemorrhage
?In childhood,rupture of saccular aneurysms is
rare,and they are seldom found at routine
postmortem examination; beyond childhood,they
gradually increase in frequency to reach their
peak incidence between 35 and 65 years of age,
?Approximately 90 to 95 percent of saccular
aneurysms lie on the anterior part of the circle of
Willis,
Clinical picture
?Prior to rupture,saccular aneurysms are usually
asymptomatic,Exceptionally,if sufficiently large
to compress pain-sensitive structures,they may
cause localized cranial pain,
?The presence of a partial oculomotor palsy with
dilated pupil may be indicative of an aneurysm of
the posterior communicating-- internal carotid
junction,
?With rupture of the aneurysm,blood under high
pressure is forced into the subarachnoid
space(where the circle of Willis lies),
Clinical picture
?Rupture of the aneurysm usually occurs while the
patient is active rather than during sleep,and in
some instances sexual intercourse,straining at
stool,lifting heavy objects,or other sustaining
exertion precipitates the ictus,In patients who
survive the initial rupture,the most feared
complication is rerupture,an event that may
occur at any time from minutes up to 2 or 3
weeks later,
?In less severe cases,consciousness,if lost,may be
regained within a few minutes or hours,but a
residual of drowsiness,confusion,and amnesia
accompanied by severe headache and stiff neck
persists for several days,
Clinical picture
?Since the hemorrhage is confined to the
subarachnoid space,there are few or no
focal neurologic signs,
?AVM is another most common cause for
SAH
?Convulsive seizures,usually brief and
generalized,
Clinical picture
?Vasospasm Delayed hemiplegia or other focal
deficit usually appears 3 to 12 days after rupture
and rarely before or after this period,These
delayed accidents and the focal narrowing of a
large artery or arteries,seen on angiography,are
refered to as vasospasm,
?Hydrocephalus If a large amount of blood
ruptures into the ventricular system or floods the
basal subarachnoid space,The patient then may
become confused or unconscious as a result of
acute hydrocephalus,A subacute hydrocephalus
due to blockage of the CSF pathways by blood
may appear after 2 to 4 weeks,
Laboratory Findings
?A CT scan will detect blood locally or diffusely in
the subarachnoid spaces or within the brain or
ventricular system in more than 90 percent of
cases and in practically all cases in which the
hemorrhage has been severe enough to cause
momentary or persistent loss of consciousness,
?In all other cases a lumbar puncture should be
undertaken when the clinical features suggest a
subarachnoid hemorrhage,Usually the CSF is
grossly bloody within 30 min of the hemorrhage,
with RBC counts up to 1 million per cubic
millimeter or even higher,
Laboratory Findings
?Carotid and vertebral angiography is the only
certain means of demonstrating an aneurysm and
does so in some 85 percent of patients in whom
the correct diagnosis of spontaneous
subarachnoid hemorrhage is made on clinical
grounds,
?MRI and MRA detect most aneurysms of the
basal vessels but are as yet of insufficient
sensitivity to replace conventional angiography,
Even when MRA or, CT angiography
,demonstrates the aneurysm,the surgeon usually
requires the kind of anatomic definition that can
only be obtained by conventional angiography,
Establish the diagnosis
?If there is a typical history,marked neck
stiffness and no focal neurological deficit,
lumbar puncture is still the best way to
make the diagnosis,revealing uniformly
blood-stained CSF,
Establish the diagnosis
?If the history is typical with marked neck stiffness,
but the patient remains in coma or shows a
marked focal neurological deficit,a CT scan is a
safer way to establish the diagnosis (revealing
blood in the subarachnoid space),since lumbar
puncture may lead to worse condition in this
group of patients (whose coma or focal
neurological deficit may indicate the presence of
an associated intracerebral blood clot),
Treatment
?This is influenced by the neurologic and general
medical state of the patient as well as by the
location and morphology of the aneurysm,
?The general medical management in the acute
stage includes the following,in all or part,
?bed rest
?fluid administration to maintain above-normal
circulating volume and central venous – pressure
?use of elastic stockings and stool softeners
?administration of beta-blockers
?calcium channel blockers
Treatment
?intravenous nitroprusside
?or other medication to reduce greatly elevated
blood pressure and then maintain systolic blood
pressure at 150 mmHg or less;
?and pain-relieving medication for headache ( this
alone will often reduce the hypertension ),
?The prevention of systemic venous thrombosis is
critical,usually accomplished by the use of
cyclically inflated whole-leg compression boots,
Treatment
?The use of anticonvulsants is controversial;
many neurosurgeons administer them early,
with a view of preventing a seizure-induced
risk of rebleeding,
?Calcium channel blockers are being used
extensively to reduce the incidence of
stroke from vasospasm,Nimodipine 50 mg,
administered intravenus,is currently
favored,
Treatment
?Notable advances in the techniques for the
obliteration of aneurysms,particularly the
operating microscope,and the management of
circulatory volume have significantly improved
the outcome of patients with ruptured aneurysms,
?Both the risk of rerupture of the aneurysm and
some of the secondary problems that arise
because of the massive amount of blood in the
subarachnoid space can be obviated by early
obliteration of the aneurysm,
?
Treatment
? lumbar puncture is carried out for
diagnostic purposes if the CT scan is
inconclusive; thereafter this procedure is
performed only for the relief of intractable
headache,to detect recurrence of bleeding,
or to measure the intracranial pressure
prior to surgery,
Treatment
?Advice from specialist neurosurgical units should
be sought,Patients who have withstood their first
bleed well are submitted to carotid and vertebral
angiography within a few days to establish
whether or not an operable aneurysm is present,
Patients who do not recover from their first bleed
well,patients with inoperable aneurysms should
be nursed in bed for a few weeks and then
mobilized over a further few weeks,being
encouraged to return to full normal activities at
about 3-4 months,
?Prevent re-bleeding
Rehabilition
?Since the incidence of significant damage
to the brain is high in patients surviving
subarachnoid haemorrhage,many will not
be able to return to normal activities,
?They will need support from relatives,
nurses,physiotherapists,speech therapists,
occupational therapists,social workers and
specialist units in rehabilitation,
Course and prognosis
? Patients with the typical clinical picture of
spontaneous subarachnoid hemorrhage in whom
an aneurysm or arteriorvenous malformation
cannot be demonstrated angiographically have a
distinctly better prognosis than those in whom
the lesion is visualized,
? Vasospasm and rebleeding were the leasing
causes of morbidity and mortality in addition to
the initial bleed,In respect to rebleeding,Aoyagi
and Hayakawa found that this occurred within 2
weeks in 20 percent of patients,with a peak
incidence in the 24 h after the initial bleed,
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