Neurology, Stroke, Localization, Medicine, CVA, Cerebrovascular Accident, Diagnosis, MBBS, Clinical Neurology, simplified

1. CVA/ Stroke localization
Arun George
CMC Vellore

2. • Stroke (or ‘Cerebrovascular accident’) is a
syndrome of 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.
• Transient Ischaemic Attack (TIA) or ‘mini stroke’
is where those symptoms resolve in 24 hours
(usually under 30 minutes).
• Strokes are divided into those with an ischaemic
or haemorrhagic cause.

3. Risk Factors

4. What type of stroke is it ?

5. Etiology
• Evidence of thrombosis: progressive
deterioration, atherosclerosis risk factors, a
carotid bruit.
• Evidence of embolism: Abrupt onset, history
of atrial fibrillation, Recent Myocardial
infarction, Prior TIA/ Stroke.
• Evidence of haemorrhage: abrupt
onset, headaches, fits, hypertension risk
factors, rapid decrease in level of
consciousness.

6. Stroke types / frequency
Ischemic 80%
• Thrombotic
• Embolic
60%
20%
Hemorrhagic 20%
• Intracerebral hemorrhage
• Subarachnoid hemorrhage
12%
8%

8. Following clinical and bedside data are helpful
1.
2.
3.
4.
5.
6.
Past , personal and family history
History of old strokes or TIAs
Time of onset of the symptoms
Activity at the time of onset of the symptoms
Temporal course and progression
Accompanying symptoms –
Headache, vomiting, decreased level of
consciousness

9. Past, present . Personal and family history
1. Presence of diabetes
&coronary heart disease
2. Prior heart disease
3. Hypertension *
4. Pt on anticoagulant
Atherosclerotic
Embolic
Hemorrhagic
Hemorrhagic

10. Activity at onset
Classical teaching –
Thrombotic strokes - during sleep – when the
circulation is least active
Hemorrhage and Embolism - during activity –
when circulation is active

11. Cortical stroke
If the cerebral cortex is involved, the CNS
pathways can be but can also produce the
following symptoms:
• Aphasia (inability to speak or understand
language from involvement of Wernicke’s or
Broca’s area)
• Apraxia (altered voluntary movement)
• Visual field defect

12. • Memory Deficits (involvement of Temporal
lobe)
• Hemi neglect (involvement of the Parietal
lobe)
• Disorganised thinking, confusion, hypersexual
gestures (with involvement of the frontal lobe)
• Anosognosia (persistent denial of the
existence of a, usually stroke-related deficit).

13. Frontal lobes
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executive function, movement and behavior.
primary motor cortex
Broca’s speech area
micturition center
inferior frontal lobes may be associated with anosmia.
behavioral disturbance.
1. medial frontal lesions- withdrawn, unresponsive and
mute (abulic), and this is often associated with urinary
incontinence, gait apraxia and the type of increase in
tone known as gegenhalten.
2. lateral convexity lesions of the frontal lobes become
disinhibited

14. Parietal
• Nondominant Parietal Lobe (Usually the Right
one) does Intellectual Processing of Sensory
Information for Visual-Spatial Tasks
• Right Parietal Lobe Lesion - refuses to accept
there is a problem, Neglects the left side, has
Constructional Apraxia

15. Temporal
• Cerebral Cortex part that does
Emotion, Memory, Language
• Commonly affected by Herpes Virus
• Medial Temporal Lobe Lesion causes learning
impairment but spares short and long-term
memory
• Dominant Temporal Lobe Lesion Euphoria, Auditory
Hallucinations, Delusions, Thought Disorders
• Right Temporal Lobe Lesion - Irritability, Dec
Visual and Music Ability

17. Internal capsule
• Anterior limb
• Genu
• Posterior limb
Corticobulbar
Corticospinal
Sensory (spinothalamic)

19. • Retrolenticular and sublenticular parts of
internal capsule – visual and auditory fibres

21. • The corticospinal tract conducts impulses from the brain to
the spinal cord.
• It contains mostly axons originated from the motor cortex.
• The corticospinal tract is made up of two separate tracts in
the spinal cord: the lateral corticospinal tract and the
anterior corticospinal tract.
• left hemisphere of the brain controls the right side of the
body, while the right hemisphere of the brain controls the
left side of the body. The signals cross in the medulla
oblongata, this process is also known as decussation.

22. • The spinothalamic
tract is a sensory
pathway originating in
the spinal cord.
• The pathway
decussates at the
level of the spinal
cord, rather than in
the brainstem like the
posterior columnmedial lemniscus
pathway and
corticospinal tract.

23. There are two main parts of the spinothalamic
tract (STT):
• The lateral spinothalamic tract transmits pain
and temperature.
• The anterior spinothalamic tract (or ventral
spinothalamic tract) transmits crude touch
and pressure.

24. posterior columnmedial lemniscus
pathway, PCML
•sensory pathway responsible for
transmitting fine touch, vibration and
conscious proprioceptive information
from the body to the cerebral cortex;
as well as tactile
pressure, barognosis, graphesthesia, s
tereognosis, recognition of
texture, kinesthesia and two-point
discrimination.
The name comes from the two
structures that the sensation travels
up: the posterior (or dorsal) columns
of the spinal cord, and the medial
lemniscus in the brainstem.
Crosses over at medulla.

27. Cranial nerve nuclei
• 3, 4 – midbrain  PCA
• 5,6,7,8 - Pons  basilar artery
• 9,10,11,12 – Medulla  vertebral artery

28. • Reticular formation – important role in arousal
– situated in the brainstem
• Connections of the cerebellum with the spinal
cord and cortex  traverse the brainstem

29. • Cerebellar signs may be produced by the
lesions in the brainstem
• Respi, CVS centres – in medulla
• Cerebellar peduncles – superior, middle and
inferior  arises from midbrain, pons and
medulla respectively

31. Internal carotid branches and their
blood supply
• Anterior cerebral artery  Medial surface of
the hemisphere and internal capsule
• Middle cerebral  Lateral surface of the
hemisphere, basal ganglia and internal capsule
• Post communicating artery – internal capsule
• Ant choroidal artery – internal capsule
• Ophthalmic artery - eye

32. • Vertebral artery
medulla and cerebellum
• Basilar artery  pons
and cerebellum
• Posterior cerebral 
midbrain, thalamus, hipp
ocampus, occipital
lobe, temporal lobe and
cerebellum

33. Internal capsule – blood supply

35. Middle cerebral occlusion
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•
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•
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Motor aphasia – frontal lobe
Sensory aphasia – superior temporal gyrus
Cortical sensory loss – parietal lobe
Homonymous hemianopia – visual radiation
Motor paralysis – internal capsule, motor
cortex

36. DDx of Stroke
• Chronic subdural hematoma – hx of
trauma, headache and drowsiness >>
hemiparesis
• Glioblastoma multiforme – rapidly growing
tumor – no recognisable vascular
territories, progression over days;
papilloedema
• Metastasis – CXR, CT to rule out

37. Signs of cortical involvement
• Left hemisphere (dominant) – aphasia
• Right hemisphere (non dominant)– dressing/
constructional apraxia

38. Signs of cortical involvement
• Apraxia is the inability to perform learned motor acts
on command due to a lesion in the cerebral
hemisphere
• Ideomotor apraxia – unable to do simple motor acts on
command. Eg: use a razor
dominant hemisphere - parietal
• Constructional apraxia- unable to reproduce simple
diagrams/ designs
non dominant parietal
• Dressing apraxia

39. • Neglect – parietal cortex
being unaware of the hemiplegia
(anosognosis), ignoring the paralyzed half of
the body
• Jacksonian seizures
• Cortical sensory loss – two point
discrimination, graphaesthesia, stereognosis

40. • Frontal lobe dysfunction – weakness of one or
both legs  occur with ACA occlusion
features include frontal lobe release signs like
sucking, snout, glabellar
tap, grasp, palmomental, urinary
incontinence, easy
distractability, behavioural, personality and
memory disturbances

41. • Anomia/ Alexia –
Anomia is inability to name objects which are shown to the
patient.
Alexia inability to read
Agraphia inability to write
Anomia for faces
• Cortical blindness – blindness due to b/l homonymous hemianopia
and presence of pupillary response and normal optic disc on
fundoscopy; patient unaware of his blindness as he has areas of
intact vision
• Korsakoff’s amnesic state – profound loss of recent memory.
Usually associated with bilateral or unilateral homonymous
hemianopia; due to infarction of hippocampus

42. • Internal capsule stroke – preservation of
consciousness
• Intracranial h’ge anywhere (even in int
capsule) causes loss of consciousness
secondary to raised ICT

43. • Broca’s area (in inf frontal gyrus)– superior
division of MCA
• Sensory aphasia (sup temporal gyrus) –
inferior division of MCA)
• Conduction aphasia (parietal cortex) – sup
division of MCA
• Global aphasia – Internal carotid artery
occlusion or main trunk occlusion of MCA

44. • Apraxia, Neglect, Focal seizures, Cortical
sensory loss – sup. Division of MCA
• Frontal lobe signs – ACA
• Anomia/ Alexia, Anomia for faces – PCA
• Cortical blindness – occipital lobe – Basilar
artery
• Korsakoff’s amnesic state – hippocampus- PCA

45. Int capsule stroke - features
• Dense uncrossed hemiplegia – CN involved is
same side of the hemiplegia
commonly seen – UMN type of weakness in
7,12, 10 and 5th cranial nerves
UMN type of weakness in these cranial nerves
due to involvement of corticobulbar fibres in the
genu of the internal capsule
• Absence of cortical involvement – no aphasia
• Preservation of consciousness
• Rapid recovery associated with power

46. Brainstem strokes
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Crossed hemiplegia
LMN lesion of cranial nerves
Vertigo
Bilateral involvement
Unconscious- reticular system is involved

47. • Consensual reflex –
because of b/l
innervation of the
edinger westphal
nucleus by the
fibres carrying the
light reflex

48. • CN 3,4,6 – no UMN lesions (as they have
bilateral innervation)
• CN 5 – jaw jerk exaggerated in
UMN, diminished in LMN lesion
• CN 7 – LMN both Upper and Lower part of
face affected; UMN only lower part affected
• CN 12 – longstanding LMN lesions produce
fasciculations and wasting on the affected
side

50. Note
• Absent corneal reflex, absent sensation in
affected area of the face LMN lesion of CN 5
• Absent sensations over the palate, pharynx
and post. third of the tongue – LMNL of CN 10
• Vertigo = brainstem stroke  due to
vestibular nuclei (largest nuclei, spread over a
great length of the brainstem)
• Bilateral involvement – in brainstem lesion 
basilar occlusion or brainstem damage

51. hemorrhage
• SAH – rupture of berry aneurysm/ av malformation 
H, V, meningeal signs, papilloedema, LOC
• Intracerebral h’ge:
a. putamenal/ capsular  dense uncrossed hemiplegia
b. thalamic hemorrhage  hemi anesthesia +/hemiparesis
c. Pontine h’ge  deep coma, bilateral fixed pinpoint
pupils, hyperpyrexia and decerebrate posturing
d. cerebellar h’ge  repeated vomiting, occipital
headache and meningeal signs

52. • Thrombosis – a/c onset, stepwise
increase, consciousness preserved (except
brainstem strokes)
• Embolism – acute, maximal deficit at onset;
probably Hx of a cardiac lesion – MS
• Hemorrhage – a/c onset, gradual
development of deficit over 10-30 minutes;
LOC common  can go into coma

53. • Pure motor hemiplegia – internal capsule or
pontine lesion
• Pure sensory stroke – thalamus
• Dysarthria, clumsy hand syndrome –
dysarthria, facial palsy, ataxia of the hand 
lesion in the internal capsule or pons

54. Pseudobulbar palsy
• capsular/cortical strokes – occur one after the
other in both sides  bilateral infarct  10th and
12th gone in both sides  like in a bulbar palsy.
This is characterised by
dysphagia, dysphonia, dysarthria, emotional
lability. Basically it’s a b/l UMN type of 10th and
12th nerve lesion.
• Features of a medullary lesion are produced by
b/l corticospinal tract infarction