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Semester 3: Mind and Movement > PBL Topic 3 Case 7 > Flashcards

PBL Topic 3 Case 7 Flashcards

1
Q

Identify three roles of the cerebellum

A
  • Timings of motor activities
  • Intensity of muscle contraction
  • Interplay between agonist and antagonist muscles
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2
Q

Identify the three lobes of the cerebellum

A
  • Anterior lobe
  • Posterior lobe
  • Flocculonodular lobe
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3
Q

Where is the vermis located and what is its function?

A
  • Longitudinal band in the centre of the cerebellum
  • Control for muscle movements of the axial body, neck, shoulders and hips
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4
Q

Identify the two zones of the cerebellar hemipsheres and their function

A
  • Intermediate zone, control of muscle contractions in hands, fingers, feet and toes
  • Lateral zone, planning of sequential movements
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5
Q

Describe the topographical representation in the cerebellum

A
  • Axial portions of the body lie in the vermis
  • Limbs and facial regions lie in the intermediate zones
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6
Q

Why does the lateral zone of the cerebellar hemisphere not have topographical representations?

A
  • It receives signals directly from the cerebral cortex
  • For the planning and co-ordination of sequential muscular activities
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7
Q

Describe the course of the corticopontocerebellar pathway

A
  • Afferent pathway from motor cortex
  • Passes by way of pontocerebellar tracts
  • Terminates in lateral divisions of the cerebellar hemispheres
  • To the opposite side of the brain
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8
Q

Describe the course of the olivocerebellar pathway

A
  • Afferent pathway from inferior olive
  • Which are excited by fibres from motor cortex, basal ganglia, reticular formation and spinal cord
  • Terminates on all parts of the cerebellum
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9
Q

Describe the course of the vestibulocerebellar fibres

A
  • Afferent pathway from vestibular apparatus and brainstem vestibular nuclei
  • Terminate in flocculonodular lobe and fastigial nucleus of the cerebellum
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10
Q

Describe the course of the dorsal spinocerebellar tract

A
  • From muscle spindles, Golgi tendon organs, tactile receptors through dorsal tracts
  • Pass into cerebellum through inferior cerebellar peduncle
  • Terminates in vermis and intermediate zones
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11
Q

Describe the course of the ventral spinocerebellar tract

A
  • From motor signals in the anterior horns
  • Through corticospinal and rubrospinal tracts
  • Tells cerebellum which signals have arrived at anterior horns and which have not
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12
Q

What is the speed of conduction in the spinocerebellar tracts?

A
  • 120 m/sec
  • Most rapid pathway transmission in any pathway in the CNS
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13
Q

Identify two other pathways that relay information to the cerebellum

A
  • Spinoreticular pathway
  • Spino-olivary pathway
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14
Q

Identify the four deep nuclei of the cerebellum

A
  • Fastigial nucleus, associated with vestibular apparatus
  • Globose nucleus, associated with co-ordination of agonist and antagonist muscles
  • Emboliform nucleus, associated with co-ordination of agonist and antagonist muscles
  • Dentate nucleus, associated with co-ordination of sequential movements
  • Globose and emboliform are known collectively as interposed nuclei
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15
Q

Outline the three layers of the cerebellar cortex, where are the deep cerebellar nuclei located relative to these layers?

A
  • Molecular layer
  • Purkinje layer
  • Granule cell layer
  • Deep cerebellar nuclei are located deep to these layers
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16
Q

Identify the efferent outputs of the cerebellum

A
  • Purkinje cell
  • Deep nuclear cell
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17
Q

Identify the afferent inputs to the cerebellum

A
  • Climbing fibres from inferior olives of the medulla, which send signals to deep nuclear cells and then to Purkinje cells
  • Mossy fibres from higher brain, brainstem and spinal cord, which synapse with granule cells before sending signals to Purkinje cells
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18
Q

Describe the impulse from a climbing fibre

A
  • Single strong impulse causes a prolonged action potential followed by several weaker spikes
  • Known as a complex spike
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19
Q

Describe the impulse from a mossy fibre

A
  • Impulse duration is much smaller and action potential is less prolonged
  • Known as a simple strike
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20
Q

How are deep nuclear cells inhibited and what is the importance of this?

A
  • Inhibited by Purkinje cells
  • So that an inhibitory signal sis to the output motor pathway
  • Damping function stops muscle movement overshooting its mark
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21
Q

Identify two other inhibitory cells of the cerebellum and in which cell layer they are located

A
  • Basket cells
  • Stellate cells
  • Molecular layer
  • Lateral inhibition
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22
Q

What is meant by vestibulocerebellum / archicerebellum?

A
  • Flocculonodular lobes and vermis
  • Involved in equilibrium and agonist/antagonist muscle contractions
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23
Q

What is meant by spinocerebellum / paleocerebellum?

A
  • Vermis and intermediate zones
  • Involved in coordinating movement in distal limbs
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24
Q

What is meant by cerebrocerebellum / pontocerebellum / neocerebellum?

A
  • Lateral zones
  • Motor imagery, planning of movements in advance to the movement
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25
Q

With regards to the vestibulocerebellum, what is meant by anticipatory correction?

A
  • Ability of cerebellum to calculate the rate and direction of movement during next few milliseconds
  • Based on signals from periphery
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26
Q

How does the spinocerebellum co-ordinate movement in distal limbs?

A
  • Receives from motor cortex red nucleus and peripheral proprioceptors
  • Deep nuclear cells of interposed nucleus send signals back to cerebral cortex through relay nuclei in the thalamus and through rubrospinal tract
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27
Q

Explain the basis of an intention tremor

A
  • Must movements are pendular and thus have a tendency to overshoot due to momentum
  • Cerebellum has a damping system to prevent this overshoot
  • Failure of which causes limb to oscillate in opposite directions
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28
Q

What is meant by ballistic movements and how is this affected by cerebellar destruction?

A
  • Rapid movements such as typing and reading
  • That are preplanned, set in to motion for a specific distance then stop
  • Cerebellar destruction results in movements that are slow to develop, weak force, and slow termination of movement
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29
Q

Describe how the cerebrocerebellum is involved in planning and timing of sequential movements

A
  • Plan begins in sensory and premotor areas
  • Two way signals sent between cerebellum and cerebral cortex
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30
Q

What is meant by dysdiadochokinesia?

A
  • Impairment of rapidly alternating hand movement
  • Because motor system fails to predict where different parts of the body will be at different times
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31
Q

What is meant by dysmetria and ataxia?

A
  • Overshoot of movements over intended mark and subsequent overcompensation (dysmetria) resulting in uncoordinated movements (ataxia)
  • Due to lesions in the spinocerebellar tract
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32
Q

What is meant by nystagmus?

A
  • Tremor of eyeballs when fixating on one side of head
  • Damage of flocculonodular lobes, with subsequent loss of equilibrium
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33
Q

What is meant by intention tremor?

A
  • Oscillation of movement caused by overshoot followed by back and forth vibration
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34
Q

What is meant by scanning dysarthria?

A
  • Failure of intensity or duration of sound results in jerky, explosive or slurred speech
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35
Q

What is meant by hypotonia?

A
  • Decreased tone
  • Caused by damage to dentate and interposed nuclei on same side of lesion and subsequent loss of facilitation of the motor cortex
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36
Q

Identify three roles of the basal ganglia

A
  • Relative intensities of separate movements
  • Directions of movements
  • Sequencing of successive movements
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37
Q

Identify the different structures of the basal ganglia

A
  • Caudate nucleus and putamen (corpus striatum)
  • Putamen and globus pallidus [internal and external] (lentiform nucleus
  • Substantia nigra [pars reticulata and pars compacta]
  • Subthalamic nucleus
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38
Q

What is meant by the direct and indirect pathways of the motor loop of the basal ganglia?

A
  • Direct loop: traverses corpus striatum and thalamus and involves consecutive sets of neurons
  • Indirect pathway, traverse subthalamic nucleus and involves seven sets of neurons
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39
Q

Which neurotransmitter is involved in projections from cerebral cortex and thalamus?

A
  • Glutaminergic
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40
Q

Which neurotransmitter is involved in projections from the striatum and globus pallidus?

A
  • GABAergic
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41
Q

What are the two different synapses involved in the nigrostriatal pathway?

A
  • Direct pathway = Facilitatory D1 receptors
  • Indirect pathway = Inhibitory D2 receptors
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42
Q

Which regions of the basal ganglia are somatotopically organised?

A
  • Putamen
  • Globus pallidus
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43
Q

Outline the direct pathay

A
  • Excitatory signals from sensorimotor cortex to striatum
  • This excites the striatum, which sends inhibitory signals to internal globus pallidus
  • This inbhits the internal globus pallidus, which inhibits the inhibitory signals to the thalamus
  • Disinhibition of the thalamus results in activation of the supplementary motor area
  • Which modifies ongoing corticostriate activity and initiates impulse trains along the corticospinal and corticoreticular fibres.
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44
Q

Outline the effect of the nigrostriatal system on the direct pathway

A
  • Excitatory dopamine signals from pars compacta to striatum
  • This further excites the striatum
  • So causes more disinhibition of the thalamus
  • Turning up motor activity
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45
Q

Outline the indirect pathway

A
  • Excitatory signals from sensorimotor cortex to striatum
  • This excites the striatum, which sends inhibitory signals to external globus pallidus
  • This inhibits the external globus pallidus, which inhibits the inhibitory signals to the subthalamic nucleus
  • The subthalamic nucleus nucleus now sends excitatory signals to the internal globus pallidus
  • Which sends inhibitory signals to the thalamus, inhibiting the signals to the supplementary motor area.
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46
Q

Outline the effect of the nigrostriatal system on the indirect pathway

A
  • Inhibitory dopamine signals from pars compacta to striatum
  • This inhibits the striatum
  • So fewer inhibitory signals are sent to the external globus pallidus
  • More inhibition of subthalamic nucleus, so it is unable to send excitatory projections to the globus pallidus internus
  • So more excitatory projections to thalamus, so more motor activity.
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47
Q

Outline 3 abnormalities of the basal ganglia

A
  • Athetosis, lesion in global pallidus, producing spontaneous and continuous writhing movements of the hand
  • Hemiballismus, lesions int he subthalamic nucleus, producing sudden flailing movements of the entire limb
  • Chorea, a lesion in the putamen, producing a flicking movement of the hand or face
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48
Q

Outline the biosynthesis of acetylcholine

A
  • Choline is acetylated by choline acetyltransferase
  • Which transfers the acetyl group from acetyl coenzyme A
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49
Q

How is acetylcholine inactivated?

A
  • Hydrolysis by acetylcholinesterase
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50
Q

Identify two types of acetylcholine receptors

A
  • Nicotinic ACh receptors (nAChRs)
  • Muscarinic ACh receptors (mAChRs)
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51
Q

What type of receptors are nAChRs?

A
  • Ligand gated ionotropic channels
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52
Q

What type of receptors are mAChRs?

A
  • G-protein coupled receptors
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53
Q

Outline three main classes of nAChRs

A
  • Muscle receptors confined to neuromuscular junctions
  • Ganglionic receptors
  • CNS-type receptors
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54
Q

Outline the subtypes of muscarinic receptors

A
  • M1-M5
  • Odd numbered are excitatory as they excite inositol phosphate pathway allowing calcium influx and depolarisation
  • Even numbered are inhibitory as they inhibit adenylyl cyclase pathway allowing potassium efflux with hyperpolarisation
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55
Q

Which muscarinic receptor is the neural type, how does it work?

A
  • M1
  • Causes a decrease in k+ conductance which causes membrane depolarisation
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56
Q

Where are cholinergic neurons located?

A
  • Nucleus basalis of Meynert
  • A forebrain nuclei
57
Q

Which nucleus provides the main cholinergic output to the hippocampus and is involved in memory?

A
  • Septohippocampal nucleus
58
Q

Outline three main functions ascribed to cholinergic pathways with relation to each pathway.

A
  • Arousal (nucleus basal to cortex)
  • Memory (septum pellucidum to hippocampus)
  • Motor control (cholinergic interneurons in striatum)
59
Q

Where is dopamine most abundant in the brain?

A
  • Corpus striatum
60
Q

Outline the biosynthesis of dopamine

A
  • L-tyrosine is converted to dihydroxyphenylalanine (dopa) by tyrosine hydroxylase
  • Dopa is then converted to dopamine by dopa decarboxylase.
61
Q

Why do dopaminergic neurons not convert dopamine to noradrenaline?

A
  • They lack dopamine beta-hydroxylase (DBH)
62
Q

How is dopamine metabolised and what is the clinical significance of the product?

A
  • Uptake into presynaptic neuron or glial cell by DAT
  • Monoamine oxidase
  • Catechol-o-methyl transferase
  • Which produces homovanillic acid (HVA)
  • Which is used as an index to dopamine turnover
  • Drugs that cause the release of dopamine increase HVA
63
Q

Outline the four main dopaminergic pathways in the brain

A
  • Nigrostriatal pathway
  • Mesolimbic pathway
  • Mesocortical pathway - Tuberohypophyseal pathway
64
Q

Describe the course of the nigrostriatal pathway and its function

A
  • Cell bodies in substantia nigra
  • Whose axons run in medial forebrain bundle
  • And terminate in corpus striatum
  • Involved in motor control
65
Q

Describe the course of the mesolimbic pathway and its function

A
  • Cell bodies in ventral tegmental area
  • Whose axons run in medial forebrain bundle
  • To nucleus accumbens and amygdaloid nucleus
  • Involved in behaviour
66
Q

Describe the course of the mesocortical pathway and its function

A
  • Cell bodies lie in ventral tegmental area
  • Whose axons run in medial forebrain bundle
  • To prefrontal cortex
  • Involved in behaviour
67
Q

Describe the course of the tuberohypophyseal pathway and its function

A
  • Cell bodies lie in hypothalamus
  • To pituitary gland
  • Involved in endocrine control
68
Q

Identify the two types of dopamine receptor, what kind of receptor are they?

A
  • D1 and D2
  • Which are G-protein transmembrane receptors
69
Q

What is the D1 family?

A
  • Contains D1 and D5
  • Excitatory, linked to stimulation of adenylyl cyclase
70
Q

What is the D2 family?

A
  • Contains D2, D3 and D4
  • Inhibitory, linked to inhibition of adenylyl cyclase, activation of K+ channels and inhibition of Ca2+ channels
71
Q

Identify a dopamine antagonist

A
  • Chlorpromazine an antipsychotic
72
Q

Why must glutamate be synthesised in neurons from local precursors?

A
  • It does not cross the blood brain barrier
73
Q

Identify two local precursors for the synthesis of glutamate

A
  • From glucose, via Krebs cycle, by action of GABA transaminase
  • From glutamine, produced by glial cells, which is converted to glutamate by glutaminase
74
Q

How is glutamate recycled?

A
  • Taken up by astrocytes
  • And converted into glutamine
75
Q

Identify the three main subtypes of ionotropic glutamate receptors

A
  • NMDA, involved in slower excitatory responses
  • AMPA, involved in fast excitatory responses
  • Kainate, involved in fast excitatory responses
76
Q

Identify three special features of NMDA receptors

A
  • Highly permeable to Ca2+ so effective in promoting Ca2+ entry
  • Blocked by Mg2+ when polarised
  • Activation requires glycine and glutamate
77
Q

Identify the metatropic glutamate receptors

A
  • mGlu1-8
  • mGlu1 receptors are excitatory postsynaptic receptors
  • mGlu2 and mGlu3 receptors are presynaptic inhibitory receptors
78
Q

Outline the biosynthesis of GABA

A
  • Glutamic acid decarboxylase
  • Which converts glutamate to GABA
79
Q

Where is GABA most abundant in the CNS?

A
  • Nigrostriatal system
80
Q

How is GABA taken up and how is it destroyed?

A
  • Taken up by GABAergic neurons and astrocytes via specific transporters
  • Destroyed by GABA transaminase, converting it to succinic acid.
81
Q

What percentage of neurons in the CNS are GABAergic?

A
  • 20%
82
Q

Identify the two main types of GABA receptors

A
  • GABAA, ligand gated ion channels, postsynaptic fast inhibition
  • GABAB, G-protein coupled receptors, presynaptic and postsynaptic inhibition by blocking Ca2+ and increasing K+ conductance
83
Q

Where is glycine most abundant?

A
  • Spinal cord grey matter
84
Q

Describe the glycine receptor

A
  • Resembles GABAA
  • Ligand gated postsynaptic channel that causes fast inhibition
85
Q

What are Lewy bodies and how do they form?

A
  • Intracellular protein aggregates
  • Caused by mutation of alpha-synuclein, a vesicular protein
  • Which becomes resistant to degradation so builds up within cells
86
Q

How do Lewy bodies result in neurotoxicity

A
  • Vesicular storage of dopamine is impaired
  • Leading to an increase in cytosolic dopamine
  • Degradation of which produces reactive oxygen species
87
Q

Outline the effect of degradation of nigrostriatal neurons on the striatum

A
  • Loss of facilitation of spiny striatal neurons bearing D1 receptors, disengaging the direct pathway
  • Loss of inhibition of D2 receptors, engaging the indirect pathway
88
Q

How does engagement of the indirect pathway result in movement problems?

A
  • Sensorimotor cortex strongly activates GABAergic neurons in striatum which act on external globus pallidus
  • Causing disinhibition of subthalamic nucleus
  • Which discharges glutamine strongly onto internal globus pallidus
  • Which discharges GABA strongly onto ventral nucleus of thalamus
  • Reduced output to fibres travelling to supplementary motor area
89
Q

What is bradykinesia, what causes bradykinesia and how does it present?

A
  • Suppression of voluntary movement
  • Due to muscle rigidity and inertia of motor system (so motor activity is difficult to stop and start)
  • Routine activities such as opening a door require deliberate planning
90
Q

What is the frequency of a resting tremor?

A
  • 3-6 hertz
91
Q

What is the commonest sequence of limb involvement of resting tremor in Parkinson’s?

A
  • One upper limb to ipsilateral lower limb in 1 year
  • Contralateral limb involvement within 3 years
92
Q

What is a pill-rolling movement?

A
  • Index and middle finger move against thumb pad
93
Q

Why do Parkinson’s patients have a stooped posture?

A
  • Rigidity mainly affecting flexors
94
Q

What is meant by lead pipe rigidity?

A
  • Limb is rigid throughout entire range of motion
  • Cogwheel sensation
95
Q

What is the first line treatment for Parkinson’s?

A
  • Levodopa
  • Combined with a decarboxylase inhibitor (co-beneldopa)
96
Q

Why is levodopa combined with a decarboxylase inhibitor?

A
  • Reduces dopamine synthesis in periphery
  • Which would cause troublesome side effects
97
Q

Why do patients become tolerant to levodopa?

A
  • Reflects natural progression of the disease
98
Q

Identify the main unwanted effects of levodopa

A
  • Involuntary writhing movements (athetosis)
  • Rapid fluctuations in clinical state, reflecting the fluctuating plasma concentration of dopamine
  • Hypotension, nausea and schizophrenia-like syndrome
99
Q

Identify two dopamine agonists and their troublesome side effects

A
  • Bromocriptine, inhibits prolactin from anterior pituitary gland, causing nausea, vomiting and somnolence
  • Pergolide, believed to cause heart disease
100
Q

Identify two replacements of dopamine agonists

A
  • Non-ergot compounds
  • Such as pramipexole and ropinirole - Which are better tolerated
101
Q

What is Selegiline and its advantages?

A
  • Selective MAO-B inhibitor which targets mainly dopamine
  • So does not provoke cheese reaction or interact with other drugs
  • Protects dopamine from extra neuronal degradation
102
Q

Explain one disadvantage of selegiline and name a similar drug that does not cause these side effects

A
  • Metabolised to amphetamine so can cause excitement, anxiety and insomnia
  • Rasagiline
103
Q

What does deep brain stimulation involve in the treatment of Parkinson’s?

A
  • Paralysis of subthalamic nucleus (inhibiting internal globus pallidus causing disinhibition of the thalamus)
104
Q

What is Complementary and Alternative Medicine?

A
  • Therapies and interventions that are
  • Non standard
  • Non prescription
  • Non surgical
105
Q

How does complementary medicine differ to alternative medicine?

A
  • Complementary medicines are taken as well as conventional treatment
  • Alternative medicines are taken instead of conventional treatment.
106
Q

What is a placebo?

A
  • Any therapy that has no specific activity for the condition being treated
  • It has no active ingredient and no direct physiological effect
  • Example is sugar pill
107
Q

What is the placebo effect?

A
  • Any psychological or psychophysiological effect produced by placebos
  • In a clinical trial, this effect can be worked out by excluding the known specific effects of the treatment under investigation.
108
Q

What is the nocebo effect?

A
  • Adverse psychological or psychophysiological effects produced by a placebo
109
Q

What are outcome expectancies with relation to placebo?

A
  • Beliefs that treatment will have positive effects on health status
110
Q

What are self-efficacy expectancies with relation to placebo?

A
  • Beliefs that one can carry out the actions necessary for successful management of a disease
111
Q

Outline four other explanations of the placebo effect

A
  • Conditioning
  • Anxiety reduction
  • Social support
  • Psychophysiological mechanisms
112
Q

Outline four examples of CAM in Parkinson’s

A
  • Nicotine
  • Cannabis
  • Caffeine
  • Acupuncture
113
Q

Why are CAM potentially harmful in the treatment of Parkinson’s

A
  • Used as alternative to traditional medicine such as levodopa
  • Harmful side effects and interactions with prescribed medicines
114
Q

Describe the course of the limbic loop of the basal ganglia

A
  • From prefrontal cortex
  • Through the nucleus accumbens (ventral striatum)
  • Returns to prefrontal cortex via the mediodorsal nucleus of the thalamus
115
Q

What is the role of the limbic lobe of the basal ganglia?

A
  • Gives motor expression to emotions
  • Such as smiling, gesturing, aggressive or submissive posture
116
Q

Outline the epidemiology of Parkinson’s disease

A
  • Increases with age (1:200 over 80)
  • More common in males (1.5:1 M:F)
  • Environmental factors include pesticide exposure, rural living and non-smokers
  • Several genetic loci designated PARK-1 to PARK-11
117
Q

Which genetic locus and subsequent protien is responsible for formation of Lewy bodies?

A
  • PARK-1
  • Alpha Synuclein
118
Q

Which genetic locus and subsequent protien is responsible for juvenile and early onset of PD?

A
  • PARK-2
  • Parkin
119
Q

Outline how PET scanning can be used to detect Parkinson’s disease

A
  • [18F]fluorodopa is injected intravenously and binds to dopamine receptors
  • In Parkinson’s disease there is reduced fluorodopa binding due to reduction in dopamine receptors
  • Intensity of uptake is seen as blue / green
120
Q

Identify two dopa decarboxylase inhibitors

A
  • Carbidopa (co-careldopa)
  • Benserazide (co-beneldopa)
121
Q

Outline the mechanism of aciton of amantadine and when it is mainly used.

A
  • Advanced disease
  • Mainly acts be incresing dopamine release
122
Q

A glycine antagonists will inhibit what type of receptor?

A
  • NMDA
123
Q

Outline the genetic basis of Huntington’s disease

A
  • Inherited as autosomal dominant disorder
  • Trinucleotide repeat disease, with expansion of CAG repeats
124
Q

How does the number of glutamine residues relate to development of Huntington’s disease?

A
  • Huntingtin gene normally possesses fewer than 30 glutamine residues
  • In HD there is increased number of glutamine residues on the N-terminal of the expressed protein
  • The mutated huntingtin possesses more than 40 glutamine residues
125
Q

What is the main clinical feature of Huntington’s? Which region of the basal ganglia is it associated with?

A
  • Chorea
  • Flicking moments of the hands, face and other body parts called chorea.
  • Putamen
126
Q

Outline the pathology of HD with relation to neurotransmitters

A
  • Reduction of glutamic acid dercarboxylase, the enzyme responbible for GABA synthesis
  • Resulting in a hyperactivity of dopaminergic synapses
  • Mirror image of Parkinson’s
127
Q

Identify 3 drugs used in the management of Huntington’s

A
  • Tetrabenazine (inhibits of a vesicular dopamine transporter that reduces dopmaine storage)
  • Chlorpromazine (dopamine antagonist)
  • Baclofen (GABA agonist)
128
Q

What is athetosis? Which region of the basal ganglia is it associated with? This condition is a side effect of which drug?

A
  • Writhing movements of the hands face and neck
  • Globus pallidus
  • Levoopa
129
Q

What is hemiballismus and what region of the basal ganglia is it associated with?

A
  • Flailing movements of an entire limb
  • Subthalamic nucleus
130
Q

Which genetic locus and subsequent protien is associated with a phenotyope identical to sporadic Parkinson’s disease?

A
  • PARK8
  • LRRK2
131
Q

Outline the role of ACh in Parkinson’s

A
  • ACh release from striatum is normally inhibited by dopamine acting on D2 receptors
  • In PD, there is a lack of dopamine in striatum
  • So there is increased release of ACh in resutling in abnormal motor activity.
  • Originally treated with mAChR antagonists though these had too many side effects e.g. dry mouth, eyes, blurred vision, urinary retention and diarrhoea
132
Q

What is hyoscine and what does it cause?-

A
  • Muscarinic antagonist
  • Amnesia
133
Q

Outline the role of the Pars Reticulata in the regulation of movement

A
  • SnPR has GABAergic projections to thalamus that inhibit the thalamus
  • As part of the direct pathway, GABAergic projections from the striatum inhibit the SnPR
  • There is disinhibition of the thalamus as a result

Same effect as on Globus Pallidus Internus

134
Q

Outline three types of care homes

A
  • Residential home: Aimed at individuals who cannot manage at home on their own
  • Nursing home: Aimed at individuals who cannot cope at home on their own and have a condition that requires 24 hour nursing care
  • Specilaist care home: Aimed at individuals who cannot cope at home on their own and have a condition that requires specialist trained staff or adapted facilities
135
Q

How does benserazide work?

A
  • Inhibitor of AADC (aromatic L-amino decarboxylase)
  • The enzyme responsible for converted levodopa to dopamine in the periphery
136
Q

What does a standards need approach to QoL assume?

A
  • Needs rather than wants are central to quality of life
137
Q

What is the difference between a subjective and objective measure of QoL?

A
  • Objective: Level of functioning
  • Subjective: Self-appraisal of one’s own wellveing
138
Q

Give an example of a unidimensional and mutlidimensional question that could be asked on a health questionnaire

A
  • Unidimensional: How woudl you rate your mood?
  • Multidimensional: How would you rate your health?

Semester 3: Mind and Movement (21 decks)

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