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-Dr. PATRALIKA NATH(PT)
Assistant Professor of Physiotherapy,
Bengal Institute of Pharmaceutical
Sciences,Kalyani
 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
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
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
 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.
 Atherosclerosis and plaque formation leading
narrowing of vessel lumen, progresssing to
interruption of blood flow at certain sites of
predilection
 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.
 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
 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.
 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
 Circle of Willis
 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
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)
 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.
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)
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]
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
 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
• Scapula: retraction and/or
elevation
• Shoulder: Abdn., ER.
• Elbow: flexn.*
• Forearm: Supn.
• Wrist & finger: flexn.*
Flexor
synergy
• Scapula: Protraction
• Shoulder: Addn*., IR*
• Elbow: Extn.
• Forearm: pronation*
• Wrist & finger: flexn.*
Extensor
synergy
•Hip: flexn*, abdn, ER
•Knee: flexn
•Ankle: dorsiflexn,inversion
•Toe: dorsiflexn
Flexor
synergy
•Hip: extn, addn*,IR
•Knee: extn*
•Ankle: plantarflexn*,inversion
•Toe: plantarflexn
Extensor
synergy
 Typical hemiplegic posture??
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)
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.
 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.
 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.
 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.
 Surgical procedures include decompressive
surgery(Hemicraniectomy) for cerebellar
haemorrhages, evacuation of supratentorial
haematomas and extraventricular drain
insertions for hydrocephalus.

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Cerebrovascular Accident

  • 1. -Dr. PATRALIKA NATH(PT) Assistant Professor of Physiotherapy, Bengal Institute of Pharmaceutical Sciences,Kalyani
  • 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
  • 11.  Circle of Willis
  • 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
  • 20. • Scapula: retraction and/or elevation • Shoulder: Abdn., ER. • Elbow: flexn.* • Forearm: Supn. • Wrist & finger: flexn.* Flexor synergy • Scapula: Protraction • Shoulder: Addn*., IR* • Elbow: Extn. • Forearm: pronation* • Wrist & finger: flexn.* Extensor synergy
  • 21. •Hip: flexn*, abdn, ER •Knee: flexn •Ankle: dorsiflexn,inversion •Toe: dorsiflexn Flexor synergy •Hip: extn, addn*,IR •Knee: extn* •Ankle: plantarflexn*,inversion •Toe: plantarflexn Extensor synergy
  • 23.
  • 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

  1. 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
  2. Aneurysm- An aneurysm is a ballooning at a weak spot in an artery wall.