NMH; Lecture 5, 6, 7 and 8 - Thalamus and Hypothalamus, Sensory pathways, Motor pathways: cortical motor function, basal ganglia and cerebellum; and motor pathways: Neuromuscular and spinal c Flashcards

1
Q

<p>How is the thalamus organised?</p>

A

<p>Divided in two by the third ventricle, collection of individual nuclei with separate functions -> ispsilateral connection with forebrain, nuclei are interconnected</p>

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2
Q

<p>What is the function of the thalamus?</p>

A

<p>Relay centre between cerebral cortex and rest of CNS, integrates information and involved in virtually all functional systems</p>

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3
Q

<p>What are the 4 different thalamus nuclei?</p>

A

<p>Specific, association, intralaminar, reticular</p>

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4
Q

<p>What is the structure of the thalamus?</p>

A

<p>x</p>

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5
Q

<p>Where does each of the 4 thalamic nuclei connect to in the cortex?</p>

A

<p>Specific to primary cortical areas; association to association cortex; intralaminar to all cortical areas; reticular not connected to cortex</p>

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6
Q

<p>What are the 6 nuclei in the specific nuclei?</p>

A

<p>Ventral lateral/anterior, ventral posterolateral/posteromedial and lateral/medial geniculate</p>

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7
Q

<p>Where do the specific nuclei connect to the cortex?</p>

A

<p>x</p>

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8
Q

<p>What are the functional cortical areas which are coloured in?</p>

A

<p>x</p>

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9
Q

<p>What are the 5 nuclei in the association nuclei?</p>

A

<p>Anterior, lateral dorsal, dorsomedial, lateral posterior and pulvinar</p>

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10
Q

<p>Where do the association nuclei connect to the cortex?</p>

A
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11
Q

<p>How are the thalamic nuclei associated with RAS?</p>

A

<p>Intralaminar nuclei diffuse cortical projections, reticular nucleus diffuses intrathalamic projection -> both receiving inputs from reticular formation</p>

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12
Q

<p>What is the Reticular Activating System?</p>

A
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13
Q

<p>What is thalamic syndrome?</p>

A

<p>Sensation is reduced, exaggerated, altered; pain, emotional disturbance (Dejerine-Roussy Syndrome)</p>

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14
Q

<p>How is the hypothalamus organised?</p>

A

<p>Divided in two by third ventricle, collection of individual nuclei with separate function, largely ipsilateral connection with forebrain</p>

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15
Q

<p>What are the different hypothalamic nuclei and how are they arranged?</p>

A
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16
Q

<p>What is the function of the hypothalamus?</p>

A

<p>Coordinates homeostatic mechanisms via the ANS, ENS and controlling behaviour</p>

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17
Q

<p>What are the associated forebrain structures?</p>

A

<p>Olfactory system, limbic system</p>

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18
Q

<p>What are the parts of the limbic system?</p>

A

<p>Hippocampus, amygdala, cingulate cortex, septal nuclei</p>

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19
Q

<p>Which behaviours does the hypothalamus control?</p>

A

<p>Eating and drinking, expression of emotion, sexual behaviour, circadian rhythm, memory</p>

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20
Q

<p>What are the presenting symptoms of a hypothalamic tumour?</p>

A

<p>Polydipsia, polyuria, absent menses</p>

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21
Q

<p>What are the later symptoms of a hypothalamic tumour?</p>

A

<p>Labile emotions, rage, inappropriate sexual behaviour, memory lapses, temperature fluctuation, hyroid, adrenal cortex, gonadal function decreases, hyperphagia</p>

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22
Q

<p>How is thalamic syndrome caused?</p>

A

<p>Posterior cerebral artery stroke</p>

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23
Q

<p>What structural damage can occur to the hypothalamus?</p>

A

<p>Craniopharyngioma, other tumours (glioma, meningioma, dermoid, chordoma, hamartoma), sarcoidosis, langerhans cell histiocytosis</p>

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24
Q

<p>What are somatosensory modalities?</p>

A

<p>Conscious senses other than vision, hearing, balance, taste and smell</p>

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25
Q

<p>What are sensory receptors?</p>

A

<p>Transducers that convert energy from the env. into the neuronal action potentials -> considered as the nerve ending</p>

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26
Q

<p>What are the kind of sensory stimuli that sensory receptors pick up?</p>

A

<p>Thermal, mechanical, light and chemical</p>

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27
Q

<p>Which modalities use a mechanoreceptor?</p>

A

<p>Touch (light touch, pressure and vibration) and proprioception (Joint position, muscle length, muscle tension)</p>

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28
Q

<p>Which modalities use a thermoceptor?</p>

A

<p>Temperature</p>

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29
Q

<p>Which modalities use a nociceptor?</p>

A

<p>Pain</p>

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30
Q

<p>How do you form a sense organ with sensory receptors?</p>

A

<p>Non-neural cells</p>

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31
Q

<p>What is the difference between response to a specific stimulus in receptors in a specific sense organ compared to other receptors?</p>

A

<p>In the specific one they respond to specific stimuli at a much lower threshold than other receptors</p>

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32
Q

<p>What do receptors require to produce a response?</p>

A

<p>An aqequate or threshold stimulus</p>

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33
Q

<p>What are some examples of mechanoreceptors?</p>

A
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34
Q

<p>What is vibration detected by?</p>

A

<p>Rapidly adapting mechanoreceptors -> with each fibre type having different threshold, with receptors generating cycles of AP</p>

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35
Q

<p>What happens if thresholds overlap?</p>

A

<p>Certain vibrations may fire different fibres simultaneously</p>

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36
Q

<p>What frequency is the body most sensitive to?</p>

A

<p>250Hz</p>

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37
Q

<p>What is the frequency range for Pacinian corpuscles?</p>

A

<p>60-400Hz (peak at 250Hz)</p>

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38
Q

<p>What is the frequency range for Meissner's corpuscles?</p>

A

<p>5-300Hz with peak at 20-50Hz</p>

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39
Q

<p>What is elevation of vibratory threshold a sign of?</p>

A

<p>Neurodegeneration</p>

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40
Q

<p>What is a tickle?</p>

A

<p>Relatively mild stimulation of something moving across the skin which may be pleasurable</p>

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41
Q

<p>What causes a tickle?</p>

A

<p>Areas of the body with naked unmyelinated afferent nerve fibres</p>

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42
Q

<p>What is an itch (pruritis)?</p>

A

<p>Annoying, relieved by scratching</p>

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43
Q

<p>What causes an itch?</p>

A

<p>Local mechanical stimulation or chemical agents (histamine, kinins) -> stratching is a stimulation of large nerve fibres overwhelming the spinal transmission (closes the gate)</p>

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44
Q

<p>When does itch occur?</p>

A

<p>Neuropathy, renal failure, dermatitis</p>

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45
Q

<p>What are temperature gated channels?</p>

A

<p>Open and closes at different ranges of temperature which detection is most sensitive on face and chest</p>

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46
Q

<p>Which stimuli are detected by TRPV?</p>

A

<p>Hot temperature and chillies</p>

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47
Q

<p>Which stimuli are detected by TRPM8?</p>

A

<p>Cold and menthol</p>

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48
Q

<p>Which stimuli are detected by TRPV1?</p>

A

<p>Hot but also cold -> ice burn</p>

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49
Q

<p>What are nociceptors?</p>

A

<p>Specialised peripheral cutaneous terminals</p>

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50
Q

<p>What is the function of nociceptors?</p>

A

<p>Respond to noxious and harmful stimuli with a high threshold required for activation</p>

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51
Q

<p>What do nociceptors activate?</p>

A

<p>Directly activate ion channel proteins -> Transient Receptor Potential channels, neurotrophin, GPCR</p>

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52
Q

<p>What are some examples of stimuli detected by nociceptors?</p>

A

<p>Heat -> TRPV1, cold ->TRPM8, pH<7 -> acid sensing ion channels, intense pressure -> K+ channels</p>

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53
Q

<p>What is the commonest cutaneous nociceptor and what is its function?</p>

A

<p>Polymodal C fibre which responds to pressure, temperature and chemical stimuli</p>

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54
Q

<p>What is the commonest skeletal muscle nociceptor and what is its function?</p>

A

<p>Chemoreceptor for lactic acid</p>

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55
Q

<p>Which substances can modulate nociception?</p>

A

<p>Prostaglandin, substance P, histamine, serotonin, CGRP, bradykinin, potassium, ACh -> substances associated with inflammation and explain why its painful</p>

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56
Q

<p>What is the stimulus threshold?</p>

A

<p>Weakest stimulus detectable; adequate stimulus required to elicit specific response or reflex -> min stimulus detected >50% of time, varying in relation to anatomical location and different in different individuals</p>

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57
Q

<p>How can stimulus intensity be conveyed?</p>

A

<p>Frequency of AP generated, number of separate receptors activated -> relationship between stimulus intensity and ultimate sensory discrimination may be linear/logarithmic</p>

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58
Q

<p>What is a receptive field?</p>

A

<p>Area from which stimulus elicits neuronal response and it overlaps -> recruitment of adjacent sensory receptors with increased stimulus intensity -> increased number of A interpreted by brain as increases intensity</p>

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59
Q

<p>What is the function of the synapse?</p>

A

<p>Allows contact from neurone to muscle or from neurone to neurone -> arrangements can be simple or complex -> contact ratio ranges from 1:1 for muscle to 10^3:1 in CNS</p>

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60
Q

<p>How can the membrane potential of the post synaptic neurone be altered?</p>

A

<p>Can be made less negative called excitatory post synaptic potential; can be made more negative called inhibitory post synaptic potential (closer to threshold for firing) -> graded effects for summation (EPSPs and IPSPs can also summate)</p>

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61
Q

<p>What does the degree of summation determine?</p>

A

<p>How readily a neuron can reach threshold to produce an AP</p>

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62
Q

<p>What is a neuromuscular junction?</p>

A

<p>Specialised synapse between the motor neuron and the motor end plate, the muscle fibre cell membrane</p>

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63
Q

<p>How is the NMJ activated?</p>

A

<p>When an AP arrives at the NM, Ca infux causes ACh release and binds to receptors on motor end plate, causing ion channels to open - Na influx causes AP in muscle fibre</p>

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64
Q

<p>What are mEPP?</p>

A

<p>At rest, individual vesicles release ACh at very ow rate causing minature end-plate potentials</p>

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65
Q

<p>What are alpha motor neurones?</p>

A

<p>Lower motor neurones of the brainstem and the spinal cord</p>

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66
Q

<p>What is the function of alpha motor neurones?</p>

A

<p>Innervate the extrafusal muscle fibres of the skeletal muscle - activation causes muscle contraction; motor neurone pool contains all alpha motor neurones innervating a single muscle</p>

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67
Q

<p>What is the motor unit?</p>

A

<p>Single motor neurone together with all the muscle fibres that it innervates -> smallest functional unit with which to produce force -> on average each otor neurone supplies about 600 muscle fibres - stimulation of one motor unit causes contraction of all muscle fibres in that unit</p>

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68
Q

<p>What are the 3 types of motor units?</p>

A

<p>Slow (S, type I), Fast/fatigue resistant (FR, type IIA) and Fast//fatigueable (FF, type IIB)</p>

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69
Q

<p>What are the characteristics of a slow type I motor unit (cell bodies, dendrites, axons and conduction velocity)?</p>

A

<p>Smallest diameter cell bodies with small dendritic trees, thinnest axons and slowest conduction velocity</p>

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70
Q

<p>What are the characteristics of a FR type IIA motor unit (cell bodies, dendrites, axons and conduction velocity)?</p>

A

<p>Larger diameter cell bodies, larger dendritic trees, thicker axons, faster conduction velocity</p>

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71
Q

<p>What are the characteristics of a FF type IIB motor unit (cell bodies, dendrites, axons and conduction velocity)?</p>

A

<p>Larger diameter cell bodies, larger dendritic trees, thicker axons, faster conduction velocity</p>

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72
Q

<p>How can the 3 motor unit types be classified?</p>

A

<p>By amount of tension generated, speed of contraction and fatiguability of the motor unit</p>

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73
Q

<p>What are the 2 mechanisms by which the brain regulates force that a single muscle can produce?</p>

A

<p>Recruitment and rate coding</p>

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74
Q

<p>What is recruitment (regulation of muscle force)?</p>

A

<p>Motor units aren't randomly recruited -> governed by the size principle, where smaller units are recruited first (slow twitch units) and as more force is required, more units are recruited allowing fine control under which low force levels are required</p>

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75
Q

<p>What is rate coding (regulation of muscle force)?</p>

A

<p>Motor unit can fire at a range of frequencies and slow units fire at lower frequencies -> as firing rate increases, force produced by unit increases; summation occurs when units fire at frequency too fast to allow muscle to relax between arriving action potentials</p>

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76
Q

<p>What are neurotrophic factors?</p>

A

<p>Type of growth factor, preventing neuronal death; promotes growth of neurones after injury</p>

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77
Q

<p>What is the effect of neurotrophic factors?</p>

A

<p>Motor unit and fibre characteristics are dependent on innervating nerve -> if fast twitch muscle and slow muscle are cross innervated, soleus becomes fast and FDL become slow -> motor neurone has some effect on properties of muscle fibres which it innervates</p>

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78
Q

<p>How can the fibre types of the motor units change and which types change under which conditions?</p>

A

<p>Type IIA/IIB change following training; type I/II in cases of severe deconditioning/spinal cord injury; microgravity during spaceflight results in shift from slow to fast muscle fibres; ageing is associated with loss of TI/II fibres but also preferential loss of tII fibres which results in larger proportion of tI fuibres in aged muscle (evidence from slower contraction times)</p>

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79
Q

<p>How are the motor tracts in the spinal cord organised?</p>

A
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80
Q

<p>What is a reflex?</p>

A

<p>Automatic and often inborn response to stimulus that involves a nerve impulse passing inward from receptor to nerve centre and then outward to effector without reaching level of consciousness; involuntary coordinated pattern of muscle contraction and relaxation elicited by peripheral stimuli</p>

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81
Q

<p>What are the components of a reflex arc?</p>

A

<p>Sensory receptor, sensory neuron, integrating centre, motor neurone, effector</p>

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82
Q

<p>What is the monosynaptic reflex (stretch)?</p>

A
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83
Q

<p>What is the Hoffman Reflex?</p>

A
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84
Q

<p>What is the flexion withdrawal polysynaptic reflex?</p>

A
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85
Q

<p>What is the flexion withdrawal and crossed extensor?</p>

A
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86
Q

<p>?What is the Jendrassik manoeuvre?</p>

A

<p>? Influencing reflexes by e.g. clenching teeth or making fist when patellar tendon is being tapped</p>

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87
Q

<p>What kind of regulation can the higher centres of CNS exert upon stretch reflex?</p>

A

<p>Inhibitory and excitatory regulation; with inhibitory control dominating in normal conditions, and decerebration revealing excitatory control from supraspinal areas -> rigidity and spasticity can result from brain damage giving overactive/tonic stretch reflex</p>

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88
Q

<p>How do higher centres influence reflexes - and which higher centres/pathways are involved?</p>

A

<p>1) Activating alpha motor neurons
2) Activating inhibitory interneurons
3) Activating propriospinal neurons
4) Activating gamma motor neurons
5) Activating terminals of afferent fibres;
Cortex (corticospinal), red nucleus (rubrospinal), vestibular nuclei (vestibulospinal), tectum (tectospinal)</p>

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89
Q

<p>What is the function of the corticospinal, rubrospinal, vestibulospinal, tectospinal control of reflexes?</p>

A

<p>Corticospinal - Fine control of limb movement, body adjustments; rubrospinal - Automatic movements of arm in response to posture/balance changes; vestibulospinal - Altering posture to maintain balance; tectospinal - head movements in response to visual information</p>

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90
Q

<p>What is the gamma reflex loop?</p>

A

<p>If the knee is extended and the muscle goes slack; the spindle is shortened to maintain its sensitivity</p>

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91
Q

<p>What is hyperreflexia?</p>

A

<p>Loss of descending inhibition after the reflex -> can be due to a stroke</p>

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92
Q

<p>What is clonus hyperreflexia?</p>

A

<p>x</p>

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93
Q

<p>What is the Babinski sign (hyperreflexia)?</p>

A

<p>x</p>

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94
Q

<p>What is hyporeflexia?</p>

A

<p>Below normal/absent reflexes; mostly associated with lower motor neuron diseases</p>

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95
Q

<p>What is functional segregation?</p>

A

<p>The motor system is organised in a number of different areas that control different aspects of movement</p>

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96
Q

<p>What is hierarchical organisation?</p>

A

<p>High order areas of hierarchy are involved in more complex tasks (programme and decide movements, coordinate muscle activity); lower areas of hierarchy perform lower level tasks (execution of movement)</p>

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97
Q

<p>What is the motor system hierarchy?</p>

A
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98
Q

<p>What are the three different areas of the frontal lobe anterior to the central sulcus?</p>

A

<p>Primary motor cortex (M1/Broadmann's area 4), Premotor cortex (Broadmann's area 6), Supplementary motor area (Broadmann's area 6)</p>

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99
Q

<p>Where is the primary motor cortex/Broadmann's area 4 located?</p>

A

<p>Frontal lobe on precentral gyrus, anterior to central sulcus</p>

100
Q

<p>What is the function of the primary motor cortex?</p>

A

<p>Controls fine, discrete, precise voluntary movements -> provides the descending signals to execute movements</p>

101
Q

<p>What is a characteristic cell in the primary motor cortex?</p>

A

<p>Betz cells present in layer V (grey matter)</p>

102
Q

<p>What are the 2 types of neurotransmission and what kind of transmission are they?</p>

A

<p>AP - generation and propagation along axon is electrical; Impulse - transmission is chemical, mediated by NT</p>

103
Q

<p>Where is glutamate a NT in the CNS?</p>

A

<p>From upper to lower motor neurons</p>

104
Q

<p>Where is ACh a NT in the CNS?</p>

A

<p>From lower motor neurones to muscles</p>

105
Q

<p>What kind of motor control does the primary motor cortex control?</p>

A

<p>Contralateral motor control</p>

106
Q

<p>How is the primary motor cortex somatotopically organised?</p>

A

<p>Motor homunculus</p>

107
Q

<p>Where is the premotor cortex located?</p>

A

<p>Frontal lobe, anterior to PMC</p>

108
Q

<p>What is the function of the premotor cortex?</p>

A

<p>Involved in planning movements - regulates externally cued movements (reaching out for an apple required moving body part relative to another body part (intrapersonal space), and movement of the body in the environment (extrapersonal space)</p>

109
Q

<p>What is the function of the supplementary motor area?</p>

A

<p>Planning complex movements, programming sequencing of movements - regulates internally driven movements (speech); Becomes active when thinking about a movement before executing that movement</p>

110
Q

<p>Where is the supplementary motor area located?</p>

A

<p>Frontal lobe, anterior to PMC - medially</p>

111
Q

<p>What are the parts of the association cortex?</p>

A

<p>Posterior parietal cortex - ensures movements are targeted accurately to objects in external space; Prefrontal cortex - involved in selection of appropriate movements for a particular course of action</p>

112
Q

<p>What are the different kind of motor neurone lesions?</p>

A

<p>Upper motor neurone lesion, lower motor neurone lesion</p>

113
Q

<p>What are the negative signs of an upper motor neurone lesion?</p>

A

<p>Loss of function - Paresis and paralysis</p>

114
Q

<p>What is paresis?</p>

A

<p>Graded weakness of movements</p>

115
Q

<p>What is paralysis?</p>

A

<p>Complete loss of muscle activity</p>

116
Q

<p>What are the positive signs of upper motor neuron lesions?</p>

A

<p>Increased abnormal function due to loss of inhibitory descending inputs - spasticity, hyperreflexia, clonus, babinski's sign</p>

117
Q

<p>What is spasticity?</p>

A

<p>Increased muscle tone</p>

118
Q

<p>What is hyperreflexia?</p>

A

<p>Exaggerated reflexes</p>

119
Q

<p>What is clonus?</p>

A

<p>Abnormal oscillatory muscle contraction</p>

120
Q

<p>What is Babinski's sign?</p>

A
121
Q

<p>How would the symptoms present in an upper motor neurone lesion?</p>

A

<p>x</p>

122
Q

<p>What is apraxia?</p>

A

<p>Disorder of skilled movement, where patients aren't paretic but have lost information about how to perform skilled movements</p>

123
Q

<p>What causes apraxia?</p>

A

<p>Lesion of inferior parietal lobe, frontal lobe (in premotor cortex or supplementary motor area) -> any disease in these areas cause apraxia but stroke and dementia are the most common causes</p>

124
Q

<p>What are the symptoms of a lower motor neurone lesion?</p>

A

<p>Weakness, hypotonia, hyporeflexia, muscle atrophy, fasciculations, fibrillations</p>

125
Q

<p>What are fasciculations?</p>

A

<p>Damaged motor units produce spontaneous AP, resulting in a visible twitch</p>

126
Q

<p>What are fibrillations?</p>

A

<p>Spontaneous twitching of individual muscle fibres, recorded during needle electromyography examination</p>

127
Q

<p>What is motor neurone disease?</p>

A

<p>Progressive neurodegenerative disorder fo the motor system with spectrum of disorders - refers to amyotrophic lateral sclerosis</p>

128
Q

<p>What are the upper motor neuron signs in MND?</p>

A

<p>Increased muscle tone (spasticity of limbs and tongue), brisk limbs and jaw reflexes, Babinski's sign, loss of dexterity, dysarthria, dysphagia</p>

129
Q

<p>What are the lower motor neuron signs in MND?</p>

A

<p>Weakness, muscle wasting, tongue fasciculations and wasting, nasal speech, dysphagia</p>

130
Q

<p>What is the function of the side loops in the motor hierarchy?</p>

A

<p>Help the cortical areas involved movement control to regulate the motor behaviour (PMC to execute movements, PC+SMA to plan movements, association cortex for selection and accuracy of movements)</p>

131
Q

<p>What is the anatomy of the basal ganglia?</p>

A

<p>Striatum (caudate and putamen), Globus pallidus externa (GPe) and globus pallidus interna (GPi), Substantia nigra pars compacta (SNc) andpars reticulata (SNr), Subthalamic nucleus (STN)</p>

132
Q

<p>What is the function of the basal ganglia?</p>

A

<p>Elaborating associated movements, moderating and coordinating movement (suppressing unwanted movements), performing movements in order</p>

133
Q

<p>What is the circuit of the basal ganglia?</p>

A

<p>Direct pathway is no projection to STN with overall excitatory effect on motor cortex; indirect pathway projection to STN and overall inhibitory effect on motor cortex -> normal functioning of basal ganglia needs balance of both</p>

134
Q

<p>What are the main NT in the basal ganglia circuit?</p>

A

<p>DA, glutamate and ACh are excitatory and GABA is inhibitory</p>

135
Q

<p>Which cortex and side of the body do the basal ganglia mediate function of?</p>

A

<p>Ipsilateral cortex so it is uncrossed but since PMC controls contralateral body, BG affects movements of contralateral body</p>

136
Q

<p>What are the 2 classes of syndromes that are caused due to damage to the basal ganglia?</p>

A

<p>Hypokinetic (Parkinson's) and hyperkinetic (Huntington's)</p>

137
Q

<p>What is Parkinson's disease?</p>

A

<p>Neuronal degeneration of substantia nigra pars compacta -> 80% DA cells</p>

138
Q

<p>How does the basal ganglia circuit work in hypokinetic disorders?</p>

A

<p>Degeneration of DA in SNc causes loss of nigro-striatal DAergic axons in caudate and putamen; disruption of fine balance of excitation and inhibition; reduction of the excitation of motor cortex</p>

139
Q

<p>What are the main signs of Parkinson's disease?</p>

A

<p>Bradykinesia (slowness of movements), hypomimic face (expressionless, mask like), akinesia (difficulty in initiation of movements because cannot initiate movements internally), rigidity (muscle tone increase, causing resistance to externally imposed joint movements), tremor at rest (4-7Hz) starts in one hand and with time spreads to other parts of the body; Parknson's gait (walking slow, small steps, shuffling feet, reduced arm swing); stooped posture (head and body bent forward and downward)</p>

140
Q

<p>What is Huntington's disease?</p>

A

<p>Neurodegenerative genetic disorder - abnormality in chromosome 4, autosomic dominant -> degeneration of GABAergic neurons in striatum: caudate first and putamen later</p>

141
Q

<p>How does the basal ganglia circuit work in hyperkinetic disorders?</p>

A

<p>Degeneration of GABAergic neurons in the striatum; disruption of the fine balance between inhibition and excitation; motor cortex gets excessive excitatory input; motor cortex continuously sends involuntary commands for movements and movements sequences to the muscles</p>

142
Q

<p>What are the main signs of Huntington's disease?</p>

A

<p>Choreic movements (rapid jerky involuntary movements of the body, with hands and face affected first; then legs and rest of body); speech impairment; difficulty swallowing; unsteady gait; and later on cognitive decline and dementia</p>

143
Q

<p>What is the cerebellum?</p>

A

<p>Horizontally divided into 3 lobes: Ant, post, flocculonodular and sagitally divided into 3 zones: vermis, intermediate hemisphere and lateral hemisphere</p>

144
Q

<p>How is the cerebellum connected with the body and the cortex?</p>

A

<p>Connections of cerebellum are with same side of body and opposite cerebral hemisphere</p>

145
Q

<p>What are the main NT in the cerebellum?</p>

A

<p>Glutamate (+) and GABA (-)</p>

146
Q

<p>What is the vestibulocerebellum?</p>

A

<p>Flocculonodular lobe or vestibulocerebellum, which is connected with the vestibular system</p>

147
Q

<p>What is the function of the vestibulocerebellum?</p>

A

<p>Regulation of gait, posture and equilibrium; coordination of head movements with eye movements</p>

148
Q

<p>What is the spinocerebellum?</p>

A

<p>Spinal afferents from axial portions of the body, trigeminal, visual and auditory inputs, project to the vermis; spinal afferents from the limbs project to the intermediate hemisphere</p>

149
Q

<p>What is the function of spinocerebellum?</p>

A

<p>Coordination of speech, adjustment of muscle tone, coordination of limb movements</p>

150
Q

<p>What is the cerebrocerebellum?</p>

A

<p>x</p>

151
Q

<p>What is the function of the cerebrocerebellum?</p>

A

<p>Coordination of skilled movements; cognitive function, attention, processing of language, emotional control</p>

152
Q

<p>What is the function of the cerebellum?</p>

A

<p>Maintenance of balance and posture, coordination of voluntary movements; motor learning; cognitive functions (language)</p>

153
Q

<p>How does the cerebellum maintain balance and posture?</p>

A

<p>Makes postural adjustments in order to maintain balance, modulates commands to motor neurons to compensate for shifts in body position</p>

154
Q

<p>How does the cerebellum coordinate voluntary movements?</p>

A

<p>Coordinates timing and force of different muscle groups to produce smooth body movements</p>

155
Q

<p>What is lateral inhibition and how does it work in receptive fields?</p>

A

<p>Activation of one neural unit which inhibits activation of other units; facilitating pinpoint accuracy in localisation of stimulus</p>

156
Q

<p>What is two-point discrimination?</p>

A

<p>Ability to detect that 2 stimuli are distinct from each other</p>

157
Q

<p>What is the two-point threshold?</p>

A

<p>Minimum distance required between 2 stimuli in order to perceive that they are 2 separate stimuli</p>

158
Q

<p>What does 2-point discrimination depend on?</p>

A

<p>Peripheral mechanoreceptors, spinal posterior column, cortical function</p>

159
Q

<p>How does magnitude of 2-point discrimination vary in the body?</p>

A

<p>65mm on back and 2mm on fingers</p>

160
Q

<p>What is the 2 point discrimination related to?</p>

A

<p>Density of innervation, area of receptive field, sensory homunculus</p>

161
Q

<p>What is neural adaptation?</p>

A

<p>Form of desensitisation, where if a stimulus of constant strength is maintained for a period of time, the frequency of AP diminishes; variable between types of neurones/receptors</p>

162
Q

<p>How fast is neural adaptation in phasic and tonic receptors?</p>

A

<p>Phasic = rapidly adaptive
Tonic = slowly adaptive; alows ability to differentiate meaningful from irrelevant information</p>

163
Q

<p>What are the different fibre types and their functions of nerve fibres?</p>

A

<p>x</p>

164
Q

<p>What is the involvement of cortical neurones in pain pathways?</p>

A

<p>In perception and interpretation of pain</p>

165
Q

<p>What is the involvement of thalamic neurones in pain pathways?</p>

A

<p>Ventrobasal complex and nucleus reticularis have important reciprocal roles in modulation of nociceptive signals</p>

166
Q

<p>What is the involvement of superficial dorsal horn neurones in pain pathways?</p>

A

<p>Crucial role in processing nociceptive signals</p>

167
Q

<p>What are the ascending pathways in the spinal tract?</p>

A

<p>Touch and proprioception; pain and temperature</p>

168
Q

<p>How are touch and proprioception laterally inhibited?</p>

A

<p>Interneurones within dorsal horn of spinal cord, facilitating enhanced sensory perception</p>

169
Q

<p>How does touch and proprioception ascend the spinal cord?</p>

A

<p>Dorsal column (Lemniscal system), decussation (crossing) in brainstem, somatotopy throughout pathway, lateral inhibition in dorsal column nuclei</p>

170
Q

<p>How does pain and temperature ascend the spinal cord?</p>

A

<p>Spinothalamic tract, decussation in spinal cord via interneurones, somatotopy throughout pathway; consider in spinal cord injury; Brown-Sequard syndrome: hemisection of spinal cord</p>

171
Q

<p>How are spinal neurones modulated?</p>

A

<p>By interneurones and descending inhibitory controls but respond to peripheral stimuli -> cortical response may not match peripheral input</p>

172
Q

<p>What is glutamate and what is its function?</p>

A

<p>Major excitatory synaptic NT, activates multiple receptor classes (AMPA, NMDA, mGluR), activates NMDAr by removing Mg plug</p>

173
Q

<p>What is the function of NMDAr?</p>

A

<p>NMDAr activation causes large Ca2+ influx leading to multiple intracellular actions; LTP of NMDAr may occur so hypersensitivity to pain happens, but NMDAr antagonists can relieve pain -> ketamine: strong painkiller, dissociative analgesia, battlefield anaesthetic, drug of abuse</p>

174
Q

<p>What is the gate control theory?</p>

A

<p>Non-painful stimulation can inhibit transmission of pain from periphery to brain -> rubbing elbow after banging t, spinal cord stimulation -> small Adelta and C fibres transmit painful stimuli and large Abeta fibres can transmit non-noxious stimuli; large Abeta fibres can prevent or reduce transmission of A delta and C fibres within the dorsal horn of the spinal horn of the spinal cord -> by activating inhibitory interneurones delta GABAa receptor</p>

175
Q

<p>What is the dorsal root ganglion?</p>

A

<p>Central spinal structure surrounded by dural sheath, bathed in minimal CSF -> nerve rootlets form a central dorsal nerve root that forms the ganglion</p>

176
Q

<p>What happens with neuronal dysfunction associated with channelopathy?</p>

A

<p>May result in depolarisation in response to minor stimuli</p>

177
Q

<p>How can the dorsal root ganglion be targeted therapeutically?</p>

A

<p>X-ray guarded techniques -> transforaminal epidural, nerve root block, neuromodulation</p>

178
Q

<p>What is the effect of electrical field stimulation on dorsal root ganglion neuronal function?</p>

A

<p>Can reduce frequency and amplitude of AP, compensates for neuronal dysfunction, useful neuropathic pain</p>

179
Q

<p>What is neuromodulation?</p>

A

<p>Non-painful stimulation can inhibit the transmission of pain from periphery to brain -> spinal cord stimulation and dorsal root ganglion stimulation; large Abeta fibres transmit non-noxious stimuli and can prevent/reduce transmission of Adelta ad C fibres within the dorsal horn of the spinal cord, closing the gate, compensates for neuronal dysfunction and can be useful in neuropathic pain</p>

180
Q

<p>How are the sensory pathways somatotopically organised?</p>

A

<p>Dorsal horns of spinal cord -> Rexed Laminae I-VII -> lamina II is substantia genlatinosa -> large myelinated Abeta(Aalpha) [mechanical stimuli LIII-VI], small myelinated Adelta [cold and fast pain nociception LI-LII], small unmyelinated C-fibres [pain and temp LI-II], projection neurones from LI which are parabrachial area/periaqueductal grey, interneurones connect between different laminae, wiide dynamic range neurones project from LV to thalamus via spinothalamic tract</p>

181
Q

<p>What is descending modulation?</p>

A

<p>Pain pathway neurones aren't inert until noxious stimulus occurs which means its always active -> physiological monitoring system; descending pathways from brainstem structures can have inhibitory/excitatory infuence on spinal nociceptive transmission -> mediated by spinal 5HT3, NA, GABAa and glycine receptors.
Loss of physiological inhibition may result in pathological hypersenisitivity</p>

182
Q

<p>What are the regions of the cerebral cortex?</p>

A
183
Q

<p>How is the cortex somatotopically organised?</p>

A

<p>Point by point representation of entire body on cortex</p>

184
Q

<p>What are the key somatosensory areas?</p>

A

<p>SI-> primary somatosensory cortex in postcentral gyrus, SII -> secondary somatosensory cortex in parietal operculum, posterior parietal cortex</p>

185
Q

<p>What is the association cortex?</p>

A

<p>Areas outside primary areas -> essential for complex mental functions and is the most developed part of the brain</p>

186
Q

<p>What is the cortical homunculus?</p>

A
187
Q

<p>Where is pain felt in the brain?</p>

A

<p>Cortices -> SI, SII, insular, anterior cingulate, prefrontal; brainstem, amygdala, cerebellum</p>

188
Q

<p>What is pain?</p>

A

<p>An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage -> NB: is subjective</p>

189
Q

<p>What is the function of pain?</p>

A

<p>Sign that something is wrong, associated with tissue damage -> has protective function</p>

190
Q

<p>Which fibres used for pain?</p>

A

<p>Fast = Adelta; slow =C fibres</p>

191
Q

<p>What are the types of pain?</p>

A

<p>Nociceptive (tissue damage = acute), muscle (lactic acidosis, ischaemia), superficial somatic (well-localised), visceral (deep and poorly localised), referred (from internal organ/structure = angina), neuropathic (dysfunction of NS)</p>

192
Q

<p>How do we feel pain?</p>

A

<p>Rene Descartes- pathology > nerve ending > neural impulse > spinal cord > brain > pain; Depolarisation > AP in afferent nerve > dorsal horn of spinal cord > brain.
Pain has underlying pathological cause</p>

193
Q

<p>What is WHO analgesic ladder?</p>

A

<p>3 step ladder for cancer pain relief in adults, which has been adopted for use in acute pain and chronic pain; controversial</p>

194
Q

<p>What medication is taken in the WHO analgesic ladder?</p>

A

<p>Paracetamol and Aspirin (Ibuprofen) > codeine and tramadol > morphine; adjuvant can be anything and drugs given by the clock no on demand</p>

195
Q

<p>What are the causes of myalgia?</p>

A

<p>Metabolic, overuse, stretching, tension, compression, ischaemia, tearing, viral infection, fibromyalgia, angina</p>

196
Q

<p>What are the features of muscle pain?</p>

A

<p>Aching, burning (lactic acidosis), cramping, tightness, crushing, tenderness</p>

197
Q

<p>What are the causes of superficial/cutaneous pain?</p>

A

<p>Type of nociceptive pain, related to skin, pressure, too hot/cold, inflammation, injury, infection, burns</p>

198
Q

<p>What are the features of somatic pain?</p>

A

<p>Often well-localised, sharp, stinging, aching, burning, throbbing, tightness, sensitive</p>

199
Q

<p>What are the dermatomes?</p>

A
200
Q

<p>What is visceral pain?</p>

A

<p>Pain arsing from internal organs/viscera (heart, oesophagus, stomach, duodenum, gallbladder, pancreas, colon</p>

201
Q

<p>How are the viscera innervated?</p>

A

<p>Low density of sensory innervation so vague, diffuse and poorly localised pain/sensation -> characteristically midline pain at level of sternum/epigastrum so not able to reliably differentiate one organ's pain from another; viscero-visceral crosstalk</p>

202
Q

<p>What symptoms are associated with visceral pain?</p>

A

<p>Autonomic symtpoms - referred pain; visceral hyperalgesia may occur where neural sensitisation occurs resulting in IBS, dysmenorrhoea, refractory angina -> multimodal treatment</p>

203
Q

<p>What is referred pain?</p>

A

<p>Occurs at sites of body wall whose innervation enters spinal cord at same level as organ's -> sharper, better localised than visceral pain</p>

204
Q

<p>What can be associated with referred pain and what is an example?</p>

A

<p>Hyperalgesia -> angina is a good example</p>

205
Q

<p>What are wide dynamic range neurones?</p>

A

<p>Receive input from Ab, Ad and C fibres, responding to full range of stimuli (touch, heat,chemical); fire APs in graded fashion -> exhibit wind-up</p>

206
Q

<p>What is the wind up phenomenon?</p>

A

<p>Short lasting synaptic plasticity, repetitive stimulation of WDRs induces increased evoked response and post discharge with each stimulus -> may precipitate long term potentiation with both related to neuropathic sensitisation</p>

207
Q

<p>What is Long-term potentiation?</p>

A

<p>long-lasting increase in efficacy of synaptic transmission</p>

208
Q

<p>What is peripheral and central sensitisation?</p>

A
209
Q

<p>What is neuropathic pain?</p>

A

<p>Pain in area of neurological dysfunction with sharp, burning, electric shocks, squeezing and poor response to usual analgesic drugs -> can last after area has healed completely</p>

210
Q

<p>What is allodynia?</p>

A

<p>Pain due to a stimulus that doesn't normally provoke pain</p>

211
Q

<p>What is hyperalgesia?</p>

A

<p>Increased pain from a stimulus that normally provokes pain</p>

212
Q

<p>What is sensitisation?</p>

A

<p>Increased responsiveness of nociceptive neurons to their normal input</p>

213
Q

<p>What is hypoalgesia?</p>

A

<p>Diminished pain in response to a normally painful stimulus</p>

214
Q

<p>What is hyperpathia?</p>

A

<p>Painful syndrome characterised by an abnormally painful reaction to a stimulus (esp. repetitive) as well as increased threshold</p>

215
Q

<p>What is paraesthesia?</p>

A

<p>Abnormal sensation, whether spontaneous or evoked</p>

216
Q

<p>What is dysaethesia?</p>

A

<p>Unpleasant abnormal sensation, whether spontaneous or evoked</p>

217
Q

<p>How do you diagnose and assess neuropathic pain?</p>

A
218
Q

<p>What are examples of neuropathic pain?</p>

A

<p>Complex Regional Pain syndrome, Phantom limb pain, chronic scar hypersensitivity/postsurgical pain, post herpetic neuralgia, central post stroke pain, radicular low back pain, diabetic neuropathy, chemotherapy induced neuropathy</p>

219
Q

<p>What is complex regional pain syndrome?</p>

A

<p>Severe form of neuropathic pain; neurogenic inflammation, overexpression of nociceptive endings</p>

220
Q

<p>How is complex regional pain syndrome diagnosed?</p>

A

<p>IASP Budapest Criteria: Sensory - hyperaesthesia/allodynia; vasomotor - temperature asymmetry/ skin colour changes/ asymmetry; sudomotor/oedema - oedema, sweating changes, asymmetry; motor/trophic - decreased range of motion, motor dysfunction (weakness, tremor, dystonia), trophic changes (hair, nail, skin)</p>

221
Q

<p>How can you treat or rehabilitate complex regional pain syndrome patients?</p>

A

<p>MDT rehab: Physio, Occ Therapy, Psychology, Pain Managment Prog; meds, spinal cord stimulation (nerve blocks)</p>

222
Q

<p>What is phantom limb pain?</p>

A

<p>Up to 80% of amputees have PL sensations, where 1/2 are painful -> may be associated with stump neuroma</p>

223
Q

<p>What can phantom limb also affect?</p>

A

<p>Eyes, breasts and genitals -> associated with remapping of brain</p>

224
Q

<p>What is the treatment for phantom limb pain?</p>

A

<p>Medication, mirror therapy, neuroma, excision, 8% capsaicin patches</p>

225
Q

<p>What occurs to cortical remapping in phantom limb pain?</p>

A

<p>There is displacement of lip representation in primary motor and somatosensory cortex correlated to intensity of phantom limb pain</p>

226
Q

<p>What are the different kind of medications that can be given for neuropathic pain?</p>

A

<p>Antidepressants (Amitriptyline, Nortiptyline, Duloxetine), anticonvulsants (Gabapentin, pregabalin), opioid trial (Tramadol, Buprenorphine, methadone, morphine), hybrid (Tapentadol), topical (5% lidocaine, Capsaicin 0.075% cream and 8% patches)</p>

227
Q

<p>How do you treat pharmacologically neuropathic pain?</p>

A

<p>Can't give just NSAIDs and opioids -> NNT is 3/4 for most dugs in chronic neuropathic pain; with response defined as 30-50% less pain; generally safe with dose titration needed for efficacy vs tolerability -> need a month trial as delayed response occurs</p>

228
Q

<p>What is the first line treatment of Chronic Neuropathic pain?</p>

A

<p>TCA, SNRI, alpha-2-delta ligands (gabapentin)</p>

229
Q

<p>What is the second line treatment of Chronic Neuropathic pain?</p>

A

<p>Opioids and Tramadol</p>

230
Q

<p>What is the third line treatment of Chronic Neuropathic pain?</p>

A

<p>Membrane stabilisers, NMDA antagonists, Capsaicin</p>

231
Q

<p>What are Qutenza patches?</p>

A

<p>Medicated patches impregnated with 8% Capsaicin -> compound that give chilli peppers their kick</p>

232
Q

<p>How are Capsaicin patches administered?</p>

A

<p>Applied to skin for a single 60-min application in hospital and can be repeated after 3-4 months</p>

233
Q

<p>Why are 8% patches of Capsaicin used as opposed to the 0.075% cream?</p>

A

<p>Cream is effective but has poor compliance; excellent compliance with patches and very minimal side effects -> can work in patients where nothing else works -> can get ling benefit from single treatment</p>

234
Q

<p>How do capsaicin 8% patches work?</p>

A

<p>Capsaicin binds TRPV1 receptor on nerve endings - previously thought to only desensitise the receptor directly but has direct toxicity to mitochondria -> kind of haircut/pruning mechanism</p>

235
Q

<p>What is the clinical pathway for high strength capsaicin patch therapy?</p>

A

<p>Must have peripheral NP (allodynia/hyperalgesia)</p>

236
Q

<p>What is vestibulocerebellar or flocculonodular lobe syndrome?</p>

A

<p>Damage (tumour) causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)</p>

237
Q

<p>What is spinocerebellar syndrome?</p>

A

<p>Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abnormal gait and stance (wide-based)</p>

238
Q

<p>What is Cerebrocerebellar/lateral cerebellar syndrome?</p>

A

<p>Damage affects mainly arms/skilled coordinated movements (tremor) and speech</p>

239
Q

<p>What are the main signs of cerebellar disorders?</p>

A

<p>Deficits only apparent upon movements -> ataxia, dysmetria, intention tremor, dysdiadochokinesia, scanning speech</p>

240
Q

<p>What is a hereditary and acquired example of a cerebellar disorder?</p>

A

<p>Friedreich's ataxia (hereditary), MS (acquired)</p>

241
Q

<p>What is ataxia?</p>

A

<p>General impairments in movement coordination and accuracy with disturbances in posture/gait (wide based, drunken gait)</p>

242
Q

<p>What is dysmetria?</p>

A

<p>Inappropriate force and distance for target-directed movements (knocking over a cup rather than grabbing it)</p>

243
Q

<p>What is an intention tremor?</p>

A

<p>Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)</p>

244
Q

<p>What is dysdiadochokinesia?</p>

A

<p>Inability to perform rapidly alternating movements (rapidly pronating and supinating hands and forearms)</p>

245
Q

<p>What is scanning speech?</p>

A

<p>Staccato, due to impaired coordination of speech muscles</p>