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PSY2003 SEMESTER 1 > PSY2003 SEMESTER 1 - WEEK 8 > Flashcards

PSY2003 SEMESTER 1 - WEEK 8 Flashcards

1
Q

what command do motor cortex issue based on

A

based on integration of sensory input via upper motor neuron

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2
Q

when motor cortex sends commands, where are copies sent, and where do these commands eventually reach

A

send copy to basal ganglia, cerebellum which feedbacks to cortex via thalamus
reaches lower motor neuron so is continually modulated by basal ganglia and cerebellum

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3
Q

where does the upper motor neuron begin

A

motor cortex

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4
Q

what are general symptoms of motor cortex damage?

A

impaired movement
poor high-level coordination
weakness of movement

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5
Q

what is cerebral palsy caused by

A

damage to motor control brain structures, like motor cortex

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6
Q

when does cerebral palsy originate

A

pre/perinatally, with 50% cases premature births
most common movement disorder in children, 2/1000 births

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7
Q

name general symptoms of cerebral palsy

A

stiffness and weakness of muscles
poor coordination
affects upper motor neurons

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8
Q

what type of motor neurons does cerebral palsy affect

A

upper motor neuron

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9
Q

what causes a stroke

A

interruption of blood supply to cortex, upper motor neuron affected, symptom depending on extent and location of damage
haemorrhage or ischaemia

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10
Q

what causes cerebral haemorrhage stroke

A

aneurism and blood toxic to our neural tissue

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11
Q

how can cerebral haemorrhage stroke be prevented

A

clip aneurism before rupture
maintain low BP, avoid strenuous activities

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12
Q

what causes cerebral ischaemia stroke

A

interruption of blood supply to part of brain due to blockage of blood vessel, by specific plugs (thrombus, emboli) or cardivascular disease (atherosclerosis)
lack of O2 and glucose cause excitotoxicity, neuronal cell death

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13
Q

what is goal of treatment for cerebral ischaemia strokes

A

rescue penumbra, via reopening blocked blood vessel

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14
Q

why is fine motor control issues a prominent symptom of motor cortical damage

A

due to homonculus (large representations for these activities) mean unlikely to be missed by damage and requires coordination across multiple subregions
in a stroke, positioning of middle cerebral artery means most likely to be damaged

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15
Q

what is upper motor neuron syndrome

A

collection of symptoms resulting from damage to upper motor neuron (in cortex where originate, or in pathway - spinal cord)

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16
Q

what does upper motor neuron syndrome cause

A

lack of voluntary control of muscles via lower motor neurons
lacking regulation of lower motor neurons/spinal reflex circuits

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17
Q

name test of upper motor neuron syndrome

A

Babinksi reflex

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18
Q

what babinski reflex indicates a problem

A

touch from heel, curving round to toes
toes curling under = normal
toes stretch out = issue, “positive response” needing further investigation
(baby shows positive response, is normal)

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19
Q

what is a difficulty in seperating impact of brain damage and cognitive/motor function

A

individual with cerebral palsy may be misdiagnosed with cognitive impairment = actually just issue with their speech

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20
Q

what are basal ganglia

A

group of nuclei lying deep within cerebral hemispheres, role in motor control not fully understood, implicated for many disorders

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21
Q

at rest, where do basal ganglia send inhibition and where do they reduce excitation

A

via thalamus, reduce excitation in motor cortex

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22
Q

when excited, what should happen to basal ganglia (via thalamus)

A

should be transiently inhibited then disinhibited by thalamus, causing increasing excitation in motor cortex

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23
Q

what disorders can basal ganglia be implicated within

A

parkinsons, huntingdons, tourettes

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24
Q

how common is parkinsons

A

2nd most common NDD (after AD)
50% more male>female

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25
Q

what % of PD is genetic

A

10% of cases due to mutation of one of several genes

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26
Q

name PD symptom

A
  1. paucity of spontaneous movement
  2. bradykinesia
  3. akinesia
  4. increases muscle tone (rigidity)
  5. resting tremor, pill rolling, 4-5Hz but not when doing purposeful movements
  6. shuffling gait, flexed posture, poor balance
  7. mask expression
27
Q

outline dopamine degeration in PD, and why this means that increasing dopamine, via L-DOPA, isn’t effective

A

due to degeneration of nigrostriatal neurons, so increasing dopamine via drug isn’t effective as too few functioning cells left to release dopamine appropriately into striatum
dopamine cannot cross BBB

28
Q

in DBS for PD, what areas are electrically stimulated, and what does this aim to do?

A

electrically stimulates specific basal ganglia structures to counteract excessive inhibitory output

29
Q

give limitations of DBS as treatment for PD

A

side effect
doesn’t deal with non-motor symptom (sleep disrupt, digestion, affective symptom) and can make non-motor symptom worse

30
Q

name some non-motor symptoms in PD

A

disruptions to sleep
digestion
affective (depression, anxiety)
constipation
fatigue
pain
orthostatic hypotension
urinary symptom
hallucination
dementia

31
Q

instead of the dopamine hypothesis of PD what may be role of Alpha-synuclein, lewy bodies

A

a-synuclein misfolds and aggregates into lewy bodies throughout brain
dopamine neurons in substantia nigra are particularly vulnerable = explanation account for non-motor symptom
no current treatment (but a developing research area)

32
Q

name challenges of NMS (non-motor symptom) in PD

A

manifest years before motor and overlap with others, harder with diagnosis

33
Q

what are cognitive impairments (NMD PD symptoms) characterised by

A

impaired attention, memory, EF, visuospatial function, affective change, hallucinations, apathy

34
Q

outline prevalence of cognitive impairment (NMD PD symptoms)

A

PD are 2-6x more likely to dev dementia
women older than men at PD onset, shorter disease duration

35
Q

what kind of hallucinations occur (NMD PD symptoms)

A

minor= sense of presence, passage, visual
key milestone in disease progression
rare to have tactile, olfactory and somatic

36
Q

outline prevalence of hallucination (NMD PD symptoms)

A

4-5x more likely than healthy
OA and women more vulnerable to meds, so a side-effect

37
Q

what are hallucinations in PD associated with

A

increased chance of going into nursing homes, mortality

38
Q

what is depression in PD associated with

A

use of antidepressants, cog impairment, disease durations, motor fluctuation, female, disability, age

39
Q

outline prevalence of depression (NMD PD symptoms)

A

x2 likely for depression than healthy, more likely for females

40
Q

how common is apathy in PD

A

40%

41
Q

what is apathy associated with in PD

A

increased caregiver burden and commonly coexists with depression

42
Q

what are risk factors of excessive daytime sleepiness (NMD PD symptoms)

A

male, using dopamine agonist, insomnia, disability, cog impairment, depression

43
Q

what is most common NMS

A

insomnia

44
Q

what are risk factors for insomnia (NMD PD symptoms)

A

depression, disease duration, female, dopamine agonists, cog impairments

45
Q

what are risk factors for impulse control disorders (NMD PD symptoms)

A

dopamine agonist use, male

46
Q

what types of impulse control disorders are common in men/women (NMD PD symptoms)

A

male = excessive sexual behaviour
women = binge eating and compulsive bullying

47
Q

why can it be useful to study genetic causes of primarily non-genetic diseases

A

most are sporadic (AD, PD, epilepsy, MND, stroke) but 1-10% genetic
focus on gene therapy development, help to develop treatment for all form of diseases, not just genetic

48
Q

where does cerebellum have projections (neurons)

A

not direct to lower motor neuron (like basal ganglia), but modulates activity of upper motor neurons

49
Q

how big is cerebellum, how many CNS neurons does it have

A

1/2 total number of CNS neurons
10% of brain total weight
project to almost all UMNs

50
Q

what can damage to cerebellum result in

A

impaired movement (ataxia)
less fluid voluntary movement (mechanical, slow, robotic)
intention tremor
dysarthria

51
Q

what are 2 classifications of ataxia

A
  1. disturbed posture/gait
  2. decomposition of movement = stages of movement initiation when muscles need to relax for movements to be formed
52
Q

what is dysarthria

A

disruption of fine control of speech, slurring

53
Q

what is ataxia, definition

A

collection of disorders, undefined by symptoms
loss of voluntary coordination of muscles (a neurological finding, but not a disease)

54
Q

what are types of ataxia (3 types of focus)

A
  1. focusing on symptoms type (cerebellar, sensory, vestibular)
  2. focusing on causes types (acquired, hereditary, late onset cerebellar dysfunction)
  3. focusing on more detailed diagnosis (Freidrich’s ataxia, ataxia-telangiectasia, spinocerebellar ataxia, episodic ataxia, vitamin-E deficiency related)
55
Q

name some ataxia type when focusing on types of symptom

A

cerebellar, sensory vestibular

56
Q

name some types of ataxia when focusing on type of cause

A

acquired, hereditary, late onset cerebellar dysfunction

57
Q

name some issues that ataxia may cause

A

oculmotor, speech, swallowing, tremor, balance, coordination, cardiac, fine motor skill, gait abnormality

58
Q

outline MND

A

progression, incurable and degenerative with 10% genetic component but 90% being unknown
2.5yr normal life expectancies

59
Q

how common in MND

A

more in men
2.6/100,000 women per year
3.9 men
risks strongly modulated by age
5,000 currently in UK

60
Q

what can MND be used interchangeably with

A

ALS (actually a subtype)

61
Q

name the 2 types of MND (difference between MND, ALS)

A

distinction based on effects on upper/lower MN
ALS affect both

62
Q

name some general symptoms of MND

A

altered cognitive function, usually mild
communicative ability, affective change
death normally impaired respiratory function

63
Q

no current treatments for MND but name some latest research

A

biomarkers of early diagnosis, risk factors
novel neuroprotective drugs and gene therapy
drug to slow progression and clinical/tech intervention to improve lives

64
Q

outline an MND Sheffield research breakthrough 2022- Prof Pamela Shaw

A

SOD1 gene, mutation causing genetic form
new drug tofersen to prevent SOD1 being produced, with CSF biomarker showing early effect but benefit at 12 months

PSY2003 SEMESTER 1 (8 decks)

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