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Stroke / Cerebro-Vascular
Accident (CVA)
By,
Ms. Ekta S Patel
Assistant Professor
Introduction:
× Cerebrovascular accident: The sudden
death of some brain cells due to lack
of oxygen when the blood flow to the
brain is impaired by blockage or
rupture of an artery to the brain. A CVA
is also referred to as a stroke.
Definition:
× “Focal neurological
deficit due to a local
disturbance in blood
supply to the brain. Its
onset is usually
abrupt, but may
extend over a few
hours or longer.”
WHO,
1971
× Its an focal neurological
deficit resulting from
cerebrovascular
disease and lasting
more than 24 hours or
causing earlier death.
Stroke is not
diagnosis, but a
clinical syndrome
with numerous
causes.
Classification:
CVA
Ischemic stroke
(87%)
Primary
hemorrhagic
stroke (13%)
Ischemic stroke (87%)
Atherosclerotic disease (20%)
(Large artery thrombosis
stroke)
Lunar stroke (small penetrating
artery thrombosis stroke) (25%)
Cardiogenic embolic stroke (20%)
Cryptogenic (30%)
Other (5%)
Primary
hemorrhagic
stroke (13%)
Subarachnoid
hemorrhage
(7%)
Intra-cerebral
hemorrhage
(8%)
Etiology:
× Smoking
× High blood pressure
(hypertension)
× Obesity
× High cholesterol levels
× Diabetes
× Excessive alcohol intake
× Atrial fibrillation.
Ischemic
stroke
× Being overweight
× Drinking excessive amounts of
alcohol
× Smoking
× A lack of exercise
× Stress
× Brain aneurysm
Hemorrhagic
stroke
Pathophysiology
Neuronal death following ischemia will be a result of necrotic,
apoptotic and necroptotic mechanisms depending on the severity of
insult.
Further, the opening of mitochondrial permeability transition pore
releases various proapoptotic molecules including cytochrome C that
activate apoptotic cell death.
Reperfusion aggravates the neuronal damage by forming free radicals
that damage the membranes, proteins and DNA.
This impairs the neuronal homeostasis leading to activation of several
calcium dependent pathways that include proteases and nucleases.
Activation of glutamate receptors following ischemic stroke leads to
excitotoxicity and calcium influx.
Common sites of hemorrhagic
stroke:
× Putamen: 35 % - 50%
× Subcortical white matter 30%
× Thalamus: 10%-15%
× Pons 5%-12%
× Cerebellar white matter <5%
Common sites of ischemic
stroke
Clinical Manifestation Of
Specific Cerebral Artery
Involvement
Middle cerebral artery involvement:
× Contra lateral paralysis (hemiplegia)
× Contralateral anesthesia loss of
proprioception, fine tough, localization
(hemiperesis.)
× Aphasia (Difficulty in communication )
× Dysmetria (difficulty in coordination)
× Conjugate gaze paralysis (inability to
move eyeball in some direction)
Anterior cerebral artery involvement
× 1. occlusion of stem
× 2. occlusion of distal anterior communicating
artery:
× Contralateral sensory and motor deficit of foot
and leg
× Contralateral weakness of proximal upper
extremities
× Urinary incontinence
× Apraxia (difficulty in movement on command)
×
× Personality changes: flat affect, loss of
spontaneity and distractibility
× Possible cognitive impairment
Posterior cerebral artery involvement
1. Thalamogeniculate branch occlusion
× Contralateral sensory loss
× Temporary hemiparesis
× Homonymous hemianopsia
× 2. paramedin branch occlusion: central
midbrain and thalamus:
× Webber’s syndrome
× Contralateral hemiplegia
× Incomplete homonymous heminopsia
× Dysphasia (Difficulty in generation of
speech)
× Disorientation
× Visual disturbances
× Dyscalculia: objects and inability to
count
× Possible memory loss
Vertebrobasilar artery involvement
× Bilateral motor and sensory deficit of
all extermities
× Ipsilateral Horner’s syndrome: miosis,
ptosis, decrease sweating
× Hoarsness
× Dysphagia
× Nystagmus, diplopia, blindness
× Nausea and vomiting
× Ataxia
Common symptoms
Motor
× Hemiparesis
× Hemiplagia
× Dysphagia
× Dysarthria (slurred speech)
Bowel and bladder
× Frequency, urgency, urinary
incontnance
× Constipation
Language
× Non fluent aphasia (motor /expressive
aphasia)
× Fluent aphasia (sensory/ receptive
aphasia)
× Alexia: inability to understand written
words
× Agraphia : inability to express self in
written
Sensory perceptual
× Diminished response to superficial
sensation : touch, pain, hot, cold
× Diminished proprioseption: knowledge
of body parts in environment
× Visual defects
× Perceptual deficit:
o Unilateral neglect syndrome: fail to
report, respond or orient to meaningful
stimuli.
o Apraxia : inability to perform learned or
familiar movement on commands
o Agnosia: loss of ability to identify objects
or people
o Anosognosia: unaware of existance.
× Depression
× Memory loss
× Short attention of span
× Early distractibility
× Loss of reasoning, judgment and
abstract thinking ability.
Diagnostic Evaluation:
× Physical examination
× Neurological examination
× Detailed history collection
× CT
× MRI
× MRA- MR Angiography
× Carotid ultrasound
× Transcranial doppler
× Cerebral angiography
× Transthoracic echocardiography
× Transesophageal echocardiography
× ECG
× Ambulatory ECG monitoring
× Prothombotic states
Medical managemet
× Hypervolemic- hemodilution therapy:
× The therapy is designed to decrease the
hematocrit and the viscosity of blood,
subsequently increasing CBF.
× The patient must have a documented SAH
and have a baseline neurologic status
compatible with aggressive intervention to
qualify for the therapy.
× The infusion technique is begun with
5% albumin and continued for 3 to 7
days
× The dosage is gradually tapered
before discontinuation.
× Effectiveness of the therapy is
measured through improvement in
neurologic function and regional CBF
measurements.
× Thrombolytic: (reteplase, urokinase, rt-
PA)
× recombinant tissue plasminogen activator:
(rt-PA)
× Treated within 3 hours of stroke
symptoms onset
× 0.9 mg/kg
× Initial 10% given IV bolus over 1minute
remaining infused over 60 min.
× Anticoagulant or aspirin should not be
given in first 24hours after rt-PA
treatment.
× Antiplatelet
× Anticoagulant
× Antihypertensive
Surgical management
× Carotid endarterectomy
Superficial temporal artery – middle temporal artery
anastomosis
Clot extraction (MERCI) Mechanical embolus removal
in cerebral embolism
aneurysm clipping and coiling
Thank You

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Guide to Stroke Types, Causes, Symptoms & Treatment

  • 1. Stroke / Cerebro-Vascular Accident (CVA) By, Ms. Ekta S Patel Assistant Professor
  • 2. Introduction: × Cerebrovascular accident: The sudden death of some brain cells due to lack of oxygen when the blood flow to the brain is impaired by blockage or rupture of an artery to the brain. A CVA is also referred to as a stroke.
  • 4. × “Focal neurological deficit due to a local disturbance in blood supply to the brain. Its onset is usually abrupt, but may extend over a few hours or longer.” WHO, 1971
  • 5. × Its an focal neurological deficit resulting from cerebrovascular disease and lasting more than 24 hours or causing earlier death.
  • 6. Stroke is not diagnosis, but a clinical syndrome with numerous causes.
  • 8. Ischemic stroke (87%) Atherosclerotic disease (20%) (Large artery thrombosis stroke) Lunar stroke (small penetrating artery thrombosis stroke) (25%) Cardiogenic embolic stroke (20%) Cryptogenic (30%) Other (5%)
  • 10. Etiology: × Smoking × High blood pressure (hypertension) × Obesity × High cholesterol levels × Diabetes × Excessive alcohol intake × Atrial fibrillation. Ischemic stroke
  • 11. × Being overweight × Drinking excessive amounts of alcohol × Smoking × A lack of exercise × Stress × Brain aneurysm Hemorrhagic stroke
  • 12.
  • 14.
  • 15. Neuronal death following ischemia will be a result of necrotic, apoptotic and necroptotic mechanisms depending on the severity of insult. Further, the opening of mitochondrial permeability transition pore releases various proapoptotic molecules including cytochrome C that activate apoptotic cell death. Reperfusion aggravates the neuronal damage by forming free radicals that damage the membranes, proteins and DNA. This impairs the neuronal homeostasis leading to activation of several calcium dependent pathways that include proteases and nucleases. Activation of glutamate receptors following ischemic stroke leads to excitotoxicity and calcium influx.
  • 16.
  • 17.
  • 18. Common sites of hemorrhagic stroke:
  • 19. × Putamen: 35 % - 50% × Subcortical white matter 30% × Thalamus: 10%-15% × Pons 5%-12% × Cerebellar white matter <5%
  • 20. Common sites of ischemic stroke
  • 21. Clinical Manifestation Of Specific Cerebral Artery Involvement
  • 22. Middle cerebral artery involvement: × Contra lateral paralysis (hemiplegia) × Contralateral anesthesia loss of proprioception, fine tough, localization (hemiperesis.) × Aphasia (Difficulty in communication ) × Dysmetria (difficulty in coordination) × Conjugate gaze paralysis (inability to move eyeball in some direction)
  • 23. Anterior cerebral artery involvement × 1. occlusion of stem × 2. occlusion of distal anterior communicating artery: × Contralateral sensory and motor deficit of foot and leg × Contralateral weakness of proximal upper extremities × Urinary incontinence × Apraxia (difficulty in movement on command) ×
  • 24. × Personality changes: flat affect, loss of spontaneity and distractibility × Possible cognitive impairment
  • 25. Posterior cerebral artery involvement 1. Thalamogeniculate branch occlusion × Contralateral sensory loss × Temporary hemiparesis × Homonymous hemianopsia × 2. paramedin branch occlusion: central midbrain and thalamus: × Webber’s syndrome × Contralateral hemiplegia
  • 26. × Incomplete homonymous heminopsia × Dysphasia (Difficulty in generation of speech) × Disorientation × Visual disturbances × Dyscalculia: objects and inability to count × Possible memory loss
  • 27. Vertebrobasilar artery involvement × Bilateral motor and sensory deficit of all extermities × Ipsilateral Horner’s syndrome: miosis, ptosis, decrease sweating × Hoarsness × Dysphagia × Nystagmus, diplopia, blindness × Nausea and vomiting × Ataxia
  • 29. Motor × Hemiparesis × Hemiplagia × Dysphagia × Dysarthria (slurred speech)
  • 30. Bowel and bladder × Frequency, urgency, urinary incontnance × Constipation
  • 31. Language × Non fluent aphasia (motor /expressive aphasia) × Fluent aphasia (sensory/ receptive aphasia) × Alexia: inability to understand written words × Agraphia : inability to express self in written
  • 32. Sensory perceptual × Diminished response to superficial sensation : touch, pain, hot, cold × Diminished proprioseption: knowledge of body parts in environment × Visual defects
  • 33. × Perceptual deficit: o Unilateral neglect syndrome: fail to report, respond or orient to meaningful stimuli. o Apraxia : inability to perform learned or familiar movement on commands o Agnosia: loss of ability to identify objects or people o Anosognosia: unaware of existance.
  • 34.
  • 35. × Depression × Memory loss × Short attention of span × Early distractibility × Loss of reasoning, judgment and abstract thinking ability.
  • 37.
  • 38.
  • 39.
  • 40. × Physical examination × Neurological examination × Detailed history collection
  • 41. × CT × MRI × MRA- MR Angiography × Carotid ultrasound × Transcranial doppler × Cerebral angiography × Transthoracic echocardiography × Transesophageal echocardiography × ECG × Ambulatory ECG monitoring × Prothombotic states
  • 42. Medical managemet × Hypervolemic- hemodilution therapy: × The therapy is designed to decrease the hematocrit and the viscosity of blood, subsequently increasing CBF. × The patient must have a documented SAH and have a baseline neurologic status compatible with aggressive intervention to qualify for the therapy.
  • 43. × The infusion technique is begun with 5% albumin and continued for 3 to 7 days × The dosage is gradually tapered before discontinuation. × Effectiveness of the therapy is measured through improvement in neurologic function and regional CBF measurements.
  • 44. × Thrombolytic: (reteplase, urokinase, rt- PA) × recombinant tissue plasminogen activator: (rt-PA) × Treated within 3 hours of stroke symptoms onset × 0.9 mg/kg × Initial 10% given IV bolus over 1minute remaining infused over 60 min.
  • 45. × Anticoagulant or aspirin should not be given in first 24hours after rt-PA treatment.
  • 48. Superficial temporal artery – middle temporal artery anastomosis
  • 49. Clot extraction (MERCI) Mechanical embolus removal in cerebral embolism
  • 50.