Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Heritability of schizophrenia

A

45% MZ and 10% DZ

some heritability but clearly environmental effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Dopamine

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Dopamine receptor families

A

D1 like (D1 and D5)

D2 like (D2, D3 and D4) ANTIPSYCHOTICS bind here
newer drugs D4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Eye tracking in Schizophrenia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Theory of mind in schizophrenia

A

Thought to be distorted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Complex intake of humans
Omnivore diet- range of key elements we have evolved to process Much variation between species, some variation within e.g. tolerance to dairy
26
Products and where they’re stored in the body
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
27
Homeostasis and detectors
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)
28
Homeostasis/set point theory: Body’s solution when low on fuel
Hunger (motivating, from low fatty acids/glucose) Craving (automatic behavioural state) Body corrects by releasing glucose and taking in more food
29
Satiety-stopping eating
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
30
Satiety cascade Leptin
(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
31
Issues with food
Nutritional deficits, starvation effects can cross generations Obesity affects multiple systems, premature death Specific problems e.g. bullying, self esteem
32
Factors other than homeostasis that affect eating- genetics
Prefer high energy sweet, fatty and salty foods more likely to contain nutrients Bitter foods associated with toxicity
33
Factors other than homeostasis that affect eating- | Learned preferences
Learned aversions- culture and upbringing, satiety to foods eaten recently Social learning theory-imitate speed, amount, what is customary
34
Eating disorder
Persistent disturbance of eating behaviour or behaviour intended to control weight Significantly impairs physical health or psychosocial functioning
35
Eating disorder (low weight) diagnoses issues
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
36
Factors other than homeostasis that affect eating- | The environment
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
37
Eating disorder change in diagnosis
Diagnoses change over time (ICD tends to follow DSM) Formal diagnoses are recent for many conditions Shift from rigid diagnoses- transdiagnostic model
38
Anorexia
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
39
Bulimia
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
40
Bulimia diagnoses issues
A ‘binge’ is subjective Vomiting may not always be self induced Exercise may be to keep healthy
41
Slade’s formulation model
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
42
Binge eating disorder
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
43
BED diagnoses issues
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
44
Other specified feeding and eating disorder (OSFED) | Avoidant restrictive food intake disorder (ARFID)
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)
45
Atypical eating disorders treatments and diagnoses
Treatments primarily behavioural, focus on anxiety/exposure 40-50% of cases do not fit into diagnoses, many don’t stay in one
46
Comorbidity with eating disorder
Anxiety disorders: social anxiety, ocd Depression: low serotonin Personality disorder: anxiety and impulse based Alcohol and substance abuse
47
Incidence and prevalence of eating disorders
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
48
Medical records and cases spotted (eating disorders)
Doesn’t spot all cases, so don’t know true amount. Can miss the underweight and focus on young white females
49
Westernisation and eating disorders
Increasing identification and prevalence, more social networks and TV exposure
50
Eating disorder | Theories of causation : neurobiological factors
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
Eating disorder | Theories of maintenance: cognitive patterns
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
Central belief systems of eating disorders
Broken cognitive link between eating and weight, drives restriction and bingeing Overvalue appearance and weight, defines self as accepted
53
Safety behaviours of eating disorders
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
Emotional factors of eating disorders
Anxiety maintain and trigger emotion Impact of anger, loneliness and boredom Depression more of a consequence (low serotonin)
55
Perceptual factors of eating disorders
See self as 25-30% larger (non clinical 15%) | Thought-shape fusion where feel getting fatter when look at food
56
Social factors of eating disorders
Widespread pressure to be thin, magazines etc worsen body image and self esteem Thinspiration websites encourage self criticism
57
Formulation of bingeing | Triggers and setting conditions
Triggers- emotional distress, available food/cue exposure | Setting conditions- starvation, disinhibition, permissive cognitions
58
Formulating cases of eating disorders
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
ABC model of eating disorders
Link antecedents, behaviour and consequences | Central role of need for control, maintenance is significant
60
Eating disorder treatments review
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
What to target in eating disorder treatments
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
Meta analysis- Preventing eating disorders
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
Prevention of obesity
NICE- interventions in schools, local government, families rather than psychological Encourage lifestyle changes, exercise and healthy eating
64
Anorexia therapies -adults
Similar effectiveness for individual CBT (40 sessions)and MANTRA (20-30 sessions) specific to anorexia Takes longer to treat
65
Anorexia therapies -children
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
Bulimia and binge eating therapies
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
Other disorders treatments
Therapy for most similar full syndrome | ARFID not addressed by NICE but some evidence for CBT as a solution
68
Treatments for eating disorders myths and evaluation
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
Intensive treatments (in and day patients)
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
NICE
clinicians make sense of data, therapies most strongly supported by evidence Should be used since resources are scarce Drives up commissioning for NHS
71
Other treatments with weaker evidence
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
The impact of therapies for eating disorders
Reduces anxiety, depression, impulsivity Reduces alcohol Enhance connive flexibility (reduced safety behaviours) Stabilise weight Enhance quality of life
73
Treatment for obesity
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
Motor control
Changing mix of conscious and unconscious regulation of muscle force affected by continuous sensory feedback Framework sculpted by evolutionary pressures
75
Types of motor control
Voluntary-running, talking Goal directed- conscious, explicit Habit- implicit, unconscious Involuntary- eye movements, facial expressions
76
Hierarchical control (evolutionary perspective of motor control)
``` NEWER Learned threat-avoidance, cortex and limbic (motor) Loom- avoidance, sensorimotor, midbrain Pain-escape, spinal cord (endocrine) OLDER ```
77
Overview of sensorimotor system
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
Sensorimotor hierarchy
``` Association cortex Sencondary motor cortex Primary motor cortex Brain stem motor nuclei Spinal motor circuits Muscle ```
79
Muscle fibres
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
Muscle contraction
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
Amount of muscle fibres innervated by single motor neuron depends on:
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
Speeds of muscle fibres
Slow-continually do not tire Fast fatigue resistant- maintain for long time but tire Fast fatigue- ballistic movements, tire quickly
83
Alpha (Lower) motor neurons | Input and output
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
Motor unit (unit of control)
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
Lower and upper motor neuron locations
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
The motor pool
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
Movement resolution and fibre amount
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
Reflexes
Simple or complex | Can operate without engaging with brain, critical for avoiding injury and for effective motor control
89
What does a good control system (SNS) need to know about the muscles
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
How do muscle spindles work
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
Innervating intrafusal muscles
Innervated separately by gamma motor neurons to keep intrafusal fibres at optimum length for detecting stretch
92
Stretch reflex and withdrawal reflex
Stretch-Maintain position and posture despite changing environment Withdraw-Muscle automatically tense when weight on one leg, relax the other Execute smooth movement
93
The righting reflex, vestibular righting
Detects body orientation and acceleration from gravity Info combined by somatosensory and proprioceptive sensory input to restore orientation Cerebellum computes motor activity
94
Brainstem structures
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
What cells does motor command originate in
Pyramidal cells Axon can project directly or indirectly to spinal cord and lower brainstem motor neurons
96
Motor cortex
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
Projections from motor cortex
Most projections are contralateral, innervate motor units on opposite side Upper motor neurons project to spinal cord down pyramidal tract
98
Types of muscle fibre
Skeletal Smooth Cardiac 40% body fat
99
4 legged animals movement without higher level control
Shift between distinct limb sequence for speed changes e,g, walking, running without higher level control
100
Dorsolateral tract
Corticospinal- Direct Indirect route- via red nucleus (brainstem) corticorubrospinal Project to DISTAL muscles e.g. fingers, one segment of spinal cord
101
Ventromedial tract
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
Exoskeleton and implants on tetraplegic patients
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
Cerebral palsy
Damage to motor control structures (before or during birth) | Causes stiffness and weak muscles, affects upper motor neurons
104
Motor cortex damage
Poor coordination, weak movement, upper motor neuron syndrome
105
Stroke
Interruption of blood supply to brain, upper motor neurons affected rapidly
106
Why is it difficult to assess impact of brain damage on cognitive function
Since behaviour involves movement e.g. speech | Impaired motor control can be wrongly interpreted as impaired cognition
107
Agency of action
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
Children and agency of action
Do not have it Cortex and basal ganglia are still wiring up Dopamine burst of reward when expected outcome
109
Basal ganglia and inhibition
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
Pathways when striatum is relaxed and excited
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
Basal ganglia conditions
Involuntary movements, issues with selecting movements and doing them at the right time Motor disorders
112
The selection problem
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
Parkinson’s description
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
Parkinson’s treatments :drugs
``` 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
Parkinson’s inhibition
No dopaminergic input from substantia Nigra so striatum is at rest Globus pallidus is tonically active, thalamus and motor cortex inhibited
116
Parkinson’s treatments: deep brain stimulation
Inhibits globus pallidus, excites thalamus allowing excitation of motor cortex Very variable, may be linked to variations in pathways
117
Reserah: cerebellum not just motor control
Circuits seem like involved in motor learning too (collar with basal ganglia and cortical circuits) fMRI activation also important for non motor (cognitive)
118
The cerebellum input and output
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
Cerebellum conditions
When damaged, movement impairment (ataxia) -disturbances of posture or gait -decomposition of movement Movement appears mechanical, intention tremor Dysarthia (disruption of speech)
120
Motor neuron disease/ALS
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
The homunculus
Reasonable representation but oversimplified | Representations are more complex and overlapping
122
Muscles rigor mortis
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions