2. Can be defined as sudden loss of neurological
function caused by an interruption of the blood
flow to the brain.
WHO defines it as “rapidly developing clinical signs
of focal (or global) disturbance of cerebral function,
with symptoms lasting 24 hours or longer or
leading to death, with no apparent cause other
than of vascular origin”
*TIA is defined to last less than 24 hrs
3. 1. Ischaemic-
Most common type
Results when a clot(thrombus) blocks or impairs
blood flow,deprives brain of nutrition and
oxygenation
Thrombotic cerebral infarction results from the
atherosclerotic obstruction of large cervical and
cerebral arteries
Embolic cerebral infarction is due to embolism of
a clot in the cerebral arteries
coming from other parts of the arterial system
4. 2. Haemorrhagic(ICH)-
Occurs when blood vessels rupture ,causing
leakage of blood in and around the brain
Spontaneous intracerebral hemorrhages (as
opposed to traumatic ones) are mainly due
to arteriolar hypertensive disease
3. Subarachnoid haemorrhages(SAH)-
mainly due to the rupture of aneurysms at the
bifurcations of large arteries at the inferior surface
of the brain
5. In 2001 it was estimated that cerebrovascular
diseases (stroke) accounted for 5.5 million deaths
world wide, equivalent to 9.6 % of all deaths.
Two-thirds of these deaths occurred in people
living in developing countries and 40% of the
subjects were aged less than 70 years.
Stroke is more common among men than women.
The prevalence of stroke in men is 1.3 times higher
than that in women.
6. Atherosclerosis and plaque formation leading
narrowing of vessel lumen, progresssing to
interruption of blood flow at certain sites of
predilection
7. Presence of thrombus or emboli may also reduce
blood flow to the brain.
Ischaemia due to atherosclerosis, thrombus or
emboli deprives brain of nutrition and oxygenation
and glucose, leading to cell death. This is k/a
cerebral infarction or tissue death.
Ischaemia may also develop from low perfusion
rates due to cardiac failure or significant blood loss
with resulting systemic hypotension.
8. Haemorrhagic strokes result from abnormal
bleeding in brain due to rupture of cerebral vessels
or as a result of direct trauma.
Intracranial Haemorrhage leads to increased ICP
Other causes are SAH and aneurysms,AVM,etc
9. It describes the relationship between
the contents of the cranium and intracranial
pressure.
As the cranium is made from solid bone, its
structure is fixed and therefore the volume
contained within cannot be changed.
Alongside the brain tissue, the other major
components found within the cranium
are blood and the CSF. The volume of each
of these components is restricted by the
fixed space within the cranium.
In normal cranial physiology, these three
components exist in equilibrium with each
other to satisfy this fixed volume. As such,
if the volume of one component increases,
the volume of another must decrease.
10. Medical factors such as hypertension,heart
disease and diabetes
Inherent biological traits such as age and sex,
physiological characteristics such as high
blood pressure, serum cholesterol,
fibrinogen;
Modifiable behaviors such as smoking, diet,
alcohol consumption, physical inactivity
12. Following ischaemia,the tissues in the brain
can be reviewed by the ‘four tissue
compartments concept”.
The compartments can be distinguished by
the various physiological imaging modalities
during acute ischemic
13. 1) the unaffected tissue;
2) the mildly hypoperfused tissue, but this is not usually at risk (the
oligemic tissue);
3) the tissue at risk (the ischemic penumbra); and
4) the tissue already irreversibly damaged (the ischemic core)
14. Ischaemic strokes lead to cerebral edema which
begins within minutes of the insult and reaches a
maximum with 3-4 days.
This results from tissue necrosis and movement of
water from blood to brain tissue.
If the edema doesnot subside, there is increased
ICP which may lead to contralateral shifting and
brainstem herniation.
15. Most common clinical features include-
1. Motor paresis/paralysis of muscles affecting one
side of the body
2. Alterations in tone (Flaccidity followed by
spasticity)
3. Impaired or abnormal sensations
(numbness,tingling,decreased sensation) and
parasthesia as in thalamic pain
4. Loss or changes in visual acuity such as visual
neglect and homonymous hemianopia
5. Slurring of speech, inability to understand
speech(Wernicke’s aphasia), slow hesistant
speech(Broca’s aphasia)
16.
17. 6. Altered reflexes (initial hyporeflexia with flaccidity,
then hyperreflexia as synergy patterns and spasticity
develop)
7. Positive Babinski sign(extension of great toe with
fanning out of other toes)
8. Problems in swallowing(dysphagia) or drooling from
one corner of mouth
9. Loss of memory
10. Altered or loss of balance and coordination
(cerebellar-ataxia, basal ganglia- bradykinesia or
involuntary movements such as choreoathetosis and
hemiballismus)
*[Chorea- involuntary jerky,dance like movts., Athetosis-slow writhing movt.
Hemiballismus-sudden violent ballistic flinging movts]
18. 12. Apraxia or loss of motor planning
13. Postural disturbances such as asymmetry in wt.
bearing and wt. shifting, increased postural sway,
etc
14. Personality changes and mood affect ( euphoria,
depressed or apathetic.)*
15. Change in perception of self such as unilateral
neglect, Pusher syndrome, etc.
16. Bladder and bowel dysfunction or incontinence
19. Synergy patterns- stereotyped,primitive patterns of
movement that dominate voluntary muscle action
and reflex actions.
Mass movement patterns in response to stimulus
or voluntary effort or both are called abnormal
synergy patterns.
Gross flexor movements flexor synergy
Gross extensor movements extensor synergy
Combination of strongest components produce
mixed synergy
Appear as spasticity develops, isolated movements
cannot be performed
24. A. History taking, clinical evaluation including
grading of severity
B. Physical examination- check for ABC, vitals,
cardiac auscultation and general appearance
Scales used for stroke-
NIH Stroke scale- 1–4 Minor
5–15 Moderate
16–20 Moderate to severe
21–42 Severe
Glasgow outcome scale- The Glasgow Outcome
Scale (GOS) has been widely accepted as a standard means of
describing outcome in head injury patients.The traditional GOS
has five categories, which were extended to eight for the
Glasgow Outcome Scale–Extended (GOSE)
25. B. General investigations-
CXR/ECG
Other laboratory tests such as CBC, blood glucose, CT/BT,
PT, serum lipid/cholesterol profiling
C. CT scan/MRI, carotid ultrasound, cerebral angiogram
CT is much faster and inexpensive than MRI, making it the
study of choice in cases of trauma and other acute neurological
emergencies. However,MRI doesnot use ioning radiations, has a
much greater range of available soft tissue contrast, depicts
anatomy in greater detail, and is more sensitive and specific for
abnormalities within the brain itself.
26.
27. In ischaemic stroke reperfusion therapy with tissue
plasminogen activator (tPA) or endovascular clot
retrieval (ECR) is used. Reperfusion therapy aims to
salvage the ischaemic penumbra and reduce mortality
and disability.
The tPA is given within 4.5 h after the patient was last
known to be well.
If there is no ICH on MRI and pt. is not receiving
reperfusion therapy, dual antiplatelet therapy (DAPT),
consisting of aspirin and clopidogrel, is given within the
first 24 h to reduce risk of stroke recurrence.
In presence of ICH, all anticoagulants are immediately
withheld.
28. Antihypertensives may be necessary. Rapid blood
pressure (BP) control during this acute phase can be
achieved through IV hydralazine and labetalol.
As secondary prevention measure, first-line
antihypertensive therapy can be chosen from the
following classes: angiotensin converting enzyme
inhibitor, angiotensin II receptor antagonists, calcium
channel blockers and thiazide diuretics.
Selection of an agent depends on comorbidities and
tolerability.
Most ischaemic stroke patients should be prescribed a
high-dose statin (e.g atorvastatin) regardless of lipid
levels, to reduce the risk of recurrent stroke. Use of
statin following ICH is not recommended as it can
increase risk of further bleeding.
29. Ischaemic stroke patients may be prescribed long-term
antiplatelet therapy: low-dose aspirin, clopidogrel or
combination of aspirin and dipyridamole.
Ischaemic stroke patients with AF on
electrocardiography or confirmed thrombus on
echocardiogram are started on long-term
anticoagulation therapy(e.g warfarin).
Neuropathic pain may be addressed by gabapentinoids
(GBP), serotonin-noradrenaline reuptake inhibitors
(SNRI) and tricyclic antidepressants (TCA).Second line
treatment may be with use of lignocaine or tramadol.
Nociceptive pain is treated with NSAIDS or paracetamol.
Generalised spasticity is treated with baclofen, while
focal/segmental spasticity require Botulinum toxin A.
30. Surgical procedures include decompressive
surgery(Hemicraniectomy) for cerebellar
haemorrhages, evacuation of supratentorial
haematomas and extraventricular drain
insertions for hydrocephalus.
Editor's Notes
Thrombus-blood clot that forms in ablood vessel
Embolus- unattached material (emboli) such as a blood clot, fat or cholesterol deposit, gas, tissue, or foreign material travels within the bloodstream and occludes flow within a vessel
Aneurysm- An aneurysm is a ballooning at a weak spot in an artery wall.
