Pain Flashcards
(136 cards)
1
Q
What is pain
A
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
2
Q
What are the two aspects pain can be divided into
A
Sensory-discriminative aspects: the location, intensity, and quality of the noxious stimulation.
Affective-motivational aspects: the unpleasant feeling, the fear and anxiety, and the autonomic activation that accompany exposure to a noxious stimulation
3
Q
How can hypnosis affect pain?
A
It might alleviate pain by decreasing the activity of brain areas involved in the experience of suffering
4
Q
What is pain without unpleasantness called?
A
Asymbolia
5
Q
What is asymbolia?
A
Patients with lesions in the anterior cingulate or insular cortex who perceive noxious stimuli as painful and can distinguish sharp from dull and identify the location and intensity but fail to display the appropriate emotional response
They perceive the noxious stimuli but fail to display the emotional response
6
Q
what is the false alarm theory of Ramachandran
A
When the insular cortex is damaged, patients giggle in response to pain, presumably because they can still sense the pain (‘danger’) but the pain is no longer aversive (‘false alarm’), thereby fulfilling the two key requirements for laughter.
7
Q
what is social pain
A
The unpleasant experience that is associated with actual or potential damage to one’s sense of social connection or social value
8
Q
what region of the brain mediates the emotional distress of pain
A
anterior cingulate cortex
9
Q
Does social rejection cause similar reactions as physical pain?
A
yes, social rejection activates the anterior cingulate cortex which mediates emotional distress of pain from physical damage
10
Q
What is nociception? What are nociceptors? Free nerve endings?
A
Nociception: the sensory neural processes of encoding and processing noxious stimuli, depends on specifically dedicated receptors and pathways distinct from the sensory processing of ordinary mechanical stimulation
Nociceptor: The unspecialized free nerve cell endings that respond to stimuli that produce tissue damage and initiate the sensation of pain
Free nerve ending: an axon that terminates in the skin without any specialized cell associated with it and that detects pain and/or changes in temperature
11
Q
What is a receptor cell
A
A specialized cell that responds to a particular energy or substance in the internal or external environment and converts energy into a change in the electrical potential across its membrane
12
Q
What are labeled lines
A
the concept that each nerve input to the brain reports only a particular type of information
13
Q
What is sensory transduction
A
The process in which a receptor cell converts the energy in a stimulus into a change in electrical potential across its membran
14
Q
What is a receptor potential
A
Also called generator potential. A local change in the resting potential of a receptor cell that mediates between the impact of stimuli and the initiation of action potentials.
15
Q
Describe the receptor type, axon type, diameter, and conduction speed of proprioception
A
Receptor type: Muscle spindle
Axon type: A alpha
Diameter: 13-20
Conduction speed: 80-120
16
Q
Describe the receptor type, axon type, diameter, and conduction speed of touch
A
Receptor type: Pacinian corpuscles, Ruffini’s endings, Merkel’s discs, Meissner’s corpuscles
Axon type: A beta
Diameter: 6-12
Conduction speed: 35-75
17
Q
Describe the receptor type, axon type, diameter, and conduction speed of pain and temperature
A
Receptor type: Free nerve endings
Axon type: A delta
Diameter: 1-5
Conduction speed: 5-30
18
Q
Describe the receptor type, axon type, diameter, and conduction speed of temperature, pain, and itch
A
Receptor type: Free nerve endings
Axon type: C
Diameter: 0.2-1.5
Conduction speed: less than 1
19
Q
Which primary afferent fibres carry first pain? Which one carries second pain?
A
Thinly myelinated fibres carry first pain (A delta)
Unmyelinated fibres carry second pain (C fiber)
20
Q
Describe the pathway of transduction of nociceptive signals
A
Noxious stimuli are transduced into electrical activity at peripheral terminals of nociceptors by specific receptors. This activity is conducted to the spinal cord and after transmission to the cortex where the sensation of pain is experienced
21
Q
Describe the TRP channel activation pathway
A
Bradykinin (BK) binds to G protein-coupled receptors on the surface of primary afferent neurons to activate phospholipase C (PLC), leading to the hydrolysis of membrane phosphatidylinositol bisphosphate (PIP2), the production of inositol 1,4,5-trisphosphate (IP3), and the release of Ca2+ from intracellular stores. Hydrolysis also results in the activation of protein kinase C (PKC) which regulates TRP channel activity. The TRPV1 channel is sensitized, leading to channel opening and Ca2+ influx.
22
Q
Order the following channels from lowest temperature to highest
TRPV1, TRPV2, TRPV3, TRPV4, TRPA1, TRPM8
A
TRPA1:
TRPM8:
TRPV4:
TRPV3:
TRPV1:
TRPV2:
23
Q
What activates TRPV1
A
Capsaicin
24
Q
What temperatures do TRPM8, TRPV1, and TRPM3 detect? Which fibres do they transmit over?
A
TRPM8: temperatures below normal body temperature, C fibres
TRPV1(Capsaicin): Moderate heat, C fibres
TRPM3: High temperatures, myelinated A-delta fibres
Transient receptor potential vanilloid type 1 (TRPV1) Also called vanilloid receptor 1. A receptor that binds capsaicin to transmit the burning sensation from chili peppers and normally detects sudden increases in temperature.
Transient receptor potential type M3 (TRPM3) A receptor, found in some free nerve endings, that opens its channel in response to rising temperatures.
TRPM8 Also called cool-menthol receptor 1 (CMR1). A sensory receptor, found in some free nerve endings, that opens an ion channel in response to a mild temperature drop or exposure to menthol.
25
What is range fractionation?
A hypothesis of stimulus intensity perception stating that a wide range of intensity values can be encoded by a group of cells, each of which is a specialist for a particular range of stimulus intensities.
26
What is hyperalgesia?
Increased sensitivity, resulting from sensitization of nociceptors
27
Describe the pathway of peripheral sensitization
Tissue injury and inflammation lead to the release of numerous chemicals from non-neuronal and neuronal cells such as mast cells and macrophages. These cells release mediators such as protons, purines, and cytokines. These may directly or indirectly alter sensitivity of peripheral nociceptors.
Mast cell degranulation
28
What is allodynia, hyperalgesia, and hypoalgesia
Allodynia: Pain caused by a normally non-painful stimulus
Hyperalgesia: A heightened experience of pain caused by a noxious stimulus
Hypoalgesia: A decreased perception of pain caused by a noxious stimulus
29
Describe the efferent actions of nociceptors
A noxious stimulus leads to action potentials in nociceptive fibers that propagate not only to the central nervous system but also antidromically into peripheral branches. These antidromic action potentials lead to the release of neuropeptides such as substance P, calcitonin gene–related peptide (CGRP), and neurokinin A (NKA). These substances can stimulate epidermal cells (1) and immune cells (2) or lead to vasodilatation (3), plasma extravasation (4), and smooth muscle contraction (5)
30
What are CGRP
Potent vasodilators
31
Describe neurogenic inflammation
Injury or tissue damage releases bradykinin and prostaglandins, which activate or sensitize nociceptors. Activation of nociceptors leads to the release of substance P and CGRP (calcitonin gene–related peptide). Substance P acts on mast cells in the vicinity of sensory endings to evoke degranulation and the release of histamine, which directly excites nociceptors. Substance P produces plasma extravasation, and CGRP produces dilation of peripheral blood vessels; the resultant edema causes additional liberation of bradykinin. These mechanisms also occur in healthy tissue, where they cause secondary or spreading hyperalgesia.
32
Which channels are particularly important in the transformation of generator potentials to action potentials?
NaV 1.7 in the pacemaker zone
33
Why do grasshopper mice not show pain in response to bark scorpion venom?
The bark scorpion toxin activates Nav1.7 channels in grasshopper mice and lab mice. But in grasshopper mice, the toxin potently inhibits the Nav1.8 channel in the same sensory neurons, tipping the balance to inhibit action potential firing in nociceptors. This evolutionary adaptation allows grasshopper mice to feed on bark scorpions with impunity. In contrast, the lab mouse Nav1.8 channel is not blocked by the toxin and the scorpion sting excites nociceptors, causing intense pain
34
describe the organization of the dorsal horn. A-delta, A-Beta, and C fiber?
Neurons in lamina I of the dorsal horn receive direct input from myelinated (Aδ) nociceptive fibres and both direct and indirect input from unmyelinated (C) nociceptive fibres via interneurons in lamina II. Lamina V neurons receive low-threshold input from large-diameter myelinated fibres (Aβ) of mechanoreceptors as well as inputs from nociceptive afferent fibres (Aδ and C fibers). Lamina V neurons send dendrites to lamina IV, where they are contacted by the terminals of Aβ primary afferents. Dendrites in lamina III arising from cells in lamina V are contacted by the axon terminals of lamina II interneurons. Aα fibres innervate motor neurons and interneurons in the ventral spinal cord (not shown).
35
What is referred pain? How does it happen? Describe the pain in myocardial infarction and angina?
Signals from nociceptors in the viscera that can be felt elsewhere in the body.
Convergence of visceral and somatic afferent fibers may account for referred pain. Nociceptive afferent fibers from the viscera and fibers from specific areas of the skin converge on the same projection neurons in the dorsal horn. The brain has no way of knowing the actual site of the noxious stimulus and mistakenly associates a signal from a visceral organ with an area of skin
Myocardial infarction and angina can be experienced as deep referred pain in the chest and left arm. The source of the pain can be readily predicted from the site of referred pain
36
What are the two classes of synaptic vesicles and which neurotransmitters to they transport?
small electron-lucent vesicles contain glutamate
Large dense-cored vesicles hold neuropeptides.
37
how does pain reach the brain?
Through the anterolateral system aka spinothalamic system
38
what is the anterolateral system
Also called spinothalamic system. A somatosensory system that carries most of the pain and temperature information from the body to the brain
39
describe the anterolateral pathway
Primary afferent axons terminate in dorsal horn --> secondary axons cross the midline --> ascend contralateral anterolateral column to thalamus
40
Describe the doral column pathway
Primary afferent axons enter spinal cord --> ascend ipsilateral dorsal columns --> synapse in medulla --> secondary axons cross the midline --> ascend to contralateral thalamus.
41
Describe Brown-Sequard syndrome
Hemicord lesion
42
What will a lesion restricted to the left half of the spinal cord result in?
Results in dissociated sensory loss and mechanosensory deficits in the left half of the body, with pain and temperature deficits on the right
43
What is naloxone
A potent antagonist of opiates that is often administered to people who have taken drug overdoses. It blocks receptors for endogenous opioids
44
What is analgesia
Absence of or reduction in pain
45
What are opiates
A class of compounds that exert an effect like that of opium, including reduced pain sensitivity
46
What are endogenous opioids
A class of peptides produced in various regions of the brain that bind to opioid receptors and act like opiates.
47
What are endorphins, enkephalins, and dynorphins?
three kinds of endogenous opioids, substances that reduce pain perception
48
What are opioid receptors
A receptor that responds to endogenous and/or exogenous opioids
49
What is periaqueductal gray
The neuronal body–rich region of the midbrain surrounds the cerebral aqueduct that connects the third and fourth ventricles. It is involved in pain perception
50
Describe the regulation of nociceptive signals at dorsal horn synapses. How do opiates affect it?
1. Activation of a nociceptor leads to the release of glutamate and neuropeptides from the primary sensory neuron, producing an excitatory postsynaptic potential in the projection neuron.
2. Opiates decrease the duration of the postsynaptic potential, probably by reducing Ca2+ influx and thus decreasing the release of transmitter from the primary sensory terminals. In addition, opiates hyperpolarize the dorsal horn neurons by activating a K+ conductance and thus decrease the amplitude of the postsynaptic potential in the dorsal horn neuron.
51
What are electroencephalograms?
Offers a window into brain function
52
Describe how the very small electrical fields are generated by synaptic currents in pyramidal cells
the active synapse is on the upper part of the dendrite. When the afferent axon fires, the presynaptic terminal releases glutamate, which opens cation channels. Positive current flows into the dendrite, leaving a slight negativity in the extracellular fluid. Current spreads down the dendrite and escapes from its deeper parts, leaving the fluid slightly positive at those sites.
53
How are large EEG signals generated?
If the inputs fire within a narrow time window, the pyramidal cell responses are synchronized, resulting in a large EEG
54
Describe delta rhythms
<4 Hz large in amplitude, a hallmark of deep sleep
55
Describe Theta rhythms
4-7 Hz associated with sleeping and waking states
56
Describe alpha rhythms
15–30 Hz activated cortex
57
describe beta rhythms
15–30 Hz activated cortex
58
describe gamma rhythms
30–90 Hz, and signal an activated or attentive cortex
59
describe spindles
brief 12–14 Hz waves associated with sleep
60
describe ripples
brief bouts of 80–200 Hz oscillations
61
How do EEG rhythms vary across different brain sizes
very little
62
When are bursts of action potentials evoked in the thalamocortical neuron
When the thalamocortical neuron is hyperpolarized sufficiently to activate low-threshold calcium channels
63
describe the EEG of an alert, awake human? Describe the frequencies and amplitude and what is the mix called?
EEG is desynchronized with a mix of high frequencies and low amplitudes called beta activity.
64
when do alpha rhythms appear
appear during relaxation during stage 1 sleep
65
What are vertex spikes
Sharp waves that appear during stage 1 sleep
66
What are the rhythms present in stage 2 sleep
Brief periods of sleep spindles and K complexes
67
what rhythm is present in stage 3 (SWS)
delta waves
68
Compare the EEG activity of Waking and REM sleep
very similar activity
69
describe the lengths of REM episodes and Stage 3 sleep as the night goes on
REM episodes lengthen and there is a loss of stage 3 sleep
70
what is NREM sleep?
Characterized by slow, rolling eye movements (stage I) followed by decreases in muscle tone, body movements, heart rate, breathing, blood pressure, metabolic rate, and temperature.
All these parameters reach their lowest values during SWS sleep
71
What is REM sleep?
Characterized by rapid, ballistic eye movements, as well as by pupillary constriction, paralysis of many large muscle groups, and the twitching of the smaller muscles in the fingers, toes, and middle ear. Blood pressure, heart rate, and metabolism increase to levels almost as high as those found in the awake state.
72
Describe the amount of REM and NREM sleep we have as we age?
Reduction in both REM and NREM sleep. Severe reduction in stage 3 sleep and frequent awakenings
73
what is fatal familial insomnia? Where do holes develop in the brain?
An inherited disorder in which humans sleep normally at the beginning of their life but stop sleeping in midlife and die 7-24 months later. Large holes develop in the frontal cortex.
74
What are Euthermic arousals
their body temperatures are restored to normal. When they go into hibernation they go into a torpid state but every couple time intervals they warm themselves up. They warm themselves up to go to sleep. They forego this massive energetic cost to get the benefit of sleep. Warm themselves up for a little while then go to sleep again for a little bit
75
T/F all mammals investigated have been shown to have REM and NREM sleep
true
76
What is unihemispheric slow-wave sleep
Sleeping one hemisphere at a time. One hemisphere exhibit wakefulness while the other exhibits characteristics of sleep
77
What is memory
The ability to retain information, based on the mental process of learning or encoding, retention across some interval of time, and retrieval or reactivation of the information
78
What is episodic memory
Memory of a particular incident or a particular time and place. comprises associations of several elements such as objects, space, and times. The associations are encoded by chemical and physical changes in neurons as well as by modifications to synapses between neurons
79
What is memory consolidation
A process that converts and stabilizes information from short-term memory into long-term storage. Hippocampal–neocortical memory consolidation involves the transfer of hippocampal episodic memory into the neocortex during an offline (such as sleep) process after waking experiences in memory acquisition.
80
What is encoding
A stage of memory formation in which the information entering sensory channels is passed into short-term memory
81
What is an engram
The physical basis of a memory in the brain. It is sometimes referred to as a memory trace on the assumption that it involves changes in a neural circuit rather than a single neuron
82
Describe the model of memory consolidation
Memory formation is initiated by synaptic changes in the hippocampus. In this schematic, the hippocampal neurons interact with neurons in three distributed areas of neocortex. A temporary memory trace is formed in the hippocampus through synaptic consolidation and engrams later develop in neocortex through systems consolidation. Over time, memory depends more on connections in neocortex and less on the hippocampus
83
describe the model for encoding, consolidation and retrieval of memories
According to this model, medial temporal lobe processes distribute the various sensory attributes of an event, and linkages between them, in corresponding regions of cortex. Before consolidation is complete, retrieval involves the hippocampus and other medial temporal structures. After consolidation, retrieval may occur independent of the medial temporal system
84
which part of the brain is important for spatial learning
hippocampus
85
What are place cells and grid cells
Place cell: A neuron within the hippocampus that selectively fires when the animal is in a particular location. Place cells encode locations
Grid cell: A neuron that selectively fires when an animal crosses the intersection points of an abstract grid map of the local environment.
86
describe the model of active system consolidation during sleep
during SWS, memories newly encoded into a temporary store (i.e., the hippocampus in the declarative memory system) are repeatedly reactivated, which drives their gradual redistribution to the long-term store (i.e., the neocortex). B: system consolidation during SWS relies on a dialogue between neocortex and hippocampus under top-down control by the neocortical slow oscillations (red). The depolarizing up phases of the slow oscillations drive the repeated reactivation of hippocampal memory representations together with sharp wave-ripples (green) and thalamo-cortical spindles (blue). This synchronous drive allows for the formation of spindle-ripple events where sharp wave-ripples and associated reactivated memory information becomes nested into succeeding troughs of a spindle
87
Describe the glymphatic system
The system provides a flow of CSF through the interior of the brain that helps to clear cellular debris, proteins, and other wastes.
CSF flows from the subarachnoid space into the periarterial space surrounding fine arterioles that penetrate the brain. CSF enters the brain tissue via aquaporins and then flows through the brain. The CSF then drains into the perivascular space surrounding the brain capillaries
Convective glymphatic fluxes of CSF and ISF propel the waste products of neuron metabolism into the paravenous space, from which they are directed into lymphatic vessels and ultimately return to the general circulation for clearance by the kidney and liver
88
What are hypnograms
constructed from EEG recordings and display the cyclic transitions between sleep stages
89
What are the 5 neurotransmitters important in the regulation of the sleep-wake cycle? (brain region, waking levels, SWS levels, REM levels)
Acetylcholine: Pons/basal forebrain/medial septum, high waking levels, low SWS levels, high REM levels
Norepinephrine: Locus coeruleus, High waking, low SWS, Low REM
Serotonin: Raphe nuclei, High waking, decreasing SWS, low REM
Histamine: Tuberomammiliary nucleus, High waking, low SWS, Low REM
Orexin: Lateral hypothalamus, High waking, low SWS, Low REM
90
Describe the rhythms of Thalamic neurons firing before and after ACh, NE, and histamine.
Before: Tendency to generate slow, delta-frequency rhythms of intrinsic burst-firing
After: Neurons depolarize and switch to a more excitable single-spiking mode
May resemble switch from non-REM to waking
91
what is the ventrolateral preoptic nucleus
The major sleep-promoting region
92
What are the major wakefulness promoting regions
The basal forebrain and pontine region (brain stem and forebrain)
93
Describe the flip-flop circuit for the sleep/wake transition. Which system is inhibited when it is off and on?
there is mutual inhibition between the sleep-promoting region in vlPOA and the wakefulness-promoting regions
When the flip flop is on the sleep-promoting region is inhibited
When the flip-flop is off the wakefulness region is inhibited
94
what are the effects of orexin neurons on the flip-flop circuit? how are orexin neurons activated?
Activation of orexin neurons holds the flip-flop on. Motivation to remain awake or events that disturb sleep activate the orexinergic neurons
95
Describe narcolepsy and cataplexy
narcolepsy A disorder that involves frequent, intense episodes of sleep, which last from 5 to 30 minutes and can occur anytime during the usual waking hours.
cataplexy Sudden loss of muscle tone, leading to collapse of the body without loss of consciousness
95
Describe narcolepsy and cataplexy
narcolepsy A disorder that involves frequent, intense episodes of sleep, which last from 5 to 30 minutes and can occur anytime during the usual waking hours.
cataplexy Sudden loss of muscle tone, leading to collapse of the body without loss of consciousness
96
which neurons are decreased in people with narcolepsy
hypocretin neurons
97
how is sleep initiated in narcoleptic patients
initiated with REM sleep, normally sleep is initiated with stage 1 sleep
98
describe the REM sleep flip-flop
During waking the LF orexinergic neurons turn on REM neurons and you are put on the off state
When switching to the sleep neurons the LH orexinergic neurons decrease and the REM-ON neurons take over
Only one state (on/off) can be on at a time (REM Sleep Flip-Flop)
99
which stage of sleep do people act out
in REM sleep
100
Describe the motor function and sleep atonia circuit during wake and sleep periods
The Atonia circuits inhibit the lower spinal neurons during REM sleep. SLD stimulates GABAergic interneurons which antagonize lower motor neurons which cause the paralysis
101
what is somnambulism and when is it most common
sleep walking and most common in slow wave stage sleep
102
What are the functions of the basal ganglia
important in the control of movement, the selection and initiation of voluntary movements
plays a supervision role in regulating the activity in upper motor neurons
103
What is Bordmann's area
plays an important role in planning of complex, coordinated movements
104
What are the grey matter structures
corpus striatum and the pallidum
105
what are the components of the corpus striatum
Putamen and caudate
106
What are the two components of the pallidum
Globus pallidus and substantia nigra pars reticulata
107
what are medium spiny neurons
Medium spiny neurons in the corpus striatum integrate inputs from cortical, thalamic, and brainstem structures in the corpus striatum via glutamatergic synapses
A single medium spiny neuron integrates thousands of cortical cells
108
describe how MSN work
They have a strong inward potassium conductance and they require lots of excitatory inputs to overcome the stabilizing influence of potassium conductance
little spontaneous activity
109
Describe the function of the substantia nigra pars compacta
They are called compacta because of the densely packed cells
Provides dopaminergic input to the corpus striatum
110
describe the inputs the putamen and the caudate receive in the corticostriatal pathway
Putamen: main/general inputs
Caudate: more specific inputs
111
Describe the topographical organization of the caudate and putamen
they have compartments called patches or striosomes surrounded by a matrix
112
Where do the matrix and patches receive and send information?
Matrix: receives input from most areas of the cerebral cortex and sends projections to the Globus pallidus and the substantia nigra pars reticulata
Patches: receive from the prefrontal cortex and project preferentially to a different subdivision of the substantia nigra
113
Where does the pallidum receive and send information
receive from subthalamic nuclei and sen to VA/VL thalamic nuclei which sends output to motor areas
114
when do the MSN, the putamen and the caudate fire
MSN firing is associated with the occurrence of a movement and increases before an impending movement
Putamen discharge in anticipation of limb and trunk movement
Caudate fires prior to eye movements
115
Medium spiny neurons of the ____ and ____ give rise to ______ _______ projections that terminate in the ____ ____ and the _____ ____ ____ ____, the major sources of output from the basal ganglia
Caudate and putamen
Inhibitory GABAergic projections
globus pallidus and substantia nigra pars reticulata
116
What do the efferent cells of the globus pallidus and substantia nigra pars reticulate also give rise to? Is the main output of the basal ganglia excitatotry or inhibitory?
GABAergic projections
inhibitory
117
What do the output GABAergic neurons from the pallidum do?
High levels of spontaneous activity that prevent unwanted movements through tonic inhibition of superior colliculus and thalamus
118
Describe the disinhibitory circuit
In the absence of movement: the globus pallidus provides tonic inhibitions to the relay cells in the thalamus.
In the presence of MSN activity, globus pallidus is inhibited, resulting in thalamic neurons being disinhibited to relay signals to motor neurons
When Striatum is excited, the inhibitions of the thalamus is disinhibited leading to movement
119
Describe the direct motor pathway
When excitatory inputs reach the corpus striatum from the cortex, the GABAergic projections will inhibit the tonically active inhibitory cells of the globus pallidus and substantia nigra pars reticulata
= ACTIVATION of intended motor programs
When the D1 substantia nigra pars compacta is activated , the caudate/putamen are activated which inhibits the globus pallidus which allows the thalamus to become activ and stimulate the frontal cortex.
120
Describe the indirect motor pathway
Via strong activation of the subthalamic nuclei from the cortex, these excitatory projections will activate the inhibitory cells of the globus pallidus
= SUPPRESSION of competing motor programs
When the D2 of the substantia nigra is activated, it inhibits the caudate/putamen which then allows for the globus pallidus to inhibit the thalamus
Indirect pathway increases inhibitory influences on the upper motor neurons
121
what is hemiballismus
violent, involuntary movements of the limbs, is the result of damage to the subthalamic nucleus. The involuntary movements are initiated by abnormal discharges of upper motor neurons that are receiving less tonic inhibition from the basal ganglia
122
What is huntington's disease characterized by? What are the sympotom?
Dramatically reduced size of the caudate and putament
Symptoms: involuntary movement, muscle rigidity, slow or abnormal eye movements, impaired posture, difficulties with speech and swallowing
123
What is huntington's disease characterized by? What are the symptoms?
Dramatically reduced size of the caudate and putament
Symptoms: involuntary movement, muscle rigidity, slow or abnormal eye movements, impaired posture, difficulties with speech and swallowing
124
What is huntington's disease
Degeneration of MSN that project to the external segment of the globus pallidus results in a reduction in the inhibitory outflow of the basal ganglia. Also results in an increase to the excitability of the upper motor neurons
125
What is the influence of Nigral D1 and D2 type neurons
Nigral neurons provide excitatory inputs mediated by D1 type dopaminergic receptors on the spiny cells that project to the internal globus pallidus (direct pathway)
Inhibitory inputs mediated by D2 type receptors on spiny cells that project to the external globus pallidus (indirect pathway)
126
Which is a hypokinetic disorder and which is a hyperkinetic disorder: Parkinson's and huntington's
Parkinson's is hypokinetic
Huntington's is hyperkinetic
127
Symptoms of parkinson's
Tremors, stiffness, slowness of movement, impaired posture and balance, changes in speech
Dopaminergic loss in substantia nigra
128
What is parkinson's disease caused by
Loss of dopaminergic neurons that produces abnormally high inhibitory outflow of the basal ganglia. Thalamic activation of upper motor neurons in the motor cortex is therefore less likely to occur.
Resulting in decrease in motor neuron activity
129
What are the common sites for deep brain stimulation for movement disorders
Internal segment of globus pallidus
Subthalamic nucleus
130
Describe the spatial maps of the primary motor cortex
disproportionate to the size of the body part, organized movements are represented by motor neurons
131
What sections of the spinal cord are affected by Quadriplegia, paraplegia, loss of feeling in the genital area
Quadriplegia: C1-7
Paraplegia: T1-12 and L1-5
Gential: S1-5
132
How does motor learning affect the mapping of the motor cortex
Remapping of motor cortex
133
What are the supplementary motor area and the premotor cortex
Supplementary motor area (SMA)
A region of nonprimary motor cortex that receives input from the basal ganglia and modulates the activity of the primary
motor cortex.
Premotor cortex a region of nonprimary motor cortex just anterior to the primary motor cortex.
134
What are mirror neurons
Important in understanding the intentions of others. They are a neuron that is active both when an individual makes a particular movement and whenn that individual sees another individual make that same movement
135
Describe mirror neurons in autism
they are less acivated in autistic people
