Download MBBS Localising a cortical sroke Lecture PPT

LOCALISING
A CORTICAL
STROKE
ASHWIN NAIR A R

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2015 MBBS

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DEFINITION OF STROKE
It is an abrupt onset of a focal neurological deficit which can be
attributable to a vascular cause.
Fever and hyperglycemia- 2 factors that worsen the prognosis of a

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stroke.
If a neurological stroke clears within 1 hour (earlier guidelines
mention 24 hour as the cut off), it is cal ed a TIA (Transient
ischemic attack).
Stroke results in liquefactive necrosis in the brain.

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Ischemic strokes (85%) are more common than Hemorrhagic strokes (15%).
Ischemic strokes can take genesis mostly from Anterior circulation (65%) and the
posterior circulation (20%) as well.
With respect to etiology, embolic strokes are more common than thrombotic
strokes.

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Artery to
Artery
EMBOLIC STROKE
Cardiac

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Causes of Thrombotic stroke:

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Causes of Embolic stroke
Atherosclerosis (MC)
Non-rheumatic AF / rheumatic AF
Takayasu arteritis
MS, AS

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Prosthetic valves
Sick sinus syndrome
Recent MI.

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LOCALISING A
STROKE/NEUROLOGICAL

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DEFICIT

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li
Areas of the cortex.
de Title - 2

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Superior division
of MCA
Inferior
division of

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Sylvian
MCA
fissure

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If there is occlusion to Superior division of MCA, because it
supplies the important areas in frontal lobe, we can look for the

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fol owing lesions:
Weakness of arms and legs of the opposite side (hemiplegia)- 30
% of UMN fibres come from area 4 or motor area, rest 30 percent
originate from pre and supplementary motor areas- area 6 mostly.
Affliction to frontal eye field (area 8) results in loss of saccadic

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movements.
In a frontal lobe lesion, patient looks towards side of lesion, the left
frontal lobe helps you look to the right side and vice versa.

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Brocas areas-44 45- located in inferior

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frontal gyrus.
"Dysarthric, effortful, telegraphic, sprase
speech"
Fluency, prosody are lost. Aggramatical
speech.

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Repetition is also lost.
Comprehension preserved.
Reading and writing impaired.
Add a Slide Title - 4
Isolated lesion of pre motor cortex- rare,

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more spasticity is seen, primitive reflexes
appear. Less paralysis.

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Pre frontal cortex- 9, 10, 11- "Makes you, you."
Deals with our personality, creativity, insight, judgement, attention,

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intelligence, motivation, social behaviour, language and problem
solving capacity.
Also has a role in retrieval of memory (What did you have for
breakfast?)
Lesions can thus affect al these areas, person may exhibit

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unacceptable behaviour, personality disorders.
PFC is also connected to caudate nucleus and putamen- hence
extrapyramidal features can spring up.

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Medial surface of frontal cortex- Supplied by A2
branch of ACA

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Important areas: Paracentral lobule
A lesion to this area- urinary incontinence
Anterior Cingulate gyrus- above cingulate sulcus
It has autonomic and limbic connections-lesions can result in
emotional, autonomic and endocrine defects.

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B/L lesion- Abulia/ Akinetic mutism
If there is a milder version of B/L frontal lobe lesion- gait apraxia or
iginition foot.

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PARIETAL LOBE- Superior division of M2 supplies

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it
Post central gyrus- areas 312- somatosensory cortex- takes care of
cortical sensations- Stereognosis, Tactile localisation, 2 point
discrimination, Graphasthesia,
Remember that pain and fine touch are carried by anterior

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spinothalamic tract, pressure and crude touch by lateral
spinothalamic tract.
A lesion here can be due to occlusion of the Superior segment of
MCA
Mild motor weakness can be seen here too. This is because 40 %

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of UMN fibres originate from area 312.
Cortical sensory loss

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Homonymous inferior Quadrantanopia (Pie on the floor)
Apraxia and loss of Optokinetic nystagmus.
Supramarginal gyrus: lesion causes apraxia. Can be ideational or

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idiomotor.
Left lobe is the dominant one.
Gerstmann syndrome- seen in lesions to Angular gyrus:
Loss of Rt and Lt discrimination
Acalculia

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Agraphia with Alexia
Dominant Lobe
Finger agnosia

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Lesions to Rt Parietal lobe:
Visuospatial inattention

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Hemispatial neglect or anosagnosia
Constructional apraxia
Dressing apraxia

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TEMPORAL LOBE- Supplies by Inferior division of

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MCA
AREAS : WERNICKES AREA 22
PRIMARY AUDITORY AREAS 41 AND 42
SECONDARY AUDITORY AREA 22
VISUAL ASSOCIATION CORTEX- AREAS 21 AND 22

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Hearing loss occurs only if there is B/L lesion.
Lesion affecting Wernickes area- Wernickes Aphasia- fluent
sensory aphasia.
Patient manufactures his own words.
Cannot register new events in memory.

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Lesion to Secondary auditory area: Auditory agnosia
Lesion to Visual association cortex: Visual agnosia

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Superior homonymous quadrantanopia. (Pie on the sky)
Limbic cortex also forms a major part- mainly deals with our fear,
aggression, feeding, sexual desire, goal directed behaviour.

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Consists of Amygdala and Hypothalamus.
B/L Amygdala lesion- Kluver Bucy Syndrome.
Remember that the temporal lobe does not have dominant or non
dominant.
So lesions can produce- Wernickes aphasia, audiotory and visual

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agnosia.
Auditory, olfactory and gustatory hal ucinations are also seen.

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ALSO REMEMBER
Medial temporal lobe is supplied by P2, a division of Posterior
cerebral artery. P2 arises distal to PCOM.

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When Medial temporal lobe is affected: visual agnosia, memory
loss (hippocampus is affected)
P2 supplies occipital cortex as well.

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OCCIPITAL LOBE Supplied by PCA- P2 division to
be specific

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AREAS
PRIMARY VISUAL CORTEX: 17
PERI AND PARASTRIATE CORTEX: 18. 19
They deal with ocular memory- fixation of size, shape and colour.
Occipital cortex lesion can give rise to homonymous hemianopia.

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An optic tract lesion gives rise to the same.
In occipital cortex lesion, pupil ary reflex is preserved. It is a
complete loss.
Tract lesion- reflex is affected, non congruous loss.

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Bilateral occipital cortex lesions-

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ANTON SYNDROME:
SIMULTAGNOSIA (MISSING THE FOREST FOR TREES)
OPTIC ATAXIA
OCCULOMOTOR APRAXIA
BALINT SYNDROME

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Cortical blindness, preserved light reflex, visual acuity impaired.
The patient denies blindness.

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Agnosias:
Colour
Prosopagnosia- inability to recognise faces.

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