Localization of Cortical Dysfunction Flashcards

1
Q

What are the 3 domains of consciousness?

A
  1. alertness
  2. attention
  3. awareness
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2
Q

Level Of Consciousness (4):

A

awake state on one end of spectrum to coma on the other

  1. awake
    • one is able to maintain alertness, attention, awareness including awareness of self & environment
  2. sleepy
    • alertness wanes after short period without stimulation
  3. stupor
    • alertness severely impaired
    • attention, awareness only maintained with continued stimulation
  4. coma
    • loss of alertness, attention, awareness
    • unarousable
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3
Q
  • delirium:
  • encephalopathy:
A
  • delirium
    • alert and aware, but attention severely impaired
    • confused
  • encephalopathy
    • all 3 domains affected, but to a lesser degree than in a coma
    • some alertness maintained
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4
Q

Where are structural or functional abnormalities that can cause an altered state of consiousness?

A
  • diffuse bilateral cerebral hemispheres
    • lesion involving half the cerebrum will typically NOT cause altered consciousness
    • although they will have focal deficits
  • bilateral thalami
    • because ARAS projects to brain, which then projects to cerebrum
  • brainstem ARAS
    • ascending reticular activation system
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5
Q

FRONTAL LOBE:
Primary motor cortex

A
  • functions to voluntarily control contralateral movement
  • lesion (eg. stroke) ⇒ contralateral hemiparesis
  • activation (eg. seizure) ⇒ contralateral clonic movements
  • Jacksonian march
    • seizures in the primary motor cortex that travels along gyrus
    • activates muscles in an order seen on the motor homunculus
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6
Q

FRONTAL LOBE:

Frontal Eye Fields

A
  • contralateral saccades
    • voluntary eye movements to contralateral field
  • lesion of FEF ⇒ ipsilateral gaze preference
    • eg. L FEF stroke ⇒ L gaze preference
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7
Q

FRONTAL LOBE:

Broca’s Area

A
  • fluency of language
  • inferior frontal lobe in dominant hemisphere
    • in most R handed and most L handed people, language is represented in the dominant (L) hemisphere
    • more L handed individuals tend to have bilateral language representation
  • loss of function causes a Broca’s aphasia = Non-fluent aphasia
    • speech is non-fluent, halting, effortful, composed of few words that usually make sense
    • agrammatic
    • repetition impaired
    • Broca’s area is supplied by MCA
    • lesion could be caused by stroke or tumor
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8
Q

FRONTAL LOBE:

Prefrontal Cortex

A
  • provides ORDER
  • mediates personality, executive function, ability to sequence & organize tasks, abstract, problem solving
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9
Q

FRONTAL LOBE:

Orbitofrontal cortex

A
  • provides RESTRAINT
  • inhibits socially inappropriate behavior
  • part of limbic system
    • plays role in memory & emotions
  • 2 most common ways to lesion this region of brain
    1. ​​head trauma as orbitofrontal cortex rubs along base of skull with jagged surface
    2. meningioma (tumor of meninges at base of skull)
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10
Q

Frontotemporal dementia (Pick’s disease):

A
  • progressive dementia due to neurodegeneration
  • affects prefrontal cortex first ⇒ causes personality changes, irritability, mood changes, poor executive function
  • eventually affects other regions of frontal cortex such as orbitofrontal cortex & also temporal cortex
  • dementia occurs in mid life (50’s), which is much earlier than most cases of Alzheimer’s
  • lifespan is shortened
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11
Q

FRONTAL LOBE:

Mesiofrontal cortex

A
  • provides INITIATIVE
  • mediates motivation, goal-directed behavior
    • micturition inhibitory center allows voluntary inhibition of urination
  • lesion causes akinetic mutism (patients do not move or talk), abulia (lack of initiative), incontinence as seen in hydrocephalus (ventricles enlarge & stretch fibers travelling medially to spinal cord)
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12
Q

PARIETAL LOBE:
Primary somatosensory cortex

A

mediates contralateral sensation

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13
Q

PARIETAL LOBE:

Parietal somatosensory association cortices

A
  • mediates higher order sensation (primary sensation must be intact):
    • graphesthesia = ability to discern what is written on skin
    • stereognosis = ability to discern object placed in hand based on sensation
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14
Q

Describe the characterstics of a deficit in the parietal somatosensory association cortex on the non-dominant side:

A
  • non-dominant parietal cortex (in most people, the R parietal cortex) drives spatial attention on both hemifields
    • R parietal cortex controls spatial attention on L hemifield >> R hemifield
    • L parietal cortex controls spatial attention on R hemifield primarily
  • lesion of non-dominant parietal cortex (R) results in contralateral neglect & apraxia
  • neglect = not paying attention to contralateral hemifield
    • eg. R parietal lesion will cause severe L neglect
    • patient “ignores” the left side of the world
    • they will bump into objects on L side, will ignore the L side of their body
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15
Q

Apraxia:

A

inability to perform a skilled task

  • brushing teeth, combing hair, dressing, tying shoe lace
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16
Q

Gerstmann syndrome:

A
  • lesion of dominant (L) parietal cortex (angular gyrus)
  • 4 components to clinical syndrome:
    1. agraphia
      • inability to write
    2. acalculia
      • inability to calculate
    3. finger agnosia
      • inability to recognize fingers
    4. right/left confusion
      • cannot discern between right & left
17
Q

TEMPORAL LOBE:
Wernicke’s area

A
  • comprehension of language
  • superior temporal gyrus in dominant hemisphere
  • loss of function causes Wernicke’s aphasia = Fluent aphasia
    • nonsensical gibberish
    • patient may be partially aware that what is said is not correct despite not comprehending
    • patient cannot follow commands
    • impaired repetition
  • Wernicke’s area is supplied by MCA
18
Q
  1. Conduction Aphasia:
  2. Global Aphasia:
A
  1. Conduction Aphasia:
    • ​​inability to repeat
    • mediated by arcuate fasciculus
  2. Global Aphasia:
    • ​​loss of comprehension, repetition, & fluency
    • these patients usually have no language
    • usually due to complete MCA stroke at its proximal origin (where ICA divides into ACA & MCA)
19
Q

Kluver-Bucy Syndrome:

A
  • due to injury to bilateral anterior temporal poles & bilateral amygdala
  • hyperorality (pt explores environment with mouth)
  • inappropriate sexual displays (removing clothes, masturbation in public, inappropriate kissing/flirting)
  • irritability & aggression
  • anterograde amnesia—due to amygdala involvement
  • alternating episodes of depression & overactivity
20
Q

What is the Function of the Medial Temporal Lobe? What can disrupt its function?

A
  • memory center of brain
  • hippocampal atrophy
    • neuronal degeneration in the hippocampus occurs early in Alzheimer’s disease
  • hippocampal sclerosis
    • scarring of hippocampus is thought to cause or be the result of uncontrolled complex partial seizures
21
Q

OCCIPITAL LOBE:
Primary visual cortex

A
  • right occipital cortex mediates vision from contralateral hemifield
  • optic radiations: originate from lateral geniculate nucleus ⇒ visual cortex
    1. LGN ⇒ optic radiations travels into parietal region ⇒ synapses onto superior bank of occipital cortex
      • inferior vision
    2. LGN ⇒ optic radiations travel into temporal region (Meyer’s loop) ⇒ synapses onto inferior bank of occipital cortex
      • superior vision
22
Q

Describe how lesions in the primary visual cortex affect vision:

A
  1. R occipital cortex lesionL homonymous hemianopia (and vice versa)
  2. monocular visual field defects ⇒ usually anterior to chiasm
  3. binocular visual field defects (ie. homonymous) ⇒ retro-chiasmal
  4. lesion of the parietal optic radiationscontralateral inferior quadrantanopia
  5. lesion of Meyer’s loopcontralateral superior quadrantanopia
23
Q

Define homonymous:

A

affecting both sides

  • R homonymous hemianopia indicates that R field on both eyes are affected
  • presence of a homonymous hemianopia indicates that lesion is in cortex/subcortex
24
Q

Homonymous hemianopia with macular sparing:

A
  • may occur due to dual blood supply to occipital pole
  • outer tip of calcarine cortexmacular vision
    • highest visual acuity
  • inner portions of calcarine cortexperipheral vision
  • primary blood supply is from PCA
    • secondary blood supply is from branch of MCA
  • PCA stroke may still allow intact macular vision due to blood from MCA branch
25
Q

Balint syndrome:

  • Simultanagnosia
  • Optic Ataxia
  • Ocular Apraxia
A
  • lesion of bilateral occipital-parietal pathways
    • ​“where” pathway
    • helps determine spatial relations of objects
    • triad below
  • Simultanagnosia
    • inability to perceive the visual field a whole
    • Pt focuses on small portions of picture but cannot conceptualize picture as a whole
  • Optic ataxia
    • inability to point/reach for objects in visual field under visual guidance
  • Ocular apraxia
    • inability to look at objects in VF using saccades
  • can be caused by b/l MCA-PCA watershed infarcts, Alzheimer’s disease
26
Q

What is a watershed infarct?

A
  • due to cerebral hypoperfusion
  • vulnerable cortex between main arterial territories are lesioned
  • ACA-MCA infarct
  • MCA-PCA infarct
27
Q

ACA-MCA infarct:

A
  • lesion of cortex that is not primarily supplied by MCA or ACA
  • results in “man in a barrel” syndrome
    • motor cortex representing torso & shoulder are more vulnerable than hands and legs/feet
    • due to arrangement of motor homunculus
    • results in relative sparing of movement of hands/feet
  • caused by stenosis of ICA with superimposed hypoperfusion
28
Q

MCA-PCA infarct:

A
  • lesion of cortex that is not primarily supplied by MCA or PCA
  • results in Balint syndrome
  • can be caused by systemic hypoperfusion
    • cardiac arrest