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Kaplan: Anatomy and Physiology Part III > Chapter 10: Cerebral Cortex > Flashcards

Chapter 10: Cerebral Cortex Flashcards

1
Q

What layer of the neocortex is the terminationn of the thalamocortical projections?

A

internal granular layer?

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2
Q

What are the 6 layers of the neocortex?

A

I. molecular
II. external granular
III. External pyramidal layer
IV. Internal granular layer
V. Internal pyramidal layer
VI. Multiform layer (layer of polymorphic cells)

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3
Q

Which layer of the neocortex give rise to the corticospinal and corticobulbar tracts?

A

multiform layer

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4
Q

What areas of the brain are supplied by the middle cerebral artery (MCA) supplies? (in general)

A
  • lateral surface of the frontal, parietal, and upper temporal lobes
  • posterior limb and genu of the internal capsule
  • most of the basal ganglia
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5
Q

Left sided middle cerebral artery occlusion can lead to what condition specific conditions?

A

Broca or Wernicke aphasia

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6
Q

Right sided middle cerebral artery occlusion?

A

left sided neglect

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7
Q

Occlusion of branches of the middle cerebral artery that supply Meyer’s loop fibers in the temporal lobe result in what condition?

A

contralateral superior quadrantanopsia

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8
Q

What structures does the ACA supply?

A

medial surface of the frontal and parietal lobes; anterior 4/5 of corpus callosum; anterior limb of internal capsule

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9
Q

What areas of the brain does the PCA supply?

A

supplies occipital lobe; lower temporal lob; splenium; midbrain

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10
Q

What is the most common site for an aneurysm?

A

where the anterior communicating artery joins an anterior cerebral artery

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11
Q

How do thrombotic cerebral infarcts appear?

A

anemic/ pale infarct; usually atherosclerotic complication

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12
Q

How do embolic cerebral infarcts appear?

A

hemorrhagic/ red infarct; from heart or atheroscelrotic plaques middle cerebral artery most vulnerable to emboli

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13
Q

how do hypotension cerebral infarcts appear?

A

“watershed” areas and deep cortical layers most affected

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14
Q

How do infarcts caused by hypertension appear?

A

lacunar infarcts; basal ganglia, internal capsule, and pones most affected

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15
Q

Cause of epidural hematoma

A

rupture of middle meningeal artery after skull fracture

almost always traumatic

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16
Q

Characteristics of an epidural hematoma?

A

lucid interval before loss of consciousness (“talk and die” syndrome)

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17
Q

What is the cause of a subdural hematoma?

A
  • usually caused by trauma
  • rupture of bridging veins (drain brain to dural venous sinuses)
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18
Q

What is the cause of subarachnoid hemorrhage?

A

ruptured berry aneurysm most commn cause

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19
Q

Predisposing factors of subarachnoid hemorrhage?

A

Marfan syndrome, Ehlers-Danlos type 4, adult polyscystic kidney disease, hypertension smoking

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20
Q

What are the causes of intracerebral hemorrhage?

A

common causes: hypertension, trauma, infarction

21
Q

Primary cortex corresponding Brodmann areas?

A

41 & 42

22
Q

Broca’s area corresponding Brodmann area?

A

44 & 45

23
Q

Frontal eye field corresponding Brodmann area?

A

area 8

24
Q

Premotor cortex corresponding Brodmann area?

A

area 6

25
Q

Primary motor cortex corresponding Brodmann area?

A

area 4

26
Q

Primary somatosensory cortex corresponding Brodmann area?

A

areas 3, 1, and 2

27
Q

Angular gyrus corresponding Brodmann area?

A

area 39

28
Q

Wernickes area corresponding Brodmann area?

A

area 22

29
Q

What would a lesion of the frontal eye field lead to?

A

inability to make voluntary eye movements toward the contralateral side

Because the activity of thee intact frontal eye field in the opposite cortex would also be unopposed after such a lesion, the result is conjugate slow deviation of eyes toward side of the lesion.

Intact frontal eye field in the opposite hemisphere deviates eyes away from the paralyzed limb

30
Q

What is Gerstmann Syndrome?

A

when a lesion is confined to anuglar gyrus and produces loss of ability to comprehend written language (alexia) and to write it (agraphia)

31
Q

Describe conduction aphasia?

A

the large fiber bundle (superior longitudinal fasiculus (or the arcuate fasiculus)_ is lesionsed.

verbal output is fluent, but there are many parapharases and word finding pauses. Both verbal and visual language comprehension but if ased to repeat words or execute verbal commands cant be done….also poor object naming example of “disconnect syndrome”

32
Q

Transcortical apraxia.

A

similar to conduction aphasia except 2 hemispheres are disconnected because of lesion at the corpus callosum

33
Q

Asomatognosia.

A

caused by lesions in the non-dominant right parietal lobe may result in unawareness or neglect of the contralateral half of the body

34
Q

What is visual agnosia?

A

when there is damage to parts of the temporal lobes involving the cone stream producing a visual agnosia.

Inability to recognize visual patterns (including objects) in the absence of a visual field deficit

lesions in the temporal lobe that also produce some destruction of adjacent occipital lobe in either hemisphere reult in prosopagnosia specific inability to recognize faces

35
Q

Alexia without agraphia?

A

“higher-order” deficit associated with occipital lobe damage is alexia without agraphia (or pure word blindness)

Patients unable to read at all and often have color anomia (inability to name colors)

can write

another example of disconnect syndrome in which information from occipital lobe is not available to the parietal or frontal lobes to understand or express what is seen

involvement of splenium of corpus callosum prevent visual informatin from intact right occipital cortex from reaching languate comprehension centers in left hemisphere

36
Q

Arterial supply to the anterior limb of the internal capsule?

A

medial striate br. of ACA

37
Q

What are the tracts reaching the anterior limb of the internal capsule?

A

thalamocortical

38
Q

Arterial supply to the genu of the internal capsule?

A

lenticulostriate br. of MCA

39
Q

What are the tracts through the genu?

A

corticobulbar

40
Q

Arterial supply to the posterior limb of the internal capsule?

A

lenticulostriate branch of MCA

41
Q

Tracts through the posterior limb of the internal capusle?

A

corticospinal, all somatosensory thalamocrotical projections

42
Q

Where is the second most common site of aneurysm in the brain?

A

posterior communicating artery

43
Q

Posterior communicating artery blockage can cause blockage of what cranial nerve?

A

CN III

44
Q

Gaze palsy aphasia is seen with which branch of the middle cerebral artery?

A

lenticulostriate branch

45
Q

What part of the brain is implicated in frontal lobe syndrome? What is frontal lobe syndrome?

A

prefrontal cortex;

symptoms can include poor judgment, difficulty concentrating and problem solving, apathy, inappopriate social behavior

46
Q

What is the lobe implicated in contralateral asterognosis/ apraxia?

A

superior parietal lobe

47
Q

What are the lobes implicated in Gerstmann syndrome?

A

Inferior parietal lobule

(angular gyrus; area 39)

48
Q

What structure is implicated in Kluver bucy syndrome?

A

amygdala

49
Q

What are some symptoms of Kluver Bucy?

A

hyperphagia, hypersexuality, visual agnosia

Kaplan: Anatomy and Physiology Part III (13 decks)

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