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LOCALISING
A CORTICAL
STROKE
ASHWIN NAIR A R
2015 MBBS
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
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.
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.
Artery to
Artery
EMBOLIC STROKE
Cardiac
Causes of Thrombotic stroke:
Causes of Embolic stroke
Atherosclerosis (MC)
Non-rheumatic AF / rheumatic AF
Takayasu arteritis
MS, AS
Prosthetic valves
Sick sinus syndrome
Recent MI.
LOCALISING A
STROKE/NEUROLOGICAL
DEFICIT
li
Areas of the cortex.
de Title - 2
Superior division
of MCA
Inferior
division of
Sylvian
MCA
fissure
If there is occlusion to Superior division of MCA, because it
supplies the important areas in frontal lobe, we can look for the
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
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.
Brocas areas-44 45- located in inferior
frontal gyrus.
"Dysarthric, effortful, telegraphic, sprase
speech"
Fluency, prosody are lost. Aggramatical
speech.
Repetition is also lost.
Comprehension preserved.
Reading and writing impaired.
Add a Slide Title - 4
Isolated lesion of pre motor cortex- rare,
more spasticity is seen, primitive reflexes
appear. Less paralysis.
Pre frontal cortex- 9, 10, 11- "Makes you, you."
Deals with our personality, creativity, insight, judgement, attention,
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
unacceptable behaviour, personality disorders.
PFC is also connected to caudate nucleus and putamen- hence
extrapyramidal features can spring up.
Medial surface of frontal cortex- Supplied by A2
branch of ACA
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.
B/L lesion- Abulia/ Akinetic mutism
If there is a milder version of B/L frontal lobe lesion- gait apraxia or
iginition foot.
PARIETAL LOBE- Superior division of M2 supplies
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
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 %
of UMN fibres originate from area 312.
Cortical sensory loss
Homonymous inferior Quadrantanopia (Pie on the floor)
Apraxia and loss of Optokinetic nystagmus.
Supramarginal gyrus: lesion causes apraxia. Can be ideational or
idiomotor.
Left lobe is the dominant one.
Gerstmann syndrome- seen in lesions to Angular gyrus:
Loss of Rt and Lt discrimination
Acalculia
Agraphia with Alexia
Dominant Lobe
Finger agnosia
Lesions to Rt Parietal lobe:
Visuospatial inattention
Hemispatial neglect or anosagnosia
Constructional apraxia
Dressing apraxia
TEMPORAL LOBE- Supplies by Inferior division of
MCA
AREAS : WERNICKES AREA 22
PRIMARY AUDITORY AREAS 41 AND 42
SECONDARY AUDITORY AREA 22
VISUAL ASSOCIATION CORTEX- AREAS 21 AND 22
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.
Lesion to Secondary auditory area: Auditory agnosia
Lesion to Visual association cortex: Visual agnosia
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.
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
agnosia.
Auditory, olfactory and gustatory hal ucinations are also seen.
ALSO REMEMBER
Medial temporal lobe is supplied by P2, a division of Posterior
cerebral artery. P2 arises distal to PCOM.
When Medial temporal lobe is affected: visual agnosia, memory
loss (hippocampus is affected)
P2 supplies occipital cortex as well.
OCCIPITAL LOBE Supplied by PCA- P2 division to
be specific
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.
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.
Bilateral occipital cortex lesions-
ANTON SYNDROME:
SIMULTAGNOSIA (MISSING THE FOREST FOR TREES)
OPTIC ATAXIA
OCCULOMOTOR APRAXIA
BALINT SYNDROME
Cortical blindness, preserved light reflex, visual acuity impaired.
The patient denies blindness.
Agnosias:
Colour
Prosopagnosia- inability to recognise faces.
This post was last modified on 12 August 2021