Stroke and its PT management.

1. STROKE

2. Outline Of
Topic
 Types
 Etiopathogenesis
 Clinical Features
 Diagnosis
 Scales
 PT management

3. Stroke
• Stroke is sudden loss of neurological function resulted due to
interruption of blood flow to the brain.
• Ischemic is the most common variant, affects 80% population of
the stroke which jeopardies the nutrients and O2.
• Hemorrhagic stroke occurs when blood vessels get ruptured and
blood sneaks out in and around brain.
• CVA is a term used interchangeably with stroke to refer vascular
conditions of brain.

4. Etiology
• Atherosclerosis is a major contributory factor in
cerebrovascular disease.
• It is characterized by plaque formation with an accumulation of
lipids, fibrin, complex carbohydrates, and calcium deposits on
arterial walls that leads to progressive narrowing of blood
vessels.
• Interruption of blood flow by atherosclerotic plaques occurs at
certain sites

5. • These generally include at the bifurcations,
angulations of arteries.
• The most common sites for lesions to occur are at the
origin of the common carotid artery.
• At its transition into the middle cerebral artery.
• At the main bifurcation of the middle cerebral artery.
• At the junction of the vertebral arteries with the
basilar artery

6. • Ischemic strokes are the product of a thrombus, embolism, or conditions
that produce low systemic perfusion pressures.
• The lack of Cerebral Blood Flow (CBF) compromises the brain’s needed
oxygen and glucose disrupts cellular metabolism leads to injury and death
of cerebral tissues.
• Haemorrhagic strokes, with abnormal bleeding into the extravascular areas
of the brain, are the result of rupture of a cerebral vessel or trauma.
• Haemorrhage results in increased intracranial pressures with injury to brain
tissues and restriction of distal blood flow.

8. Risk Factors & Preventions
• Cardiovascular diseases affecting the brain and heart share number of
common risk factors important to the development of atherosclerosis.
• Major risk factors for stroke are hypertension, heart disease, disorders of
heart rhythm, and diabetes mellitus.
• Individuals with hypertension (blood pressure [BP] (140/90 mm Hg or
higher) have twice the lifetime risk of stroke.
• Hypertension (140/90 mm Hg or higher) have twice the lifetime risk of
stroke. Risk is increased with elevated total blood cholesterol
(hypercholesterolemia), 240 mg/dL or greater

9. • Risk is elevated with raised levels of low-density lipoprotein (LDL bad)
cholesterol. LDL levels are defined as borderline high levels of 130 to 159
mg/dL, high levels of 160 to 189 mg/dL, and very high levels of 190 mg/dL
or greater.
• Low levels of high-density lipoprotein (HDL-good) cholesterol, defined as
below 40 mg/dL in adult males and below 50 mg/dL in adult females, also
increases risk of stroke.
• Modifiable risk factors include cigarette smoking, physical inactivity,
obesity, and diet.
• Current smokers have 2 to 4 times increased stroke risk compared to non-
smokers or those who have quit for more than 10 years.

10. • Physical activity (moderate to vigorous exercise) is associated with an
overall 35% reduction in stroke risk whereas light exercise (walking) does
not appear to have the same benefit.
• Nonmodifiable risk factors include family history, age, gender, and race.
• Lifestyle changes can significantly reduce the risk of stroke, most
importantly it includes controlling BP, diet (cholesterol and lipids free),
weight loss, quitting smoking, and increasing physical activity, as well as
effective existing systemic disease management.

11. PATHOPHYSIOLOGY
• Sudden cessation of cerebral blood flow and oxygen- glucose deprivation
sets in motion a series of pathological events.
• Within couple of minutes neurons die within the ischemic core tissue, the
greater part of neurons located in the surrounding penumbra survive for a
slightly longer time.
• This Cell survival mechanism purely depends on the severity and the
duration of the ischemic episode.
• Without timely reperfusion, cells in the penumbra will die, neuronal
activity ceases, and the infarct expands.

12. • Ischemia triggers a number of damaging cellular events, called it as
ischemic cascade.
• The release of excess neuro- transmitters (e.g., glutamate and aspartate)
produces a progressive disturbance of energy metabolism and anoxic
depolarization, this results in an inability of brain cells to produce
energy(ATP).
• This is followed by excess influx of calcium ions and pump failure of the
neuronal membrane, so this excess calcium reacts with intracellular
phospholipids to form free radicals.
• Calcium accumulation, stimulates the release of nitric oxide and cytokines
this furthermore damage the brain cells.

13. Source: Internet

14. • Ischemic strokes produce cerebral edema, an accumulation of fluids
within the brain that begins within minutes of the insult and reaches a
maximum by 3 to 4 days.
• It is the result of tissue necrosis and widespread rupture of cell membranes
with movement of fluid from the blood into brain tissues.
• The swelling gradually subsides and generally disappears by 2 to 3 weeks.
Significant edema can elevate intracranial pressures and neurological
deterioration associated with contralateral and caudal shifts of brain
structures (brainstem herniation)

15. Source: Internet

16. • Clinical signs of elevating intracranial pressure (ICP) include decreasing
level of consciousness (stupor and coma), widened pulse pressure,
increased heart rate, irregular respirations (Cheyne-Stokes respirations),
vomiting, unreacting(Dilated/No response to Light) pupils (cranial nerve
CN-III signs), and papilledema.
• Cerebral edema is the most frequent cause of death in acute stroke and is
characteristic of large infarcts involving the middle cerebral artery and the
internal carotid artery.
• Cheyne-Stokes Respiration - YouTubewww.youtube.com › watch

17. Clinical Features

18. Anterior Cerebral Artery Syndrome
(HSLE>UE/“HASLE”)
• The anterior cerebral artery (ACA) is the first and smaller of two terminal
branches of the internal carotid artery.
• It supplies the medial aspect of the cerebral hemisphere (frontal and
parietal lobes) and subcortical structures, including the basal ganglia
(anterior internal capsule, inferior caudate nucleus), anterior fornix, and
anterior four-fifths of the corpus callosum.
• More distal lesions leads to more significant impairments.
• The clinical manifestations of anterior cerebral artery (ACA) syndrome
include contralateral hemiparesis and sensory loss with greater involvement
of the lower extremity (LE) than the upper extremity (UE) because the
somatotopic organization of the medial aspect of the cortex includes the
functional area for the LE.

19. Signs and Symptoms Structures Involved
• Contralateral hemiparesis involving mainly
the LE (UE is more spared)
• Primary motor area, medial aspect of
cortex, internal capsule
• Contralateral hemisensory loss involving
mainly the LE (UE is more spared)
• Primary sensory area, medial aspect of
cortex
• Urinary incontinence
• Posteromedial aspect of superior frontal
gyrus
• Problems with imitation and bimanual
tasks, apraxia
• Corpus callosum

20. Middle Cerebral Artery Syndrome (FUEL)
• The MCA is the second main branches of the internal carotid artery and supplies
the entire lateral aspect of the cerebral hemisphere. Mainly it covers frontal,
temporal, and parietal lobes and subcortical structures, including the internal
capsule posterior portion, corona radiata, globus pallidus (outer part), most of the
caudate nucleus, and putamen.
• Occlusion of the proximal MCA produces extensive neurological damage along
with marked cerebral edema, increased intracranial pressures typically lead to
loss of consciousness, brain herniation, and possibly death.
• The most common characteristics of the syndrome are contralateral spastic
hemiparesis and sensory loss of the face, UE, and LE, with the face and UE
more involved than the LE.
• Lesions of the parieto-occipital cortex of the dominant hemisphere (usually the
left hemi- sphere) typically produce aphasia. Lesions of the right parietal lobe of
the nondominant hemisphere (usually the right hemisphere) typically produce
perceptual deficits (e.g. unilateral neglect, anosognosia, apraxia, and spatial
disorganization).

21. Signs and Symptoms Structures Involved
• Contralateral hemiparesis involving
mainly the UE and face (LE is more
spared)
• Primary motor cortex and internal
capsule
• Contralateral hemisensory loss involving
mainly the UE and face (LE is more
spared)
• Primary sensory cortex and internal
capsule
• Motor speech impairment: Broca’s or
nonfluent aphasia with limited
vocabulary and slow, hesitant speech
• Broca’s cortical area (third frontal
convolution) in the dominant hemisphere,
typically the left hemisphere
• Receptive speech impairment:
Wernicke’s or fluent aphasia with
impaired auditory comprehension and
fluent speech with normal rate and
melody
• Wernicke’s cortical area (posterior
portion of the temporal gyrus) in the
dominant hemisphere, typically the left

22. Signs and Symptoms Structures Involved
• Global aphasia: nonfluent speech with
poor comprehension
• Both third frontal convolution and
posterior portion of the superior temporal
gyrus
• Contralateral homonymous hemianopsia
• Loss of conjugate gaze to the opposite side
• Ataxia of contralateral limb(s) (sensory
ataxia) Pure motor hemiplegia (lacunar
stroke)
• (https://youtu.be/5ji0ZwcP4vs)
• Optic radiation in internal capsule.
• Frontal eye fields or their descending
tracts.
• Parietal lobe.
• Limb-kinetic apraxia
• Premotor or parietal cortex
• Perceptual deficits: unilateral neglect,
depth perception, spatial relations, agnosia
• Parietal sensory association cortex in the
nondominant hemisphere, typically the
right

23. Posterior Cerebral Artery Syndrome
• Arise as terminal branches of the basilar artery and each supplies the
corresponding occipital lobe and medial and inferior temporal lobe.
• It also supplies the upper brainstem, midbrain, and posterior diencephalon,
including most of the thalamus.
• Occlusion of thalamic branches may produce hemianesthesia
(contralateral sensory loss) or central post-stroke (thalamic) pain,
Occipital infarction produces homonymous hemianopsia, visual agnosia,
prosopagnosia, or if the lesion is bilateral, cortical blindness are common,
whereas Temporal lobe ischemia results in amnesia

24. Signs and Symptoms
(Peripheral Territory) Structures Involved
• Contralateral homonymous hemianopsia
• Bilateral homonymous hemianopsia with
some degree of macular sparing
• Visual agnosia
• Primary visual cortex or optic radiation
• Calcarine cortex (macular sparing is due to
occipital pole receiving collateral blood
supply from MCA)
• Left occipital lobe
• Prosopagnosia (difficulty naming people
on sight)
• Visual association cortex
• Dyslexia (difficulty reading) without
agraphia (difficulty writing), colour
naming (anomia), and colour
discrimination problems
• Dominant calcarine lesion and posterior
part of corpus callosum
• Memory defect
• Topographic disorientation
• Lesion of inferomedial portions of
temporal lobe bilaterally or on the
dominant side only
• Nondominant primary visual area, usually
bilaterally

25. Signs and Symptoms
(Central Territory)
Structures Involved
• Central post-stroke (thalamic) pain
Spontaneous pain and dysesthesias;
sensory impairments (all modalities)
• Ventral posterolateral nucleus of
thalamus
• Involuntary movements; choreoathetosis,
intention tremor, hemiballismus
• Subthalamic nucleus or its pallidal
connections
• Contralateral hemiplegia
• Weber’s syndrome
Oculomotor nerve palsy and contralateral
hemiplegia
• Cerebral peduncle of midbrain
• Third nerve and cerebral peduncle of
midbrain
• Paresis of vertical eye movements, slight
miosis and ptosis and sluggish pupillary
light response
• Supranuclear fibres to third cranial nerve

26. Lacunar Stroke
• Lacunar strokes are caused by small vessel disease deep in the cerebral
white matter.
• They are strongly associated with hypertensive haemorrhage and diabetic
microvascular disease & are consistent with specific anatomical sites.
• Pure motor lacunar stroke are associated with involvement of the posterior
limb of the internal capsule, pons, and pyramids. Pure sensory lacunar
stroke is associated with involvement of the ventrolateral thalamus or
thalamocortical projections.
• Other lacunar syndromes include dysarthria/clumsy hand syndrome
(involving the base of the pons, genu of anterior limb, or the internal
capsule)

27. • Ataxic hemiparesis (involving the pons, genu of internal capsule, corona
radiata, or cerebellum).
• Sensory/motor stroke which involving the junction of the internal capsule
and thalamus, or dystonia/involuntary movements such as choreoathetosis
with lacunar infarction of the putamen or globus pallidus; hemiballismus
with involvement of the subthalamic nucleus.