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YEAR 2 Semester 1👩🏼‍🎓 > Neuro + Clin🧠 > Flashcards

Neuro + Clin🧠 Flashcards

1
Q

Symptoms of schizophrenia

Positive and negative

A

Positive- (excess of typical function)
Delusions, inappropriate affect, hallucinations, incoherent thoughts

Negative (loss of typical function)
Affective flattening, avolition, catatonia, lack of interest

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2
Q

R.D Laing and Freud on Schizophrenia

A

R.D Laing- label from the majority or being different. Family difficulties lead to Schizophrenia but had no control condition

Freud- paranoid delusions from repressed homosexual urges

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3
Q

Heritability of schizophrenia

A

45% MZ and 10% DZ

some heritability but clearly environmental effects

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4
Q

Environmental causes of Schizophrenia

A

Infections, autoimmune reactions, traumatic injury

Stress- exposure to stressors and severity of stress related to episodes
Bullying- more severe and frequent childhood bullying
BUT own recollections may be biased, psychosis may affect this, retrospective and subjective

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5
Q

Pharmacological treatments for Schizophrenia

A

Chlorpromazine-agonist, binds to post synaptic dopamine receptors, stop dopamine getting to receptors
Risperine- depletes dopamine by breaking vesicles

2-3 weeks to work, Parkinson like symptoms emerge (lack of dopamine)

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6
Q

Dopamine

A

In substantia nigra, ventral tegmental area and project up to striatum

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7
Q

Evidence for Dopamine hypothesis

A

Drugs increasing dopaminergic neurone e.g. Cocaine transmission can produce symptoms of Schizophrenia

Drugs that reduce dopaminergic neurone transmission reduce psychotic symptoms

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8
Q

Efficacy of antipsychotics

And the drugs with their potency

A

More effective if drug has greater potency so binds to more dopamine

HOWEVER Haliperidol is very potent but doesn’t bind to dopamine receptors (multiple receptors) When only D2 receptors are measured: haliperidol appears potent and with good binding
Chlorpromazine has average potency and binding

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9
Q

Dopamine receptors types- D1 and D2

A

D1- positively coupled to adenlyate cyclase (helps send messages inside the cell)

D2-good at dopamine binding
Negatively coupled to adenlyate cyclase

Can not explain why effects take weeks to emerge or why only works on positive symptoms

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10
Q

Dopamine receptors structure

A

Metabolic structures, cross the cell membrane many times

When drug binds to receptors, G proteins are released to cell

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11
Q

Dopamine receptor families

A

D1 like (D1 and D5)

D2 like (D2, D3 and D4) ANTIPSYCHOTICS bind here
newer drugs D4
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12
Q

Study showing more dopamine receptors in schizophrenics

A

Receptor density measured by making dopamine agonist radioactive, use PET compare to control
Dopamine binds to receptors (level of dopamine) chemical dye binds to remaining receptors to measure unoccupied receptors
Deplete dopamine with risperine to show up unoccupied receptors
SZ has more D2 receptors so more dopamine,

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13
Q

Link between recovery and amount of unoccupied dopamine receptors

A

With more D2 receptors to begin with, respond not as well to treatment (less change in positive symptoms after 6 week treatment)

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14
Q

Schizophrenia copy number variants

A

Mutations in genes that copy abnormal DNA (deletion or duplication)
Found to be associated with Schizophrenia
Mutations are rare, failure to replicate findings

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15
Q

The schizophrenic brain

A

Apparent at first episode so may be causal, develops through lifetime continually

Enlarged ventricles, reduced grey matter in prefrontal cortex (less executive function), temporal cortex abnormalities e.g. in temporal cortex, hippocampus (affects memory) and basal ganglia

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16
Q

Eye tracking in Schizophrenia

A

Difficultly making smooth pursuit eye movements, jerky (saccadic)
Can be a genetic marker

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17
Q

Cognitive deficits in Schizophrenia

A

Cognitive defects- Reduced orientation
Cognitive biases- Over confrontational interactions
Attentional biases-Over attend to negative stimuli
Reasoning biases- Jump to conclusions with little evidence
Interpretational biases-hear voices, cognitive intrusions
Attributional biases- attribute negative life events to external causes, stable

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18
Q

Seligman’s attributional model SZ

A

EXTERNAL, GLOBAL, STABLE
=delusions, others causing something sinister

Theory of mind thought to be missing in Schizophrenics, may think others are hiding intentions, hostile

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19
Q

Theory of mind in schizophrenia

A

Thought to be distorted

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20
Q

The family and Schizophrenia

A

Double bind and paradoxical communication- contradictory messages from family, feel conflicted and may withdraw
Communication deviance-difficult to follow and focus the topic
Expressed emotion-overly harsh emotions, criticism and hostility
Correlated with relapse rates

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21
Q

Socioeconomic status and Schizophrenia

A

Low SES, more stressors and psychosis (sociogenic hypothesis)

Downward drift- SZ fall to bottom of social ladder, no job or relationship
Social selection theory-drift down to unemployment, less social pressure to achieve
Social labelling-development and maintenance of symptoms from the diagnosis

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22
Q

Psychological therapies for schizophrenia

A

Social skill training-role playing, modelling, transferable skills to help with stress, find job etc
CBT for psychosis-target and challenge psychotic symptoms and biases of interpretation
Personal therapy-develop skills for day to day living after hospitals
Family interventions-counselling and sharing experiences, training

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23
Q

How we process food

A

Chewing to break down food, mix alkaline saliva to lubricate
Swallow move food down oesophagus
Stomach churns, breaks down with hydrochloric acid, pepsin breaks down proteins to amino acids
Enzymes in small intestine (gall bladder, pancreas)break protein to amino acids and starch to sugars. Pass through wall to bloodstream and carried to liver
Fats emulsified to bile, water removed by large intestine. Packed as waste
Liver and kidneys filter out toxins from excretion, waste expelled

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24
Q

Pancreatic hormones (insulin, glucagon)

A

Insulin makes glucose (carbohydrate) to glycogen

Glucagon makes glycogen to glucose. Free fat stores to use as fuel when glucose stores are low

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25
Q

Complex intake of humans

A

Omnivore diet- range of key elements we have evolved to process
Much variation between species, some variation within e.g. tolerance to dairy

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26
Q

Products and where they’re stored in the body

A

Lipids/fats to fats (largest, most efficient energy store)
Amino acids to proteins (muscle tissue)
Glucose to glycogen (stored in muscles and liver, fast release)

Minerals and vitamins to body structure and cells
A gram of fat can store more energy and will not hold water

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27
Q

Homeostasis and detectors

A

Homeostasis when body’s set point is violated

DETECTORS: Brain sensitive to low glucose (hypothalamic regulatory nuclei)
Liver sensitive to low glucose and lipids
Stomach signals brain (ghrelin released when unstimulated by food)

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28
Q

Homeostasis/set point theory: Body’s solution when low on fuel

A

Hunger (motivating, from low fatty acids/glucose)
Craving (automatic behavioural state)
Body corrects by releasing glucose and taking in more food

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29
Q

Satiety-stopping eating

A

Short term signals:
Adequate glucose and lipid acid levels detected in brain and liver
Stomach distension
Buccal activity: chewing
High sensory stimulation:taste and smell
Appetite suppressants e.g. caffeine

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30
Q

Satiety cascade

Leptin

A

(Long term feedback mechanism)
Fatty tissues secrete leptin which:

Increases metabolism
Decreases food intake by desensitising brain to hunger signals and inhibits effect of other hormones which drive eating

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31
Q

Issues with food

A

Nutritional deficits, starvation effects can cross generations
Obesity affects multiple systems, premature death
Specific problems e.g. bullying, self esteem

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32
Q

Factors other than homeostasis that affect eating- genetics

A

Prefer high energy sweet, fatty and salty foods more likely to contain nutrients
Bitter foods associated with toxicity

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33
Q

Factors other than homeostasis that affect eating-

Learned preferences

A

Learned aversions- culture and upbringing, satiety to foods eaten recently

Social learning theory-imitate speed, amount, what is customary

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34
Q

Eating disorder

A

Persistent disturbance of eating behaviour or behaviour intended to control weight
Significantly impairs physical health or psychosocial functioning

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35
Q

Eating disorder (low weight) diagnoses issues

A

No explanations ‘why’ and is subjective
Models and gymnasts etc required to sanction weight: muscle weighs more and athletes could never reach such a low BMI
May have naturally low BMI or weight loss from illness or famine
Healthy BMI varies with ethnicity and younger people
Overweight >25 obese>30

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36
Q

Factors other than homeostasis that affect eating-

The environment

A

Environmental-eat more in dark, cold, smell of food and proximity
Industry- cheap processed in large quantities for profit, expensive healthy foods out of season
Toxic environment-obesity stigmatised when culture has lots of food, evolved to get high energy food as fat stores. Less exercise and greater adverts

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37
Q

Eating disorder change in diagnosis

A

Diagnoses change over time (ICD tends to follow DSM)
Formal diagnoses are recent for many conditions

Shift from rigid diagnoses- transdiagnostic model

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38
Q

Anorexia

A

Persistent restriction of energy intake leading to significantly low body weight
Intense fear of gaining weight or becoming fat
Disturbed self evaluation or lack of recognition of the seriousness of current low body weight
At least 15% below expected weight of BMI<17.5
Subtypes: restricting, binge eating, purging

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39
Q

Bulimia

A

Recurrent episodes of binge eating in discrete time with lack of control, inappropriate behaviour to prevent weight gain e.g. vomiting
Binges occur at least once a week for 3 months

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40
Q

Bulimia diagnoses issues

A

A ‘binge’ is subjective
Vomiting may not always be self induced
Exercise may be to keep healthy

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41
Q

Slade’s formulation model

A

Low self esteem and perfectionism
Initial sense of success in controlling self and world but then leads to starvation and fear of lack of control

Develops with immediate trigger

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42
Q

Binge eating disorder

A

Recurrent binge eating with lack of control
Episodes= 3 of the following:
Eating more rapidly than normal, until uncomfortably full, when not physically hungry, feel embarrassed/disgusted/depressed
No purging or compensatory behaviours
At least once a week for 3 weeks

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43
Q

BED diagnoses issues

A

Binge is subjective and formal diagnoses very recent, some debates about definitions
New category:could be to access insurance money for clinicians to treat overweight patients
BUT they have trouble accessing services

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44
Q

Other specified feeding and eating disorder (OSFED)

Avoidant restrictive food intake disorder (ARFID)

A

OSFED- Atypical cases, many symptoms of other eating disorders but do not meet full criteria for diagnoses

ARFID- Primarily found in children, nutritional deficiency, atypical beliefs about food or weight gain
Sensory based avoidance (refuses food on smell, texture)
Lack of interest (in consuming or tolerating)
Food associated with fear evolving stimuli (learning)

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45
Q

Atypical eating disorders treatments and diagnoses

A

Treatments primarily behavioural, focus on anxiety/exposure

40-50% of cases do not fit into diagnoses, many don’t stay in one

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46
Q

Comorbidity with eating disorder

A

Anxiety disorders: social anxiety, ocd
Depression: low serotonin
Personality disorder: anxiety and impulse based
Alcohol and substance abuse

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47
Q

Incidence and prevalence of eating disorders

A

Incidence- new cases in set window of time
Prevalence-Current cases over past year, 1% of population

Slow onset and secrecy so hard to calculate incidence so focus on prevalence

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48
Q

Medical records and cases spotted (eating disorders)

A

Doesn’t spot all cases, so don’t know true amount. Can miss the underweight and focus on young white females

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49
Q

Westernisation and eating disorders

A

Increasing identification and prevalence, more social networks and TV exposure

50
Q

Eating disorder

Theories of causation : neurobiological factors

A

Genetics- some evidence twin studies but genes may be responsible for perfectionism or low serotonin
Hypothalamus damage- may prevent hunger however anorexics report lots of hunger
May be an effect of disorder not other way around

51
Q

Eating disorder

Theories of maintenance: cognitive patterns

A

Low self esteem, do not look for positivity

Negative self attribution and perfectionism so avoid getting things wrong and keep striving
Self maintaining cycle

52
Q

Central belief systems of eating disorders

A

Broken cognitive link between eating and weight, drives restriction and bingeing
Overvalue appearance and weight, defines self as accepted

53
Q

Safety behaviours of eating disorders

A

Temporary calm (sense of control with eating behaviour) but feel worse in the long run so calm self with the behaviour in vicious cycles

Affects energy and eating cycle hugely

54
Q

Emotional factors of eating disorders

A

Anxiety maintain and trigger emotion
Impact of anger, loneliness and boredom
Depression more of a consequence (low serotonin)

55
Q

Perceptual factors of eating disorders

A

See self as 25-30% larger (non clinical 15%)

Thought-shape fusion where feel getting fatter when look at food

56
Q

Social factors of eating disorders

A

Widespread pressure to be thin, magazines etc worsen body image and self esteem
Thinspiration websites encourage self criticism

57
Q

Formulation of bingeing

Triggers and setting conditions

A

Triggers- emotional distress, available food/cue exposure

Setting conditions- starvation, disinhibition, permissive cognitions

58
Q

Formulating cases of eating disorders

A

To understand functions of eating disorders
Shows individuals differ in their history and causes/maintaining factors but assumes some core functions underpinning most cases

E.g. slade model (maintenance elements)

59
Q

ABC model of eating disorders

A

Link antecedents, behaviour and consequences

Central role of need for control, maintenance is significant

60
Q

Eating disorder treatments review

A

Over 600 therapies , many lack evidence
Key elements removed, use favourite methods
6% stuck with one treatment (evidence based)
May be untrained in the therapy they use
Men and women equally benefit

61
Q

What to target in eating disorder treatments

A

Target age when disorders typically appear e.g. adolescents
FOOD as key element, reduce fear of eating
Reduce/increase eating and concerns about the present
Reduce risk of eating disorder developing in future
Risk management to monitor patient
BUT can get worse with education about their condition

62
Q

Meta analysis- Preventing eating disorders

A

Meta analysis on 58 studies
MEDIA LITERACY reduces shape and weight concerns for young males and females
COGNITIVE DISSONANCE approaches (counter arguments to their beliefs) reduce eating behaviours and attitudes in high risk
CBT reduces risk of dieting

63
Q

Prevention of obesity

A

NICE- interventions in schools, local government, families rather than psychological
Encourage lifestyle changes, exercise and healthy eating

64
Q

Anorexia therapies -adults

A

Similar effectiveness for individual CBT (40 sessions)and MANTRA (20-30 sessions) specific to anorexia
Takes longer to treat

65
Q

Anorexia therapies -children

A

AN focused family therapy: non blaming, family takes control over child’s eating , slowly give control back to child
Relapse prevention

CBT or adolescent focused psychotherapy as second option

66
Q

Bulimia and binge eating therapies

A

BED adults or adolescents- group or individual CBT
Bulimia adults- individual CBT
bulimia children and adolescents- family therapy

Teach to sit with the emotion long enough for it to go away

67
Q

Other disorders treatments

A

Therapy for most similar full syndrome

ARFID not addressed by NICE but some evidence for CBT as a solution

68
Q

Treatments for eating disorders myths and evaluation

A

Brief therapies can be as effective for non underweight eating disorders
Therapeutic alliance with clinicians does not facilitate treatment
Early change is critical
No evidence that severity or duration reduces effectiveness of treatment
50% recovery rate but 30% underweight cases
Recovery rates drop if therapy not followed exactly

69
Q

Intensive treatments (in and day patients)

A

Necessary off high risk cases
Can be good for weight restoration but almost no evidence recovery
Very expensive
Risk of dependence
Best for stage 1 of anorexia for weight gain, cognitive change

70
Q

NICE

A

clinicians make sense of data, therapies most strongly supported by evidence
Should be used since resources are scarce
Drives up commissioning for NHS

71
Q

Other treatments with weaker evidence

A

All have little evidence

Medication-may enhance serotonin, reduce bingeing, antipsychotics may reduce anxiety but has withdrawal
Neuromodulation- transcranial stimulation
Leucotomy- used for chronic anorexia with extreme OCD
Dialectical behaviour therapy- reduces impulses
Interpersonal psychotherapy-not as good as CBT
Focused psychodynamic approaches-not replicated in other countries
Integrative cognitive affect-less effective than CBT

72
Q

The impact of therapies for eating disorders

A

Reduces anxiety, depression, impulsivity
Reduces alcohol
Enhance connive flexibility (reduced safety behaviours)
Stabilise weight
Enhance quality of life

73
Q

Treatment for obesity

A

Poor outcomes long term so developed new CBT but wasn’t effective
Continuing care models (reviewing progress seemed to work best)
Bariatric surgery an option but very expensive, needs therapy

74
Q

Motor control

A

Changing mix of conscious and unconscious regulation of muscle force affected by continuous sensory feedback

Framework sculpted by evolutionary pressures

75
Q

Types of motor control

A

Voluntary-running, talking
Goal directed- conscious, explicit
Habit- implicit, unconscious
Involuntary- eye movements, facial expressions

76
Q

Hierarchical control (evolutionary perspective of motor control)

A 
NEWER
Learned threat-avoidance, cortex and limbic (motor)
Loom- avoidance, sensorimotor, midbrain
Pain-escape, spinal cord (endocrine)
OLDER
77
Q

Overview of sensorimotor system

A

Descending control system with ascending feedback to all levels of hierarchy
Basal ganglia and cerebellum have a copy of motor command, feed back to cortex via thalamus
Command reaches the lower motor neurons, continually modulated by basal ganglia and cerebellum

78
Q

Sensorimotor hierarchy

A 
Association cortex 
Sencondary motor cortex 
Primary motor cortex
Brain stem motor nuclei 
Spinal motor circuits 
Muscle
79
Q

Muscle fibres

A

All or nothing activation
Force depends on lower motor neurons activating different types of muscle force
Antagonistic arrangement-Combined co ordinated action, oppose each other
Fibres appear to be genetically determined

80
Q

Muscle contraction

A

Acetylcholine released from motor neuron, activates myosin bead (calcium ions, magnesium ions, ATP) to change shape and bind to actin filament
Myosin walk along actin filament heads when contacts or relaxes

ATP breaks bonds between myosin head and actin filament

81
Q

Amount of muscle fibres innervated by single motor neuron depends on:

A

Level of control- e.g. eye high control low force, 3 units
Strength- e.g. trunk high force low precision, 1000 units

Units recruited smallest first
More motor units fire=more fibres contract=more power

82
Q

Speeds of muscle fibres

A

Slow-continually do not tire
Fast fatigue resistant- maintain for long time but tire
Fast fatigue- ballistic movements, tire quickly

83
Q

Alpha (Lower) motor neurons

Input and output

A

Originate in grey matter (cell bodies) of spinal cord

Sensory input from FROM RECEPTOR down DORSAL root to BRAIN
Motor output from BRAIN through VENTRAL root TO MUSCLE
More distal muscles cell bodies further out from spinal cord while more proximal are closer in

84
Q

Motor unit (unit of control)

A

Smallest unit of motor activity
Single alpha motor neuron and all the muscle fibres it connects to (innervates)

All or nothing, final pathway for motor control, activation causes depolarisation and contraction of all muscle fibres in that unit

85
Q

Lower and upper motor neuron locations

A

Upper motor neurons-originate in brain (motor cortex) and project to spine and meet lower motor neurons

Lower (alpha) motor neuron- cell body in spine or brain stem and project to muscle

86
Q

The motor pool

A

All the lower motor neurons that innervate single muscle e.g. bicep Pool contains both alpha and gamma motor neurons

Arranged in rod like shape within the ventral horn of spinal column

87
Q

Movement resolution and fibre amount

A

Fewer fibres mean greater movement resolution e.g. fingers
Muscle fibres evenly distributed to provide force (same type of fibres)

Fine control at lower force

88
Q

Reflexes

A

Simple or complex

Can operate without engaging with brain, critical for avoiding injury and for effective motor control

89
Q

What does a good control system (SNS) need to know about the muscles

A

How much TENSION in muscles (current force)
-Golgi tendon organ senses, sends ascending sensory info to brain via spinal cord

The LENGTH (stretch of the muscle)
-muscle spindles sense this (intrafusal fibres)
90
Q

How do muscle spindles work

A

Sensory fibre know when muscle stretched (length), wraps around intrafusal muscle (senses force)
Extrafusal muscle is the force itself

Sends signal (dorsal) to brain, return(ventral) muscle return to how it was

91
Q

Innervating intrafusal muscles

A

Innervated separately by gamma motor neurons to keep intrafusal fibres at optimum length for detecting stretch

92
Q

Stretch reflex and withdrawal reflex

A

Stretch-Maintain position and posture despite changing environment

Withdraw-Muscle automatically tense when weight on one leg, relax the other
Execute smooth movement

93
Q

The righting reflex, vestibular righting

A

Detects body orientation and acceleration from gravity
Info combined by somatosensory and proprioceptive sensory input to restore orientation
Cerebellum computes motor activity

94
Q

Brainstem structures

A

Ancient pathways connect sensory input to motor output in brain stem. Modern motor cortex has sculpted it to become sophisticated over time

Control respiration, speech

95
Q

What cells does motor command originate in

A

Pyramidal cells

Axon can project directly or indirectly to spinal cord and lower brainstem motor neurons

96
Q

Motor cortex

A

Direct top down control of muscle movement with as few as one synapse between a cortical neuron and innervated muscle cells.

Regulated by basal ganglia and cerebellum, copy of motor command sent to them, feedback to lower motor cortex

97
Q

Projections from motor cortex

A

Most projections are contralateral, innervate motor units on opposite side
Upper motor neurons project to spinal cord down pyramidal tract

98
Q

Types of muscle fibre

A

Skeletal
Smooth
Cardiac
40% body fat

99
Q

4 legged animals movement without higher level control

A

Shift between distinct limb sequence for speed changes e,g, walking, running without higher level control

100
Q

Dorsolateral tract

A

Corticospinal- Direct
Indirect route- via red nucleus (brainstem) corticorubrospinal

Project to DISTAL muscles e.g. fingers, one segment of spinal cord

101
Q

Ventromedial tract

A

Cortiospinal route- Direct
Indirect route- via tectum, vestibular nuclei, reticular formation (brain stem)

Project to PROXIMAL muscles e.g. trunk, multiple segments of spinal cord

102
Q

Exoskeleton and implants on tetraplegic patients

A

Implanted two implants on the surface of sensorimotor cortex
Robot exoskeleton :made virtual or real movements with limbs

  • works due to direct connection from motor cortex to muscle and factors in cerebellum and basal ganglia input BUT is carried out without lower level sensory feedback etc
  • Can cortically move, re usable up to 7 weeks without calibration
103
Q

Cerebral palsy

A

Damage to motor control structures (before or during birth)

Causes stiffness and weak muscles, affects upper motor neurons

104
Q

Motor cortex damage

A

Poor coordination, weak movement, upper motor neuron syndrome

105
Q

Stroke

A

Interruption of blood supply to brain, upper motor neurons affected rapidly

106
Q

Why is it difficult to assess impact of brain damage on cognitive function

A

Since behaviour involves movement e.g. speech

Impaired motor control can be wrongly interpreted as impaired cognition

107
Q

Agency of action

A

Knowing you did something
Violations give perceptual shock, take for granted

Retrospectively created. Connections between frontal areas (motor plans) and parietal areas that monitor outcomes
You often think it was YOU when you perceive the effect on the world (final stage)

108
Q

Children and agency of action

A

Do not have it
Cortex and basal ganglia are still wiring up
Dopamine burst of reward when expected outcome

109
Q

Basal ganglia and inhibition

A

Basal ganglia inhibits systems from taking cognitive resources
Disinhibits if salient enough what is most important from a survival point, allows it to have motor resources

Nuclei connected circuit
Receive excitatory info and inhibits thalamus, feeds back to cortex, return to basal ganglia

110
Q

Pathways when striatum is relaxed and excited

A

RELAXED- striatum at rest, globus pallidus active, thalamus inhibited so reduced excitation in motor cortex

EXCITED-striatum excited, globus pallidus inhibited, thalamus excited and excited motor cortex

111
Q

Basal ganglia conditions

A

Involuntary movements, issues with selecting movements and doing them at the right time
Motor disorders

112
Q

The selection problem

A

Multiple command systems, spatially distributed, processing together in final motor path so cannot do more than two things well at once= basal ganglia

Do what you NEED to do from survival point

113
Q

Parkinson’s description

A

Around 10% from genetic mutation of a gene (monogenic)
No cure but some effective treatments, 19 gene locations

Cannot initiate movement: Paucity of spontaneous movement, slow movements, akinesia, rigidity, pull rolling

114
Q

Parkinson’s treatments :drugs

A 
Increase dopamine with drugs but cells themselves are dying 
Levo Dopa (dopamine doesn’t cross the blood brain barrier)
If mutation associated with phenotype, may show cellular events responsible. Drugs to target proteins, gene therapy to alter faulty genetic messages
115
Q

Parkinson’s inhibition

A

No dopaminergic input from substantia Nigra so striatum is at rest

Globus pallidus is tonically active, thalamus and motor cortex inhibited

116
Q

Parkinson’s treatments: deep brain stimulation

A

Inhibits globus pallidus, excites thalamus allowing excitation of motor cortex

Very variable, may be linked to variations in pathways

117
Q

Reserah: cerebellum not just motor control

A

Circuits seem like involved in motor learning too (collar with basal ganglia and cortical circuits)
fMRI activation also important for non motor (cognitive)

118
Q

The cerebellum input and output

A

INPUTS- Copy of motor command (motor cortex) also visual, somatosensory, excitatory
Spinal cord (proprioceptive info)
Vestibular info, body position

OUTPUT- Projects to motor cortex via thalamus

Computes MOTOR ERROR and adjusts motor commands accordingly

119
Q

Cerebellum conditions

A

When damaged, movement impairment (ataxia)

-disturbances of posture or gait
-decomposition of movement
Movement appears mechanical, intention tremor
Dysarthia (disruption of speech)

120
Q

Motor neuron disease/ALS

A

Loss of upper and lower motor neurons (affects all muscles)
Degeneration and muscle wasting from not being activated

No cure and 10% have genetic component, modulated by age
Symptoms an life expectancy variable
Atrophy (muscle wastage) a good indicator

121
Q

The homunculus

A

Reasonable representation but oversimplified

Representations are more complex and overlapping

122
Q

Muscles rigor mortis

A

Release of acetylcholine causes release of calcium from inside the muscle
ATP is produced from metabolism (oxidation)
Which stops at death, muscles remain contracted

YEAR 2 Semester 1👩🏼‍🎓 (6 decks)

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