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CARDIOVASCULAR ACCIDENTS
1. Dr. AISHWARYA RAI (PT)
BPT, Fellow in Regenerative
Rehabilitation, CKTP.
2. DEFINITION
It is an acute onset of neurological dysfunction due
to an abnormality in cerebral circulation with
resultant signs and symptoms that correspond to
involvement of focal areas of brain.
If neurological deficits persist for less than 24 hours-
TIA
If neurological deficits persist for more than 24
hours- stroke.
9. •In the normal brain, cerebral blood flow to a particular part varies depending on the
metabolic requirements, i.e. the supply of O2 and glucose is ‘coupled’ to the tissue
needs. After infarction, between areas of reduced flow and areas of luxury perfusion, lie
areas of relative luxury perfusion where reduced flow exceeds the tissue requirements,
i.e. ‘uncoupling’ of flow and metabolism occurs.
•Progression from reversible ischaemia to infarction depends upon the degree and
duration of the reduced blood flow along with presence of collateral circulations.
•A mismatch between CBF and metabolic demands lead to either electrical failure of
lactic acidosis (in case glucose is available).
•A cascade of events take place that ultimately lead to accumulation of toxic compounds
and apoptosis.
•Interruption in this blood flow hence leads to a series of pathoneurological events that
leads to irregular cell damage with a core area of focal infarction within minutes.
•Ischaemic penumbra- Area surrounding the core that consists of viable but
metabolically lethargic cells.
10.
11. •It is an anastomosis formed by
the ICA, VA and their branches at
the base of brain.
•Also known as circulus arteriosus
12.
13. The anterior cerebral artery is a branch of
the internal carotid and runs above the
optic nerve to follow the curve of the
corpus callosum. Soon after its origin the
vessel is joined by the anterior
communicating artery. Deep branches pass
to the anterior part of the internal capsule
and basal nuclei. Cortical branches supply
the medial surface of the hemisphere:
1. Orbital
2. Frontal
3. Parietal
ANTERIOR CEREBRAL
ARTERY SYNDROME
14. MIDDLE CEREBRAL ARTERY SYNDROME
The middle cerebral artery is the largest branch of the internal carotid
artery. It gives off (1) deep branches (perforating vessels –
Lenticulostriate) which supply the anterior limb of the internal capsule
and part of the basal nuclei. It then passes out to the lateral surface
of the cerebral hemisphere at the insula of the lateral sulcus. Here it
gives off cortical branches (2) temporal, (3) frontal, (4) parietal.
15. POSTERIOR CEREBRAL
ARTERY SYNDROME
The posterior cerebral arteries
are the terminal branches of the
vertebral arteries. Small
perforating branches supply
midbrain structures, choroid
plexus and posterior thalamus.
Cortical branches supply the
undersurface of the temporal
lobe – temporal branch; and
occipital and visual cortex –
occipital and calcarine branches.
16.
17. INTERNAL CEREBRAL ARTERY
SYNDROME
In the most extreme cases there may be:
Deterioration of conscious level
Homonymous hemianopia of the contralateral side
Contralateral hemiplegia
Contralateral hemisensory disturbance
Gaze palsy to the opposite side – eyes deviated to the side of the lesion
A partial Horner’s syndrome may develop on the side of the occlusion
(involvement of sympathetic fibres on the internal carotid wall).
Occlusion of the dominant hemisphere side will result in a global aphasia.
Course occlusion can result in herniation, coma and death.
18. VERTEBRO BASILAR ARTERY
SYNDROME
It supplies the pons, inner ear and cerebellum.
A complete occlusion of VA can result be fatal.
A progressive lesion often starts with occipital headache, diplopia,
hemiplegia, quadriplegia and coma.
Complete basilar syndrome affecting pontine nuclei (without
affection of reticular system) results in locked in syndrome.
Locked in syndrome results in anarthria, quadriplegia with preserved
conciousness, alertness and vertical eye movements.
Vertebrobasilar artery system occlusion can result in either ipsilateral
or contralateral symptoms depending on whether tracts involved are
crossed or uncrossed.
DROP ATTACK: Sudden loss of tone in LL muscles due to involvement
of medullary pyramids. Symptoms include visual loss, diplopia,
homonymous hemianopia, facial numbness or weakness, tinnitus,
dysarthria or dysphagia.
19. DIAGNOSTIC
TESTS
1. Routine and special blood investigations: CBC,
TSH, T3, T4, Lipid profile and blood glucose
levels, serum electrolytes,
2. Carotid duplex
3. CT Scan
4. ECG
5. Echocardiography
6. MRI
7. MRA
8. Cerebral angiogram
9. PET
20. DIRECT IMPAIRMENTS
1. Motor deficits- flaccidity, spasticity, stage of
spontaneous recovery.
2. Sensory deficits
3. Presence of abnormal reflexes- ATNR, STNR, STLR, etc.
4. Presence of associated reactions- Souque’s
phenomena, Ramiste’s phenomena, homolateral limb
synkinesis.
5. Speech and Language disorders- aphasia
6. Perceptual deficits- apraxia, agnosia
7. Cognitive dysfunction
8. Dysphagia
9. Bladder bowel impairment
10. Sexual dysfunction
27. PERCEPTUAL DEFICITS
AGNOSIA- INABILITY TO RECOGNISE
OR MAKE SENSE OF UPCOMINING
INFORMATION DESPITE SENSORY
CAPACITIES.
APRAXIA- INABILITY TO PERFORM A LEARNED
MOVEMENT EVEN THOUGH THE PATIENT HAS
GOOD MUSCLE STRENGTH, COORDINATION,
INTACT ATTENTION AND SENSES. CAUSED DUE
TO LESION OF PARIETAL LOBE OF DOMINANT
HEMISPHERE.
34. MANAGEMENT
1. Medical: Maintain circulation oxygenation, blood
pressure, CO, fluid and electrolyte balance. Prevent
oedema, seizures and other complications.
2. Pharmacological: Thrombolytic, anticoagulant,
antiplatelet, antihypertensives, antispastics, etc.
3. Neurosurgical: AVM management, Carotid
endarterectomy, etc.
4. Rehabilitation
35. references
1. NEUROLOGY AND NEUROSURGERY ILLUSTRATED
KENNETH W LINDSAY, IAN BONE & GERAINT FULLER
2. PHYSICAL REHABILITATION, ASSESSMENT AND TREATMENT
SUSAN B. O’SULLIVAN & THOMAS J. SCHMITZ
3. PHYSIOTHERAPY IN NEUROLOGICAL CONDITIONS WITH
ASSESSMENT AND TREATMENT PROTOCOLS.
GOWRISHANKAR POTTURI
