Neuro case studies Flashcards

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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
Q

What caused S.M.’s inability to feel fear?

A

Bilateral destruction of her amygdala due to Urbach-Wiethe disease.

26
Q

How did S.M.’s condition affect her behavior?

A

No fear in dangerous situations.

Disinhibited social behaviors, such as reduced awareness of personal space.

27
Q

What did Feinstein et al. (2011) find about S.M.’s fear responses?

A

She showed little to no fear in response to frightening film clips.
She found them exciting or entertaining instead.

28
Q

What did Adolphs et al. (2005) discover about S.M.’s gaze?

A

She made fewer fixations to eyes when viewing faces but improved fear recognition when instructed to focus on eyes.

29
Q

What distinguished Einstein’s brain from others?

A

Thicker, denser corpus callosum.

Larger parietal lobes linked to mathematical and spatial abilities.

30
Q

What does the corpus callosum contribute to intelligence?

A

It facilitates efficient communication and integration of information between hemispheres.