Cerebral Cortex Flashcards

1
Q

What layer of the neocortex give rises to the axons that form corticospinal and corticobulbar tracts?

A

Internal pyramidal layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the presentation of anterior cerebral artery occlusion?

A
  • spastic paralysis and anesthesia of contralateral lower limbs
  • urinary incontinence (usually bilateral lesion)
  • Transcortical apraxia of the left limbs
  • frontal lobe abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Presentation of the middle cerebral artery occlusion

A
  • spastic paralysis of contralateral lower face and upper limb
  • anesthesia contralateral face and upper limb
  • aphasia (broca, Wernicke, or conduction, Gerstman sx) (left middle cerebral artery branches affected)
  • left-sided neglect (right middle cerebral artery branches affected, no dominant hemisphere)
  • contralateral superior quadrantanopsia (Meyer’s loop)
  • gaze palsy (brodmann 8)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Presentation of posterior cerebral artery occlusion

A

Homonymous hemianopia of contralateral visual field with macular sparing.
*alexia without agraphia may occur if dominant hemisphere involved - splenium involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Most common site of aneurysm

A

When anterior communicating artery joins an anterior cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Initial presentation of an aneurism of internal carotid, and first nerve of cavernous sinus involved when expand laterally.

A
  • compression temporal axons or lateral aspect of chiasm ▶️ ipsilateral nasal hemianopia
  • VI CN ▶️ internal strabismus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Features of a embolic infarct and most vulnerable artery to them

A
  • hemorrhagic/red infarct

- middle cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What mechanism can cause a “watershed” areas and involvement of deep cortical layers in brain infarct?

A

Hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What sites and type of infarct do you expect in hypertension patients?

A
  • basal ganglia, internal capsule and pons

- lacunar infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mention 5 predisposing factors to aneurysm rupture? Presentation

A
  • Marfan syndrome, ehlers-danlos type 4, adult polycystic kidney disease, hypertension, smoking
  • subarachnoid hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What area of brain is possible damage when you have a inability to make voluntary eye movement toward contralateral side?

A

Lesion of the frontal eye field (brodmann 8)

- result: conjugate slow deviation of the eyes toward the side of the lesion (intact side make it)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Signs and symptoms is lesion in prefrontal area

A
  • difficult concentrate, easily distracted, lack of initiative, foresight and perspective
  • apathy (severe emotional indifference), abulia
  • slow intellectual faculties, slow speech, decreased participation in social interactions
  • suckling or grasp reflexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lesion in Broca area, brodmann 44 and 45. Signs and symptoms.

A
  • Broca (expressive) aphasia
  • Agraphia (often affected in all aphasias)
  • they can understand but lack of ability to verbalize their thoughts orally or writing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Findings in clinical presentation of lesion at left (dominant) hemisphere at Brodmann area 5,7 (posterior parietal association cortex)

A
  • apraxia (bilateral)
  • astereognosia (contralateral)
  • apraxia results of loss of input to premotor cortex (area 6)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Inability to comprehend spoken and reading (alexia) language (base extend of lesion). Patient paraphasic.

A

Wernicke aphasia (receptive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical presentation of the lesion at angular gyrus (area 39) in dominant hemisphere. Cause

A
  • Gerstman syndrome: alexia, Agraphia, but understand spoken language. Acalculia, finger agnosia, right-left disorientation
  • infarction of the left MCA
17
Q

What structure is damage in conduction aphasia? Which are the signs?

A
  • superior longitudinal fasciculus (arcuate fasciculus): connect Wernicke and Bronca areas. Inability to send information between them
  • verbal output fluent, but many paraphrases and word-finding pauses, no repeat words or verbal commands, poor object naming, frustration
18
Q

Patient with apraxia, no motor weakness, inability to execute commands to move left arm, understanding it, can execute commands to move right arm. Name of the description and cause.

A
  • Transcortical apraxia (disconnect syndrome)
  • infarct of the anterior cerebral artery ▶️ lesion at corpus callosum

*disconnection of Wernicke area (left) from right primary motor cortex. Execute command with right arm because Wernicke area at left hemisphere can communicate with ipsilateral primary motor cortex without corpus callosum

19
Q

What is the result of a wide spread lesion in areas 7, 39, 40 in no dominant right parietal lobe?

A
  • asomatognosia: neglect contralateral half of body ▶️ no dress, undress, wash, etc. deny existence of things at left visual side (they can see)
  • anosognosia: deny the deficit
20
Q

Cause of homonymous contralateral hemianopia with macular sparing, what cortical area involve?

A
  • infarct of a branch of posterior cerebral artery

- primary visual cortex, brodmann 17 (striate)

21
Q

What lesion may cause achromatopsia, prosopagnosia and visual agnosia?

A
  • inferior part of temporal lobe (area 20, 21)

* visual association cortex: form and color

22
Q

Lesion at parietal lobe in areas 18, 19 (visual cortex - extrastriate, visual association cortex)

A

Deficit in perceiving visual motion and depth

*unaffected visual fields, colors, reading.

23
Q

Patient with Alexia without Agraphia, unable to read and to name colors (color anomia, curious), can write, and associated with homonymous hemianopia with macular sparing, where is the lesion? And cause of it.

A
  • left occipital cortex (anterior part) and splenium of corpus callosum
  • infarction of left posterior cerebral artery
  • impair visual info from intact right occipital cortex (left visual field) to reach language comprehension center in left side ▶️ not understand what you see
24
Q

Symptoms in a lesion of primary auditory cortex

A
  • Little loss auditory sensitivity

- some difficult localizing sounds in contralateral sound field

25
Q

What clinical presentation do you expect in a hypertensive stroke involving lenticulostriate branch of MCA?

A
  • contralateral spastic paralysis, weakness, anesthesia upper, lower limbs, trunk and face
  • irrigate genu and posterior limb of internal capsule ▶️ corticospinal, all somatosensory thalamocortical projections and corticobulbar tracts
26
Q

Which are the disconnect syndromes and their damage structures?

A
  • conduction aphasia - superior longitudinal fasciculus (arcuate)
  • Transcortical aphasia - corpus callosum
  • alexia without agraphia - splenium of corpus callosum
27
Q

When occur a sensory dysphrosodia?

A
  • Wernicke area lesion (22) in no dominant hemisphere (right)
  • MCA stroke
28
Q

What happen if premotor cortex (brodmann 6) is damaged?

A
  • apraxia: unable to perform movements in correct sequence
  • no weakness and individual movements normal
  • planning motor activities (function of premotor cortex)
29
Q

Second most common site of cerebral aneurysm, what sign is frequently associated?

A
  • posterior communicating artery

- III CN palsy