Stroke

Introduction
Stroke is a clinical syndrome of sudden
focal or global cerebral dysfunction lasting
more than 24 hours, of presumed vascular
origin. It may occur as a result of cerebral
infarction (ischaemic stroke), intracerebral
haemorrhage or subarachnoid
haemorrhage. Ischaemic stroke is the
commonest type, accounting for about
85%.
Pathophysiology of ischaemic
stroke
Thrombo-embolic occlusion of blood flow triggers a sequence
of events, the ischaemic cascade. Failure of energy production
leads to anaerobic glycolysis and lactic acidosis, and failure of
the ion pumps results in neuronal depolarisation and
intracellular calcium overload. These events lead to the
release of neurotoxic substances such as excitatory
neurotransmitters (chiefly glutamate), inflammatory mediators
(eg. prostaglandins, leukotrienes), toxic free radicals (eg.
nitric oxide) and activated lytic enzymes (lipases, proteases),
ultimately causing neuronal death (1).
Ischaemic damage depends on the degree and the duration
of ischaemia. Following complete occlusion of a vessel, a
central core of densely ischaemic tissue is irreversibly
damaged (infarction) within minutes.
Around the infarction is an area of critical ischaemia
(ischaemic penumbra), which is inadequately perfused.
Neurones in the penumbra are energy deficient and
electrically quiescent, but have intact ion pumps and are
viable. Prolonged ischaemia will lead to their death and
extension of the infarct. If perfusion is restored within a
certain period of time, neurones in the penumbra can
be salvaged; this constitutes a therapeutic window of
opportunity. In humans, this window period is believed
to be 3 to 6 hours.
Early treatment
Components of the early treatment of ischaemic stroke
are shown in Box 1.
Box 1. Early treatment of
ischaemic stroke
1. General care
2. Specific treatment: thrombolysis,
anticoagulants, antiplatelet agents and neuro-
protective agents
3. Emergency approach
4. Stroke unit care
5. Treatment of complications
6. Treatment of co-morbidity
7. Rehabilitation
1. General care
1. General care
General care of a stroke patient in the early stages aims at sustaining life
(eg. airway, breathing, circulation) and maintaining vital bodily
functions (eg. fluid and electrolyte balance, blood glucose, nutrition,
swallowing, temperature, and bladder, bowel and skin care).
Autoregulation of regional cerebral blood flow is defective in the ischaemic
penumbra, and blood flow is dependent on cerebral perfusion pressure.
Volume depletion or a fall in blood pressure will reduce perfusion
pressure and lead to extension of the infarct (2,3). Attention to fluid
and electrolyte balance is essential. Volume overload can lead to
cerebral oedema, and volume depletion with accompanying
hypotension and electrolyte disturbances can adversely affect outcome.
Volume replacement should be by the oral route, or a nasogastric tube
when swallowing is impaired. Intravenous fluids when required should
be given as isotonic saline. Aspiration is a concern in the early stages,
as swallowing difficulties are common. A simple bedside test of
swallowing is to give 1 or 2 teaspoonfuls of water with the patient
seated; coughing or `developing a wet voice' indicates impaired
swallowing and oral feeding should not be attempted.
Blood pressure management is critical after a stroke. A
transient rise in blood pressure is seen in up to 80% of
patients. This resolves spontaneously in most cases by 7 to
10 days. Injudicious treatment of reflex elevation in blood
pressure may lead to a fall in perfusion pressure in the
penumbra. Treatment should be started only when definite
indications (Box 2) are present (2,3,4). In their absence
blood pressure should be monitored regularly but treatment
withheld for 10 days. Antihypertensive therapy is
commenced if blood pressure remains persistently elevated
after 10 days.
Blood pressure reduction should be gradual, with a targeted
reduction of about 10 to 15% over 24 hours. Reducing
blood pressure to below systolic <180, diastolic <110 mmHg
can be harmful (3,4). Short acting oral agents (eg.
captopril) are particularly useful.
Box 2. Indications for early
treatment of elevated blood
pressure in acute stroke
Evidence of pre-existing hypertension
documented previous hypertension - clinic
records etc. evidence of hypertensive target
organ
damage, hypertensive retinopathy, left
ventricular hypertrophy on ECG
Evidence of a hypertensive emergency eg.
hypertensive encephalopathy, left heart failure.
Blood pressure is very high: systolic >220-240,
diastolic >120 mmHg
Blood glucose content is another critical determinant of
outcome after stroke. Both hypoglycaemia and
hyperglycaemia can be detrimental (4). Hypoglycaemia
should be corrected with dextrose infusions. Hypergly-
caemia is associated with aggravation of cerebral
oedema and increased mortality, and needs treatment
with insulin. Fever should be actively treated with
antipyretics, and the cause, usually an infection, sought
and treated.
Bladder dysfunction is common after a stroke, and both
urinary retention and incontinence can occur. Urinary
retention needs urethral catheterisation. In patients with
urinary incontinence, residual bladder volume after
micturition should be assessed by bladder ultrasound
scan or by catherisation; an indwelling catheter is
indicated where the residual volume is high, but others
can be managed with external devices such as condom
catheters
2. Specific therapy
a) Thrombolysis
The success of thrombolytic therapy in acute myocardial
infarction has rekindled interest in its use in stroke.
Intravenous thrombolytic therapy has changed the
treatment of acute ischaemic stroke. It appears that
both the type of drug and the timing of administration
are important determinants of outcome. Initial studies
that used streptokinase did not show a definite benefit.
However, the NINDS trial which used r-tPA within 3
hours of onset showed significant improvements in
outcome (5).
The main complication of thrombolytic therapy is
bleeding, which may be intracranial or extracranial.
Spontaneous haemorrhagic transformation, a recognised
complication of cerebral infarction, may be aggravated
by thrombolytic therapy. Thrombolysis increases the
severity of haemorrhage, rather than the incidence.
Early CT scans are useful not only to exclude
haemorrhage before thrombolysis, but also to identify
infarcts that may be at a higher risk of haemorrhagic
transformation. The dose of r-tPA is 0.9 mg/kg up to a
maximum of 90 mg, the first 10% as a bolus, and the
balance as an infusion over 60 min. There are many
contraindications for r-tPA including seizure at onset, pre-
treatment BP systolic >185, diastolic>110 mm Hg, major
infarct on CT scan, previous intracranial haemmorhage,
recent myocardial infarct, recent or intended surgery, use
of anticoagulant recently etc. IV r-tPA is now standard
acute treatment in the USA, Australia and most European
countries. Many concerns still remain largely owing to the
risk of bleeding and the difficulties in initiating treatment
within 3 hours (5). Intra-arterial thrombolysis using r-tPA
has been shown to be beneficial in posterior circulation
strokes due to basilar artery thrombosis. Its place in
carotid territory strokes is under evaluation.
b) Anticoagulants
Anticoagulants are of two main types, and include
parenteral heparin (unfractionated heparin and low
molecular weight heparin _ LMWH) and oral warfarin.
Oral warfarin is of proven benefit in prevention of stroke.
Unfractionated heparin has been used in acute ischaemic
stroke, especially in stroke-in-evolution or cardio-embolic
stroke, without much evidence of benefit. Many recent
studies have failed to demonstrate an improvement in
outcome (7), and unfractionated heparin has no place in
the management of acute ischaemic stroke. LMWH may
be equally effective as unfractionated heparin, with a
lower risk of bleeding. More large trials are necessary
before they can be considered in routine clinical practice.
c) Antiplatelet agents
Aspirin and other antiplatelet agents are of proven value
in primary and secondary prevention of stroke. Two
large trials, each randomising about 20 000 patients,
addressed the value of early use of aspirin in acute
ischaemic stroke. Data from both trials have shown that
early use of aspirin (160 to 300 mg within 48 hours) is
beneficial in reducing deaths and dependency (7,8). The
benefits appear to be mainly related to prevention of
early recurrences. The place of other antiplatelet agents
(such as dipyridamole, clopidogrel, ticlopidine and
glycoprotein IIb/IIIa receptor antagonists) as acute
treatment needs evaluation
d) Neuro-protective agents
Preserving the intergrity of the ischaemic neurones is
important. Avoid factors that aggravate ischaemic damage;
these include hypotension, hypoxia, hyperglycaemia and
hyperpyrexia (1). Reducing the energy requirements of
ischaemic neurones by high dose barbiturate therapy and
hypothermia have shown promising results (1). Treatment
with pharmacological agents that target specific events of
the ischaemic cascade (neuro-protective agents) within the
therapeutic window period is under evalution, and this may
become first-line therapy in the future (4,9). Such agents
include calcium channel blockers (eg nimopidine), GABA
antagonists (eg clomethiazole), glutamate antagonists (eg
eliprodil), free radical scavengers (eg tirilazad) and sodium
channel blockers (eg lubeluzole).
3. Treating stroke as an emergency
The main difficulty in using r-tPA and other potential therapies
is the need to initiate treatment within 3 hours. Many
countries have sucessfully overcome this challenge by
developing public educational campaigns, emergency pre-
hospital medical care systems with trained ambulance crews,
rapid triage and 'fast-track' systems on admission to hospital,
stroke units and stroke teams. Stroke is now treated as an
emergency.
4. Stroke units
A stroke unit is a multidisciplinary team of health care
professionals, providing organised inpatient stroke care in a
defined area. Compared with conventional care in a general
medical ward setting, stroke unit care produces significant
improvements in short term and long term outcome measures.
Death, disability, dependency and hospital stay are reduced,
and functional capacity is improved (10).
5. Treatment of complications
Early detection and treatment of complications are essential to
improve outcome after a stroke. Cerebral oedema, or brain
swelling, is probably the most important early complication.
Treatment of cerebral oedema should ideally be guided by
intracranial pressure monitoring. In the absence of such
facilities, patients with alteration of consciousness, large infarcts,
and evidence of mass effect (midline shift, compression of
ventricles) on CT scanning should be treated (Box 3). Other
complications of stroke include haemorhagic transformation,
seizures, respiratory and urinary infection, deep vein thrombosis
and pulmonary embolism, acute peptic ulcer, pressure sores,
neuropsychiatric sequelae such as anxiety or depression and
musculo-skeletal sequelae such as contractures, spasticity and
adhesive capsulitis of the shoulder.
Box 3. Management of raised
intracranial pressure after stroke
(3,4)
Elevate head end by 30
Avoid or correct aggravating factors _ hypoxia,
hyperglycaemia
Moderate fluid restriction
Avoid hypoosmolar fluids eg. dextrose
Giving osmotic agents (eg iv. mannitol) as
indicated
Hyperventilation
IV barbiturates
NB. Steroids are of no value
6. Treatment of co-morbidity
Patients with stroke are usually old and may have associated co-
morbid conditions. These may interfere with the rehabilitation process
(eg. chronic lung disease), or the treatment (eg. aspirin or warfarin in
peptic ulcer disease), and need assessment and treatment in their own
right.
7. Rehabilitation
Rehabilitation is the process by which patients after a stroke are
restored to their previous functional, mental and social capacity. This is
best carried out by a multidisciplinary stroke team with the active
participation of patients and care givers.
Conclusion
Stroke is an emergency, a 'brain attack'. Recent developments in drug
therapy and service organisation have led to an aggressive approach
to treatment of ischaemic stroke, replacing the widespread sense of
therapeutic nihilism in the past. Many new treatment modalities are
being increasingly used, more are being developed and evaluated, and
the future looks brighter for stroke patients.
The vascular diseases of cerebrum occupy one of the first places in the
structure of organic pathology of the central nervous system (about
17%).

HAEMORRHAGIC STROKE
Haemorrhagic stroke develops as a result of involuntary break of
intracerebral vessel and is accompanied by forming of
haematoma. A intracerebral hemorrhage is one of the heaviest
forms of vascular defeat of cerebrum. As a rule, a hemorrhage
of brain develops as a result of hypertensive illness (50 60%),
pathological changes in the vessels of brain, more frequent
after atherosclerosis.
Physical examination, births, emotional stresses, fluctuation in
the temperature of body, alcoholic intoxication and others like
that often predetermine the temporal increase of arterial
pressure. A spontaneous hemorrhage of brain mainly occurred
in women. In clinical practice hemorrhage is distinguished on
lateral and medial simultaneously on both sides of internal
capsule. A medial hemorrhage is often accompanied with
penetration of haematoma in the cavity of lateral or III ventricle.

Clinic. Haemorrhagic stroke develops mainly sharply, often without
some forecasters. A clinic is characterized by a sudden fainting fit and
local neurological symptoms. Sometimes there is vomits. The face of
patient becomes crimson-red, pulse tense, slow, breathings vowel, the
temperature of body rises. A head and eyes is often returned aside.
Another local symptoms are paresis or paralysis of extremities on a side
opposite to the cell of hemorrhage, which arise up as a result of
compression of the haematoma on formations of internal capsule or
vessels. If a hemorrhage is comparative small, motive violations are
poorly expressed, while a massive hemorrhage, squeezing an internal
capsule, results in hemiplegia.
Exposure of other local symptoms, in particular violations of
sensitiveness, hemianopsia, disorders of language, becomes possible
after the exit of patient from the comatose state and renewal of
consiousness. During short time from the moment of origin of stroke
there are considerable vibrations of vegetative violations: a pallor of
person changes by hyperemia or, opposite, he covered by sweat, the
distal departments of extremities are cold, often all these phenomena
prevail on the side of paralysis. In beginning of disease the increase of
tone of muscles with violation of motive function is characteristic.
For diagnostics the most important method is computer tomografy. If
at the persons of middle and young ages young the pressure of
cerebrospinal liquid is frequently promoted, at the senile age people it
can be normal or even reduced. The promoted maintenance of
albumen is often exposed. On G we can observed the -cho signal
on opposite to hemorrhage site
Very frequent is horizontal large amplitude tonic nistagm which often
unites with vertical, connected with asymmetrical position of eyes,
floating eyeballs. Disorders of breathing appear in the case of heavy
defeat of trunk.
Treatment. As lethality as a result of brain hemorrhage treated with
conservative treatment is extraordinarily high, and in the case of
surgical treatment goes down, that is why the necessary operation is a
method of choice.
A lateral hemorrhage is an absolute testimony for surgical treatment. In
the case of medial hemorrhage the prognosis for surgical treatment is
worse.
In the case of penetration of blood in the ventricles of brain the
conservative treatment is uneffective
Two types of operations are applied: 1) dissection of brain and delete
of haematoma; 2) urgent punction of haematoma through a brain with
sucking of blood. The cavity of haematoma once or twice is washed by
isotonic solution of sodium chloride.
In the case of presence of blood clots in the cavity of ventricle washing
is ineffective.
In the case of hemorrhage in a cerebellum haematoma is treated on
the same principle, like the haematoma of large brain.
SHARP VIOLATION OF CEREBRAL CIRCULATION OF BLOOD
Sharp violation of cerebral circulation by the mechanism of
development is related either to the hemorrhage in subdural space
(haemorrhagic stroke) or with an ischemia of brain (ischemic stroke).
Sometimes there is transition of ischemic stroke in haemorrhagic stroke.
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