CNS 5 Flashcards

1
Q

Cerebellum (“Little Brain”)

Inputs:

A

1) sensory input form spinal cord

2) motor commands from cerebral cortex

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2
Q

Functional divisions:

Cerebellum

A
  1. Vermis : posture, neck and axial (Trunk) musculature
  2. Intermediate zone: locomotion
  3. Lateral zone: coordinating complex, skilled movements of arms, hands & fingers
  4. Flocculonodular lobe: balance
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3
Q

Ba sal Ganglia (Extrapyramidal System)

• Anatomy:

A
  • Large, deep cerebral nuclei
    1. Involved in initiating movement
    2. Involved in suppressing activity of muscles that would resist the intended movement
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4
Q

Basal Ganglia (Extrapyramidal System)

Dysfunction:

A

either:

  • poverty of movement (bradykinesia (slow movement) and rigidity and tremor)
    Parkinson’s disease (PD)
  • Involuntary movement:
    eg. Chorea, Tourette’s syndrome, hemiballismus
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5
Q

Brainstem

Function:

A
  1. Control of respiratory & cardiovascular musculature
  2. Control of transmission in sensory, motor, reflex & pain pathways
  3. Initiation of locomotion (Midbrain locomotor area (MLA))
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6
Q

Sleepy states

A
  • alert wakefulness
  • relaxed wakefulness
  • relaxed drowsiness

NREM (slow wave) sleep

  • stage N1
  • stage N2
  • stage N3

REM (periodoxical) sleep

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7
Q

El ectroencephalogram (EEG)

A

• Vo l t a g e f l u c t u a t i o n s r e c o r d e d b e t w e e n p a i r s o f e l e c t r o d e s o n t h e s c a l p

• Made up of summed, synchronous, post-synaptic potentials of many
neurons

• Waveforms vary with behavioural states: attention, arousal, sleep,
dreaming

  • Abnormal in epilepsy and over brain tumours
  • Used to verify brain death ie. To allow organs to be removed
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8
Q

Brainstem Control of Sleep,
Wakefulness, Arousal

• Controlled by the reticular activating system (RAS):

A

nuclei in brainstem and hypothalamus

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9
Q

Br ainstem Control of Sleep,
Wakefulness, Arousal

• Controlled by the reticular activating system (RAS): nuclei in brainstem and hypothalamus

A
  1. Visual and other sensory inputs activate RAS neurons
  2. Brainstem RAS supplies the monoamines norepinephrine (Noradrenaline), serotonin and histamine to hypothalamus and other brain areas
  3. Hypothalamus supplies orexins (Neuropeptide hormones) to thalamus and cortex, maintaining wakefulness
  4. Suprachiasmatic nucleus activates orexin-producing neurons at first light in the morning, promoting wakefulness. It also secretes melatonin at dusk. These mechanisms set the “circadian rhythm”.
  5. “Sleep centre” in pre-optic nucleus of hypothalamus delivers GABA-ergic inhibition of RAS, reducing orexin levels
  6. RAS is inhibited by GABA agonist sedatives like Valium and Xanax, by anti-histamines like Benadryl, by barbiturates like Nembutal and other anaesthetics
  7. Small lesions in RAS can produce coma
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10
Q

Conscious Experiences

A

• Awar enes s of pas s age of time, exter nal s ens or y inputs and internal states such as fatigue, thirst, happiness, memories, reasoning, ideas

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11
Q

Two main aspect of conscious experiences

A

Selective attention and conscious perception

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12
Q

Selective Attention

A
  • Attention shifts from one focus or attractor to another
  • Coincident attractors ( eg. Visual and auditory inputs coming from the same direction) are more likely to trigger a shift than separate attractors
  • CNS areas implicated in triggering shifts: Thalamus and locus ceruleus in brainstem RAS
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13
Q

Conscious Perception

• Theory:

A

there isn’t a single cluster of
“consciousness neurons”. Rather, specific sets of neurons in widely separated brain areas temporarily function together:
“Temporary Sets”.

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14
Q

Destruction of specific brain areas can

abolish selective parts of

A

consciously perceived inputs ie. Hemi-neglect after a stroke affecting the parietal lobe: the person is unaware of half of their visual field.

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15
Q

Primary motivated behavior:

A

directly related to homeostasis eg.

Maintaining water balance, nutrition, body temperature.

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16
Q

Secondary motivated behavior:

A

that which results in pleasure. Can be

disadvantageous eg. Over-eating, taking recreational drugs.

17
Q

Emotion

A
  • Internal attitudes toward events and the environment ( eg. Being happy, sad, fearful)
  • External responses (emotional behaviour)
18
Q

Emotion: Neuroanatomical Mechanisms

• Theory:

A

there is no single cluster of neurons that generate all emotions.

19
Q

Electrical stimulation in lateral hypothalamus elicits

A

Rage

20
Q

Lesions of amygdala results in an absence of

A

Fear

21
Q

Serotonin re-uptake inhibitors counteract

A

Depression by main ting levels of serotonin and norepinephrine at
synapses. They may thereby enhance
neurogenesis eg. In the hypothalamus

22
Q

Working Memory (Shortterm Memory)

A

– Episodic: recent events, places

– Visuo-spatial: recent sights, locations – Phonological: recent words, sounds

23
Q

Long-term Memory

A

Declarative (Involves consciousness)

  • Semantic (Facts: ice is cold, fire is hot)
  • Episodic (Personal experiences)

Procedural (Motor, mainly sub-conscious)

  • Stimulus-response behaviours
  • Motor skills: playing piano, skiing…
24
Q

Transfer from s.t.m. to l.t.m. (Laying down, or consolidation of the memory trace) probably occurs in

A

temporal lobes

25
Q

“Reward” system involving _________ is also implicated

A

hypothalamus

26
Q

The caudate nucleus is implicated in consolidating stimulus-response
associations taught during

A

operant conditioning and in solving sequence tasks

27
Q

Amnesia: retrograde & anterograde loss of s.t.m.

A

– Concussion: measured by type and duration of amnesia

– Retrograde → loss of memory of events prior to the injury

– Anterograde → loss of memory of event after the injury

28
Q

Korsakoff’s Syndrome

A

(Damage to hippocampus) complete

anterograde amnesia

29
Q

Alzheimer’s disease:

A

degeneration of memory-holding neurons, perhaps due to amyloid precursor proteins causing “excitotoxicity”
ie. Neurons are damaged by over-excitation