Neuro case studies Flashcards

1
Q

what is the function of the frontal lobe?

A

executive function (e.g. attention, inhibition), personality, voluntary movement, speech / language
production

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2
Q

what is the function of the temporal lobe?

A

auditory processing, lang comprehension, visual object recog, links with limbic system

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3
Q

what is the function of the parietal lobe?

A

somatosensory cortex, spatial orientation

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4
Q

what is the function of the occipital lobe?

A

visual processing

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5
Q

what is the function of the cerebellum?

A

coordination of movement (incl eyes), balance

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6
Q

What connects the brain’s hemispheres?

A

The corpus callosum.

essential re-integration of info transferred between R/L hem

Grey matter – cortex

White matter – fibres, myelin sheath insulates axon

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7
Q

What is the role of grey and white matter?

A

Grey matter: Cortex; contains neuron cell bodies.
White matter: myelin sheath insulates axons that transmit signals.

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8
Q

What role does the hippocampus play?

A

Hippocampus
- consolidation of new info - memory

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9
Q

What role does the amygdala play?

A

controls emotional responses

  • assess threats
  • fear – part of fight-or-flight
  • physiological response – avoid danger
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10
Q

What is neural plasticity?

A

Intact part of brain takes over function
of damaged area

Brain does not physically change
shape!

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11
Q

what happened to Phineas Gage in 1848?

A

tampering iron shot through cheek bone and frontal lobe but he physically recovered, though with significant personality changes.

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12
Q

What were the psychological impacts on Gage?

A

disinhibition, impulsivity, hostility, and unpredictability.
Evidence of frontal lobe function in personality and executive processes.
- good psych recovery - behaviours exaggerated

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13
Q

Evidence from neuroimaging

A

-rep of damage (Damasio et al, 1994) - sim trajectory of entry - compared scans - 27 normal brains matched size

  • multiple frontal regions damaged - pg atypical beahv explained
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14
Q

what about Individual anatomical differences?

A

no systematic assessment of pg psych defects

but - supports understanding of function of frontal brain regions

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15
Q

How did connectivity studies (e.g., Van Hom et al., 2012) refine our understanding of Gage’s injury?

A

MRI RH males [25-36] - sim to find extent of GM+WM damage

Damage - localised to LFC

Affected other brain areas - contributor to PG behave change

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16
Q

What led to H.M.’s surgery, and what was done?

A

severe epilepsy
surgeons removed large portions of:
- both medial temporal lobes
- most of his hippocampus.

17
Q

What were the effects of the surgery on H.M.’s memory?

A

Deficits: Severe anterograde amnesia (can’t form new explicit memories) and moderate retrograde amnesia (some loss of past memories).

Intact abilities: Procedural memory, short-term working memory, and intellect.

18
Q

What tasks could H.M. still perform post-surgery?

A

Learn motor skills (e.g., mirror tracing) without remembering learning them. [Corkin, 2002]

Recall information temporarily, such as a phone number while dialing it.

19
Q

What caused Clive Wearing’s memory impairment?

A

Herpesviral encephalitis damaged his hippocampus, resulting in profound amnesia.

20
Q

How did T.T.’s hippocampal damage affect his spatial memory?

A

Could navigate main roads but unable to find way on unfamiliar routes

Shows the hippocampus’s role in detailed spatial memory.

21
Q

What did H.M., Clive Wearing, and T.T. teach us about the hippocampus?

A

Essential for long-term memory consolidation.

Not as critical for implicit and procedural memory.

Crucial for spatial navigation.

22
Q

What caused D.F.’s visual impairment?

A

Carbon monoxide poisoning damaged her lateral occipital cortex, causing visual form agnosia

23
Q

What abilities were preserved in D.F.?

A

Impairment: Couldn’t recognize objects.

Preserved: Could act upon objects accurately.

24
Q

What does the two-visual streams model explain?

A

Ventral stream: Object perception and recognition.

Dorsal stream: Real-time visual control for movements.

25
What caused S.M.’s inability to feel fear?
Bilateral destruction of her amygdala due to Urbach-Wiethe disease.
26
How did S.M.’s condition affect her behavior?
No fear in dangerous situations. Disinhibited social behaviors, such as reduced awareness of personal space.
27
What did Feinstein et al. (2011) find about S.M.’s fear responses?
She showed little to no fear in response to frightening film clips. She found them exciting or entertaining instead.
28
What did Adolphs et al. (2005) discover about S.M.’s gaze?
She made fewer fixations to eyes when viewing faces but improved fear recognition when instructed to focus on eyes.
29
What distinguished Einstein’s brain from others?
Thicker, denser corpus callosum. Larger parietal lobes linked to mathematical and spatial abilities.
30
What does the corpus callosum contribute to intelligence?
It facilitates efficient communication and integration of information between hemispheres.