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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
what % of PD is genetic
10% of cases due to mutation of one of several genes
26
name PD symptom
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
outline dopamine degeration in PD, and why this means that increasing dopamine, via L-DOPA, isn't effective
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
in DBS for PD, what areas are electrically stimulated, and what does this aim to do?
electrically stimulates specific basal ganglia structures to counteract excessive inhibitory output
29
give limitations of DBS as treatment for PD
side effect doesn't deal with non-motor symptom (sleep disrupt, digestion, affective symptom) and can make non-motor symptom worse
30
name some non-motor symptoms in PD
disruptions to sleep digestion affective (depression, anxiety) constipation fatigue pain orthostatic hypotension urinary symptom hallucination dementia
31
instead of the dopamine hypothesis of PD what may be role of Alpha-synuclein, lewy bodies
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
name challenges of NMS (non-motor symptom) in PD
manifest years before motor and overlap with others, harder with diagnosis
33
what are cognitive impairments (NMD PD symptoms) characterised by
impaired attention, memory, EF, visuospatial function, affective change, hallucinations, apathy
34
outline prevalence of cognitive impairment (NMD PD symptoms)
PD are 2-6x more likely to dev dementia women older than men at PD onset, shorter disease duration
35
what kind of hallucinations occur (NMD PD symptoms)
minor= sense of presence, passage, visual key milestone in disease progression rare to have tactile, olfactory and somatic
36
outline prevalence of hallucination (NMD PD symptoms)
4-5x more likely than healthy OA and women more vulnerable to meds, so a side-effect
37
what are hallucinations in PD associated with
increased chance of going into nursing homes, mortality
38
what is depression in PD associated with
use of antidepressants, cog impairment, disease durations, motor fluctuation, female, disability, age
39
outline prevalence of depression (NMD PD symptoms)
x2 likely for depression than healthy, more likely for females
40
how common is apathy in PD
40%
41
what is apathy associated with in PD
increased caregiver burden and commonly coexists with depression
42
what are risk factors of excessive daytime sleepiness (NMD PD symptoms)
male, using dopamine agonist, insomnia, disability, cog impairment, depression
43
what is most common NMS
insomnia
44
what are risk factors for insomnia (NMD PD symptoms)
depression, disease duration, female, dopamine agonists, cog impairments
45
what are risk factors for impulse control disorders (NMD PD symptoms)
dopamine agonist use, male
46
what types of impulse control disorders are common in men/women (NMD PD symptoms)
male = excessive sexual behaviour women = binge eating and compulsive bullying
47
why can it be useful to study genetic causes of primarily non-genetic diseases
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
where does cerebellum have projections (neurons)
not direct to lower motor neuron (like basal ganglia), but modulates activity of upper motor neurons
49
how big is cerebellum, how many CNS neurons does it have
1/2 total number of CNS neurons 10% of brain total weight project to almost all UMNs
50
what can damage to cerebellum result in
impaired movement (ataxia) less fluid voluntary movement (mechanical, slow, robotic) intention tremor dysarthria
51
what are 2 classifications of ataxia
1. disturbed posture/gait 2. decomposition of movement = stages of movement initiation when muscles need to relax for movements to be formed
52
what is dysarthria
disruption of fine control of speech, slurring
53
what is ataxia, definition
collection of disorders, undefined by symptoms loss of voluntary coordination of muscles (a neurological finding, but not a disease)
54
what are types of ataxia (3 types of focus)
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
name some ataxia type when focusing on types of symptom
cerebellar, sensory vestibular
56
name some types of ataxia when focusing on type of cause
acquired, hereditary, late onset cerebellar dysfunction
57
name some issues that ataxia may cause
oculmotor, speech, swallowing, tremor, balance, coordination, cardiac, fine motor skill, gait abnormality
58
outline MND
progression, incurable and degenerative with 10% genetic component but 90% being unknown 2.5yr normal life expectancies
59
how common in MND
more in men 2.6/100,000 women per year 3.9 men risks strongly modulated by age 5,000 currently in UK
60
what can MND be used interchangeably with
ALS (actually a subtype)
61
name the 2 types of MND (difference between MND, ALS)
distinction based on effects on upper/lower MN ALS affect both
62
name some general symptoms of MND
altered cognitive function, usually mild communicative ability, affective change death normally impaired respiratory function
63
no current treatments for MND but name some latest research
biomarkers of early diagnosis, risk factors novel neuroprotective drugs and gene therapy drug to slow progression and clinical/tech intervention to improve lives
64
outline an MND Sheffield research breakthrough 2022- Prof Pamela Shaw
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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