PSY2003 SEMESTER 1 - WEEK 8 Flashcards
what command do motor cortex issue based on
based on integration of sensory input via upper motor neuron
when motor cortex sends commands, where are copies sent, and where do these commands eventually reach
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
where does the upper motor neuron begin
motor cortex
what are general symptoms of motor cortex damage?
impaired movement
poor high-level coordination
weakness of movement
what is cerebral palsy caused by
damage to motor control brain structures, like motor cortex
when does cerebral palsy originate
pre/perinatally, with 50% cases premature births
most common movement disorder in children, 2/1000 births
name general symptoms of cerebral palsy
stiffness and weakness of muscles
poor coordination
affects upper motor neurons
what type of motor neurons does cerebral palsy affect
upper motor neuron
what causes a stroke
interruption of blood supply to cortex, upper motor neuron affected, symptom depending on extent and location of damage
haemorrhage or ischaemia
what causes cerebral haemorrhage stroke
aneurism and blood toxic to our neural tissue
how can cerebral haemorrhage stroke be prevented
clip aneurism before rupture
maintain low BP, avoid strenuous activities
what causes cerebral ischaemia stroke
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
what is goal of treatment for cerebral ischaemia strokes
rescue penumbra, via reopening blocked blood vessel
why is fine motor control issues a prominent symptom of motor cortical damage
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
what is upper motor neuron syndrome
collection of symptoms resulting from damage to upper motor neuron (in cortex where originate, or in pathway - spinal cord)
what does upper motor neuron syndrome cause
lack of voluntary control of muscles via lower motor neurons
lacking regulation of lower motor neurons/spinal reflex circuits
name test of upper motor neuron syndrome
Babinksi reflex
what babinski reflex indicates a problem
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)
what is a difficulty in seperating impact of brain damage and cognitive/motor function
individual with cerebral palsy may be misdiagnosed with cognitive impairment = actually just issue with their speech
what are basal ganglia
group of nuclei lying deep within cerebral hemispheres, role in motor control not fully understood, implicated for many disorders
at rest, where do basal ganglia send inhibition and where do they reduce excitation
via thalamus, reduce excitation in motor cortex
when excited, what should happen to basal ganglia (via thalamus)
should be transiently inhibited then disinhibited by thalamus, causing increasing excitation in motor cortex
what disorders can basal ganglia be implicated within
parkinsons, huntingdons, tourettes
how common is parkinsons
2nd most common NDD (after AD)
50% more male>female
what % of PD is genetic
10% of cases due to mutation of one of several genes
name PD symptom
- paucity of spontaneous movement
- bradykinesia
- akinesia
- increases muscle tone (rigidity)
- resting tremor, pill rolling, 4-5Hz but not when doing purposeful movements
- shuffling gait, flexed posture, poor balance
- mask expression
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
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
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
name some non-motor symptoms in PD
disruptions to sleep
digestion
affective (depression, anxiety)
constipation
fatigue
pain
orthostatic hypotension
urinary symptom
hallucination
dementia
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)
name challenges of NMS (non-motor symptom) in PD
manifest years before motor and overlap with others, harder with diagnosis
what are cognitive impairments (NMD PD symptoms) characterised by
impaired attention, memory, EF, visuospatial function, affective change, hallucinations, apathy
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
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
outline prevalence of hallucination (NMD PD symptoms)
4-5x more likely than healthy
OA and women more vulnerable to meds, so a side-effect
what are hallucinations in PD associated with
increased chance of going into nursing homes, mortality
what is depression in PD associated with
use of antidepressants, cog impairment, disease durations, motor fluctuation, female, disability, age
outline prevalence of depression (NMD PD symptoms)
x2 likely for depression than healthy, more likely for females
how common is apathy in PD
40%
what is apathy associated with in PD
increased caregiver burden and commonly coexists with depression
what are risk factors of excessive daytime sleepiness (NMD PD symptoms)
male, using dopamine agonist, insomnia, disability, cog impairment, depression
what is most common NMS
insomnia
what are risk factors for insomnia (NMD PD symptoms)
depression, disease duration, female, dopamine agonists, cog impairments
what are risk factors for impulse control disorders (NMD PD symptoms)
dopamine agonist use, male
what types of impulse control disorders are common in men/women (NMD PD symptoms)
male = excessive sexual behaviour
women = binge eating and compulsive bullying
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
where does cerebellum have projections (neurons)
not direct to lower motor neuron (like basal ganglia), but modulates activity of upper motor neurons
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
what can damage to cerebellum result in
impaired movement (ataxia)
less fluid voluntary movement (mechanical, slow, robotic)
intention tremor
dysarthria
what are 2 classifications of ataxia
- disturbed posture/gait
- decomposition of movement = stages of movement initiation when muscles need to relax for movements to be formed
what is dysarthria
disruption of fine control of speech, slurring
what is ataxia, definition
collection of disorders, undefined by symptoms
loss of voluntary coordination of muscles (a neurological finding, but not a disease)
what are types of ataxia (3 types of focus)
- focusing on symptoms type (cerebellar, sensory, vestibular)
- focusing on causes types (acquired, hereditary, late onset cerebellar dysfunction)
- focusing on more detailed diagnosis (Freidrich’s ataxia, ataxia-telangiectasia, spinocerebellar ataxia, episodic ataxia, vitamin-E deficiency related)
name some ataxia type when focusing on types of symptom
cerebellar, sensory vestibular
name some types of ataxia when focusing on type of cause
acquired, hereditary, late onset cerebellar dysfunction
name some issues that ataxia may cause
oculmotor, speech, swallowing, tremor, balance, coordination, cardiac, fine motor skill, gait abnormality
outline MND
progression, incurable and degenerative with 10% genetic component but 90% being unknown
2.5yr normal life expectancies
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
what can MND be used interchangeably with
ALS (actually a subtype)
name the 2 types of MND (difference between MND, ALS)
distinction based on effects on upper/lower MN
ALS affect both
name some general symptoms of MND
altered cognitive function, usually mild
communicative ability, affective change
death normally impaired respiratory function
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
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
