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100 Cards in this Set
- Front
- Back
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Cholinergic (Ach)
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- basal forebrain and midbrain/pons
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Gabaergic (GABA)
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- inhibitor
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Dopamine
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- substantia nigra, ventral tegmentum
- projects to frontal lobe, basal ganglia |
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Noradrenoline
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- locus coeruleus
- projects to all of cortex |
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Serotonin (tryptophan)
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- raphe nucleus
- projects to spinal cord and all of cortex |
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Histamine (histidine)
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- hypothalamus (tuberomammilary n.)
- projects to spinal cord and all of brain |
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evoked potentials or EP's
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responses of the sensory system to stimulation of the sensory receptor or sensory pathway
-used to assess the integrity of sensory pathways that could be caused by MS, tumors, vascular abnormalities, bony compression, trauma, neurodegenerative disorders |
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somatosensory evoked potentials, SEP's
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response to stimulation of whole nerve such as the medial or tibial nerve or of stimulation to the skin
-reflect conduction in the dorsal column/medial lemniscus pathway |
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brainstem auditory evoked potentials, BAEP's
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auditory evoked potentials usually in responce to a click or pure tone in headphones, can provide info about legions at different levels of the brainstem
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visual evoked potentials VEP's
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best when the stim is a changing pattern of equal luminosity
-only occipital cortical activities can be recorded, not subcortical |
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electroencephalography EEG
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tests ongoing static activity of the cerebral cortex
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an awake individual with eyes open generates what kind of activity
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bete
-low voltage, fast frequency 13-35 hertz |
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a person that is aler with eyes closed generates what kind of activity
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alpha
-low voltage, slower frequency 8-13 hertz |
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as a person closes their eyes and falls asleep they generate what kind of activity
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theta and delta
-theta is slightly higher voltage and slower frequency (3-7 hertz) than alpha or beta -delta activity is high voltage, very slow frequency .5-3 hertz and reflects synchronization of neural activity |
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EEG is abnormal when...
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slow frequency high voltage is demontrated during wakefulness
-may reflect focal damage due to tumors or absesses, metabolic abnormalities, or damage to reticular formation |
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epileptic EEG is...
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common to slowactivity with large amplitude and accational large amplitude spikes of activity
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REM sleep
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low voltage, high frequency
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the EEG sleep cycle
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beta alpha delta REM, repeat
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prefrontal association area function
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organization of cognitive behavior
planning of responses (aka dorsolateral frontal lobe) |
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limbic association area's function
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frontal lobotomy for calming effect
motivation memory (aka orbitofrontal region and the cingulate gyrus) |
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temporal-parietal-occipital associationg area's function
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body image and spatial relations/organization
language |
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legion of prefrontal association area (dorsolateral frontal lobe)
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deficits in delayed spatial response
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legion os orbitofronal area (frontal lobotomy)
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decreased emotional behavior, calming effect
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legion of frontal lobe (dorsolateral/orbitofrontal)
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lack of goal oriented behavior and initiative
perseverance of Wisconsin card sort task irreverent/inappropriate social behacior abnormailty of gaze |
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megative syptoms of Schizophrenia
(non-psychotic period) |
ocial isolation
Psychomotor poverty Poor attention span Flat affect Lack of motivation |
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positive symptoms of Schizophrenia
(psychotic period) |
Disorganization syndrome (disorganized thought and
behavior) Delusion syndrome (delusions and persecutions) Alienation syndrome (auditory hallucinations and disturbance of self - internal images are alien) |
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DOPAMINE HYPOTHESIS
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Psychotic episodes triggered by DA elevation
- amphetamine (blocks NA and DA reuptake) overuse leads to psychotic attacks - antipsychotic drugs (neuroleptics) block DA transmission (chlorpromazine haloperodol, droperodol) |
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in schitophrenia, Dopamine changes may be secondary to what?
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structural
changes in: temporal lobe hippocampus and amygdala prefrontal regions incl. Orbitofrontal and cingulate gyrus |
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schizophrenics show...
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attention deficits
memory deficits problem solving deficits |
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how does dopamine levels relate to prefrontal and hippocampal outputs?
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Prefrontal and hippocampus output is inversely related to dopamine levels
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In the Rat model for schizophrenia
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Hippocampal lesions lead to increased stress
response (startle ) Entorhinal lesions lead to increased dopamine in amygdala |
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Depression (unipolar depression)
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5% incidence
loss of energy insomnia slowed thoughts, feeling of worthlessness recurrent thoughts of death |
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Mania (bipolar depression)
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.6-1% incidence
- overactivity overtalkative socially intrusive decreased need for sleep reckless involvement |
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Disorder of mood affective disorders
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depression and mania
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Anxiety disorders - 15% incidence
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panic disorder, phobias, social phobias, agoraphobia, obsessive compulsive
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panic disorder
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intense terror
palpitations, sweating, trembling, fear of dying |
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obsessive compulsive disorder
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repetitive behaviors
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phobias
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anxiety to a specific fear object
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social phobias
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anxiety to social exposure or performance situations
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agoraphobia
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fear of not escaping a certain situation (crowds, bridges)
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overview of the hypothalamic-pituitary-adrenocortical axis, or HPA axis
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amygdala stimulates the HPA system and the stress response, hippocampal activation supresses the HPA system, the hippocampus has gluticocorticoid receptors that are sensative to circulating cortisol, thus hippo is neg. feedback
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HPA system responce produces
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cortisol
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no amygdala
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no understanding of fear
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HPA axis
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amygddala excites the hypothalamus, which excites the pituitary whic releases adrenocorticotropic hormone, which stimulates the adrenal gland to produce cortisol, which mobilizes glucose, which excites the hippocampus which inhibits the entire system at the level of the hypothalamus
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what is associated with too much cortisol
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depression, anxiety, and schizophrenia
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too much cortisol does what
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increases glutimate which is excitotoxic and causes cell death and a reduction in hippocampus volume... which causes less inhibition of the HPA system
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three types of memory
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implicit or nondeclaritive or procedural
explicit or declarative emotional |
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parkinson's pt's have problems with what type of memory
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procedural
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amnesia pt's have problems with what type of memory
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declaritive
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two types of learning for procedural memory
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nonassociative learning
-responce to sing stim. habitual/sensitization associative learning -ass. between events classical conditioning/operant conditioning |
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depressed pt's have increased bloodflow where?
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amygdala
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the body's stress responce
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avoidance
arousal increased SNS responce- cortisol energizes increased cortisol production from adrenal |
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shitzophrenics have a decreased level of what in their blood
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glycine, and also impaired phsphorylation of serine, a precursor of glycine
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phencyclidine (PCP) elicits what type of symptoms?
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phychotic symptoms
-PCP is an NMDA antagonist |
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NMDA
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requires Mg, voltage, and glycine
-a receptor for glutamate |
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Ketamine elecitis what
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pschycotic syptoms and is a NMDA antagonist
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What are similarities of presynaptic
actions in the central nervous system, compared to synaptic action at the neuromuscular junction? |
Voltage-activated calcium entry
Fusion of synaptic vescicles with the axon terminal membrane Release of neurotransmitter Reuptake of transmitter or its product into the synaptic terminal for re-packaging and release |
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What are differences of presynaptic
actions in the central nervous system, compared to synaptic action at the neuromuscular junction? |
Many presynaptic axons converge on a
single postsynaptic cell in the CNS Connections can be axon-dendritic, axo-somatic, dendro-dendritic, or axo-axonic in the CNS There are many different neurotransmitter substances in the CNS, and sometimes a presynaptic element releases more than one |
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What are similarities of postsynaptic
actions in the central nervous system, compared to synaptic action at the neuromuscular junction? |
Transmitters bind to postsynaptic
receptors Postsynaptic receptors can couple directly to channels (ionotropic receptors) |
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What are differences of postsynaptic
actions in the central nervous system, compared to synaptic action at the neuromuscular junction? |
Receptors can be coupled directly
or indirectly to ion channels Transmitter actions can be excitatory (depolarizing) or inhibitory (hyperpolarizing) |
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What are common excitatory
neurotransmitters? |
Glutamate
Acetylcholine |
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Glutimate acts of what type of receptors
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Kainate/AMPA receptors (ligand-activated, fast
channel) NMDA receptor Requires intense depolarization first to open it Allows calcium, as well as sodium, to enter Thought to be important in at least some memory mechanisms (more later) |
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What are common inhibitory
neurotransmitter substances? |
Glycine (esp. in the spinal cord)
Gamma-amino-butyric-acid (GABA) |
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excitatory ion movement
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Na+ in
K+ out |
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inhibitory ion movement
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Cl- in
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How do G-protein mediated synaptic
actions differ from direct transmitter actions on ligand-gated channels? |
Transmitter does not directly contact channel
GTP binds to a protein on the receptor (G- protein) Diffusible portion of the protein is released to act as or on a second messenger The second messenger can affect channels, and can also cause other actions THE ACTIONS ARE SLOW |
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excitotoxicity
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large amount of excit. nt are released and causes postsynaptic cell death
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what class of cells degenerate in alzhiemers?
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acetlchline
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What experimental evidence is
there for neural plasticity? |
Long term changes in single cell
responses to sensory stimuli Changes in cortical maps Changes in synaptic potentials produced by stimulation of presynaptic axons (Long term potentiation, LTP) |
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evidence of plasticity
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finger amputation-cortico map change
stim of monkey finger-change in map |
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consequences of LTP
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more receptors
increased receptor sensativity dendritic changes |
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Summary of some potential
mechanisms for neural plasticity |
Changes in receptor sensitivity (perhaps by protein phosphorylation; relatively short term)
Structural changes in dendritic spines (longer term) Structural changes in axonal branching (longer term) |
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decerebrate posture may signal
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midbrain legion
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decorticate posture may signal
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legion on cortex
presents of tonic labyrinthine reflex |
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primary motor cortex is active during what kind of movements
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all, simple and complex
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what is active during complex movements
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primary and both sides of the supplemental motor cortex
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lateral premotor cortex is important for
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paying attention to sensory info that guides movement
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optic ataxia
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characterized by inaccuracies in body movements under visual control, and is a common consequence of damage to the posterior parietal lobes in humans
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basal ganglia seems very active during
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overlearned activities
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What happens when dopaminergic
neurons degenerate, as in Parkinsons disease? |
Motor symptoms
Bradykinesia Tremor (at rest) Rigidity Disturbances of balance and gait Cognitive symptoms Slowness of thought Inability to switch between different cognitive strategies or rules |
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what activates dopamine nerurons
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rewards, stimuli that predict awards
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dopamine neurons may fail to discharge when
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something is overlearned
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huntington's desease
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caudate and putamen, or striatum degenerates
invol jerky movements |
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complete loss of globud palitus causes
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dystonia
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too much dopamine
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invol mevements, dyskinesias
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What are the most prominent
symptoms following damage to the cerebellum? |
Ataxia
Intention tremor Inaccurate targeted limb movements Dysarthria Nystagmus |
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alpha (group I)
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proprioception, light touch, vibration
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beta (group II)
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touch, proprioception
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delta (group III)
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sharp pain, temp
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large diameter fibers
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posterior column
proprio vib ligth tough |
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small diameter fibers
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anterolateral column/spinothalamic tract
pain, temp |
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legion in anterior sensory cortex
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texture loss
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legion in post sensory cortex
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shape loss
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A delta pain fibers
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small myl
fast pain helps with local of pain |
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C pain fiber
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small unmyl
slow aching pain less localized |
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large sensory fibers supress
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pain/ small fibers
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touch and pressure receptors
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merkles disks and ruffini organs
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vibration receptors
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pacinian and meissners sorpuscles
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large diameter fibers carry
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proprio vib fine touch
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small diam fibers carry
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pain, temp, crude touch
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