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From Flashcardlet > Neuro 45 & 46: Cortex > Flashcards

Neuro 45 & 46: Cortex Flashcards

1
Q

PET scan

A

-measures changes in cerebral blood flow or metabolism via short lived isotopes that are injected

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2
Q

fMRI

A

-measures changes in cerebral blood flow based on how Hb/O2 affects protons

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3
Q

2 types of cortical areas

A
  1. primary areas:
    - sensory - have thalamic relays
    - motor
  2. association areas- assist nearby primary areas
    - sensory association cortex
    - motor association cortex
    - also includes mutlimodal/integrative areas
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4
Q

Post-central gyrus

A

-somatosensory homunculus

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5
Q

Pre-central gyrus

A

-motor homunculus

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6
Q

Which 3 deeps axons play a role in cortical communication?

A
  1. association fibers
  2. projection fibers
  3. commissural fibers
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7
Q

Association fibers

A
  • interconnect cortical areas in one hemisphere
  • there are short ones to interconnect adjacent gyri –> important for communication w/in an area
  • there are long fibers to innerconnect more distant areas –> important for distance communication
  • diseases that damage/interrupt these fibers will cause cognitive deficits
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8
Q

Uncinate fasiculus

A

-association fibers that travel btwn the temporal and frontal lobes

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9
Q

Cingulum

A

-association fibers that travel btwn the temporal and frontal lobes

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10
Q

Superior longitudinal fasiculus

A

-association fibers that travel btwn the frontal, parietal, occipital, and temporal lobes

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11
Q

Projection fibers: what are they? list the 4?

A
  • input and output fibers of the cortex to other areas of the CNS
  • damage to these cause major sensory or motor deficits
    1. corona radiata
    2. internal capsule
    3. thalamocortical fibers
    4. corticospinal fibers
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12
Q

Commissural fibers

A
  • interconect the cortex of the right and left hemispheres
    1. corpus callosum
    2. anterior commissure
    3. hippocampal commisure
  • *damage or agenesis often do not result in obvious functional deficits!!
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13
Q

Neocortex layers

A
  • outer layer of the cerebral hemispheres
  • has 6 lyrs
  • organization of the layers is essential for information processing –> developmental problems can cause seizures, mental retardation, or cog deficits!
  • involved in higher fctns such as sensory perception, generation of motor commands, spatial reasoning, conscious thought, and language
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14
Q

Pyramidal neuron

A
  • type of cortical neuron

- long axon projection neurons

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15
Q

Golgi neuron

A
  • type of cortical neuron

- short axon interneurons

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16
Q

Asterognosis

A
  • inability to identify an object by touch alone

- caused by lesions in the posterior parietal lobe

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17
Q

Apraxia

A
  • inability to produce familiar purposeful mvmnts
  • NO sensory or motor impairment
  • caused by a lesion in the posterior parietal lobe
  • sometimes the pt can perform tasks on their own, but have trouble when they need to perform tasks on command
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18
Q

Agraphesthesia

A
  • inability to identify letters or numbers “drawn” on the skin –> disorientation of the skin’s sensation across its space
  • caused by posterior parietal lesions
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19
Q

Neglect

A
  • denial of self-image of one side of the body or external world
  • lesions usually in the RIGHT hemisphere in the posterior parietal lobe
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20
Q

Aphasia

A

-disruption of language capacity, there are different forms

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21
Q

Hemispheric dominance

A
  • in some locations damage on the right may cause different deficits from damage in the same area on the left
  • so each hemisphere has different capabilities
  • dominance is clearly known for language, but is less clear for other functions
  • plays a role in handedness too
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22
Q

Delirium

A
  • usually a temporary change & is reversible with tx
  • acute/sudden onset/medical condition
  • inattention, confusion, reduced comprehension, can have change in consciousness
  • common in hopitalized older adults –> often drug induced
  • *frequently mistaken for dementia or unrecognized!!!
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23
Q

Dementia

A
  • usually permanent & irreversible
  • ongion medical condition
  • slow onset
  • no change in consciousness
  • memory impairment
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24
Q

Plasticity

A
  • probably a general feature of the cortex
  • reorganization of cortical maps
  • experiences shape brain fctn
  • can occur in developmental deficits –> ex. blindness/deaftness, stroke, hemispherectomy pts
  • the cortex expects sensory input from the periphery, so when sensory info is elimintated it will create its own info! –> ex. phantom limb, tinnitus, chronic pain, etc.
25
Q

Control of consciousness

A
  • ability to remain alert/awake is controlled by brainstem/system network that influences cortical function –> damage = coma
  • all sensory systems –> reticular activating system (RAS -midbrain) –> relay in thalmus –> cortical activation = alertness, awake status
  • need BOTH cerebral cortex and RAS to be conscious!
26
Q

Damage to primary areas v. damage to association areas

A

Primary:
-cause loss of contralateral sensation or wkness
-damage to single hemisphere is sufficient enough to cause deficit
Association:
-more complex deficits
-often patient is not aware of deficit
-usually bilateral damage is necessary to cause more complex deficits of association areas

27
Q

3 common ways to get bilateral cortex lesions?

A
  1. trauma
  2. infection - encephalitis, meningitis
  3. vascular
28
Q

What 3 lobes does the visual system involve?

A
  1. occipital lobe
  2. parietal lobe
  3. temporal lobe
29
Q

Dorsal visual pathway

A
  • extends into the parietal lobe
  • analyzes the POSITION & MOTION of an object = “where”
  • *a bilateral lesion in this pathway causes motion agnosia = deficits in perceiving object motion
30
Q

Ventral visual pathway

A
  • involves the occipitotemporal gyrus
  • analyzes an object’s FORM & COLOR = “what”
  • *bilateral deficits cause color/form agnosia or prosopagnosia (inability to recognize faces of familiar people)
31
Q

Visual word form area

A
  • unique to humans
  • specific area in the ventral pathway
  • involved in reading & face recognition
  • left-sided unilateral lesions will impair reading, but not auditory recognition of words
32
Q

Propagnosia

A
  • inability to recognize faces of previously familiar people

- caused by a lesion in the occipitotemporal gyrus

33
Q

Anton’s syndrome

A
  • cortical blindness
  • pt lacks awareness of deficit = agnosia
  • caused by a lg bilateral lesion in the visual areas
34
Q

Posterior paritetal lobe

A
  • integrates tactile and proprioceptive info and info from the 2 hands
  • mediates sterognosis and 2-pt discrimination
  • sends info to the motor cortex to provide sensory info to guide mvmnt
  • *lesions cause astereognosis, agraphesthesia, neglect, and apraxia
35
Q

Emotional component of pain: what 2 areas are involved and what do lesions cause?

A
  • anterior cingular gyrus and the insula are involved

- lesions lessen the emotional component of pain

36
Q

Transverse temporal gyri

A

-primary auditory cortex

37
Q

Wernicke’s area

A
  • for language comprehension/understanding –> speech, written, or sign
  • found in posterior temporal lobe
38
Q

Broca’s area

A
  • inferior frontal gyrus, adjacent to motor cortex

- essential for motor aspects & vocalization of language –> speech, written, sign

39
Q

Multimodal auditory areas

A
  • found superior to wernicke’s area
  • receive visual, auditory, and somatosensory info important for language fctns of reading braille and sign lang
  • *lesions = affect reading and writing from visual cues = dyslexia & agraphestheisa
40
Q

Word memory

A
  • anterior temporal lobe

* *lesions = deficits in naming and word finding

41
Q

Wernicke aphasia

A
  • inability to understand the meaning of words
  • pt cannot comprehend speech, but they can verbalize well
  • spontaneous speech is fluent and word articulation is good, but content is meaning less
  • unaware of deficit
42
Q

Broca’s aphasia

A
  • inability to vocalize words
  • speech is sparse, slow, and words are mispronounced
  • writing can also be effected
  • aware of deficit
43
Q

Conduction aphasia

A
  • damage to arcuate fasiculations disconnects wernicke’s and broca’s areas w/out directly damaging them
  • comprehension is good, speech is fluent, but contains errors
  • question-answer tasks are difficult
44
Q

Language localization and handedness

A
  • in most adults language is localized on the left
  • rt handed ppl = most have lang localized to left
  • lft handed ppl = most have lang localized to left, and the rest are spilt btwn right and bilateral localization
45
Q

Bilingual localization

A
  • both languages are localized to the same hemisphere

- lesions can preserve one lang but damage the other!

46
Q

Right hemisphere (nondominant) and language

A
  • has simpler language capabilities

- can understand printed and spoken words, understand verbal descriptions of objects, write 3-4 words, and read braille

47
Q

Damage to the right hemisphere?

A
  1. can cause loss of tonal/emotional content of language
  2. neglect of tactile and space on left side
  3. difficulty with visual discrimination –> face discrimination & recognition of expression of emotion
  4. difficulty w/ spatial/geometric orientation
  5. apraxia for left mvmnts
  6. cheerful/elated mood if its a right pre-frontal lesion
48
Q

Split brain experiments

A
  • hemisphere was surgically isolated
  • stimuli presented to the rt visual field only = pt names the object
  • simuli presented to the left feild only = pt says nothing –> but when a pencil is placed in the left hand the pt will draw the object but doesnt know why! –> pt is not conciously aware of info in the rt hemisphere
  • *so: speech is localized to the left hemisphere & info in the rt hemisphere must be transfere to the left tot speak about it!
49
Q

Damage to left hemisphere?

A
  1. Broca’s aphasia
  2. Wernicke’s apahsia
  3. depressed mood if its is a left pre-frontal lesion
50
Q

Motor association cortex

A
  • anterior to precentral gyrus:
    1. ventrolateral premotor cortex
    2. supplementary motor area (SMA)
  • mvmnts are learned and stored in motor areas –> lesions will impair access to the stored info!
51
Q

Premotor cortex

A
  • important in mvmnts triggered by sensory events or requiring sensory GUIDANCE
  • *lesions = apraxia and deficits in visually guided mvmnts (hand-eye coordination)
52
Q

Supplementary motor area (SMA)

A
  • involved in planning of mvmnts
  • active when mentally rehearsing
  • stimulation can cause bilaterally mvmnts
  • *lesions = apraxia & disrupt bimanual coordination
53
Q

Dorsolateral area of PRF

A
  • important in long-term planning, problem solving, and working memory
  • deals with info thats logical in nature
54
Q

Ventromedial area of PFC

A
  • for cortical control of emotional (limbic) centers

- deals with info that is emotional in nature

55
Q

What are the 5 areas involved in the limbic system?

A

Areas in the frontal, parietal, and temporal lobes:

  1. subcallosal
  2. cingulate gyrus
  3. parahippocampal
  4. amygdala**
  5. hippocampus**
    * *most important areas
56
Q

Hippocampus

A
  • in the temporal lobe
  • necessary to convert short-term memory into long-term memory
  • controls the process of memory conversion rather than storing the memory itself
  • *lesions = severe memory deficits –> cant remember anything past the lesion
57
Q

Amygdala

A
  • in the temporal lobe
  • controls emotional responses involving fear, anxiety, & anger
  • influences our ability to associate stimuli w/ their negative consequences
  • *lesions = fearlessness
58
Q

Brainstem cause of coma & how to test brainstem fctns

A
  • can be due to uncal herniation which causes damage to the brainstem
  • if important respiratory or cardiovascular control centers are damages = death!
  • brainstem fctn can be assessed in a comatose pt via testing brainstem reflexes

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