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72 Cards in this Set
- Front
- Back
Basal Ganglia
(group of _ nuclei, general function is _) |
subcortical brain nuclei
generation and control of voluntary movements: internal generation of movement automatic execution of motor plans and to some degree the acquisition and retention of learned motor skills |
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Basal Ganglia
(name all components) |
striatum (caudate + putamen)
pallidum (globus pallidus) substantia nigra amygdala subthalamic nucleus |
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Basal Ganglia
(dysfunction notable in what 2 diseases) |
Parkinson's disease
Huntington's disease |
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Striatal connections
(major input from what structures) |
major inputs to caudate and putamen from:
cerebral cortex intralaminar thalamic nuclei substantia nigra |
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Striatal connections
Major inputs (name fibers) |
Corticostriate fibers
Thalamostriate fibers Nigrostriatal fibers |
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Striatal inputs
Corticostriate fibers (input originate from) |
widespread regions of neocortex that terminate in mosaic pattern of patches or clusters
inputs from widely separate cortical areas are overlapping somatosensory and motor are somatotopically organized |
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Striatal inputs
Corticostriate fibers (excitatory and/or inhib?, NT) |
excitatory
glutamate |
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Striatal inputs
Thalamostriate fibers (inputs originate from) |
intralaminar nuclei of thalamus and project to caudate and putamen
|
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Striatal inputs
Thalamostriate fibers (excite and/or inhib?) |
excitatory
|
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Striatal inputs
Nigrostriatal fibers (inputs originate from) |
substantia nigra pars compacta (SNc)
both caudate and putamen receive these inputs |
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Striatal inputs
Nigrostriatal fibers (pathway important for?, disease correlation) |
important afferent input conveying dopamine (DA) to the striatum
striatum is deprived of DA in Parkinson's |
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Striatal inputs
Nigrostriatal fibers (excite and/or inhib?) |
dopamine has both excite and inhit actions on striatal neurons
|
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Striatal outputs
(outputs to what structures) |
globus pallidus
substantia nigra pars reticulata (SNr) |
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Striatal outputs
(name fibers) |
Striatonigral fibers
Striatopallidal fibers |
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Striatal outputs
Striatonigral fibers (project from _ to _) |
striatum to SNr
(caudate projects to rostral part of SNr, putamen projects to more caudal parts) |
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Striatal outputs
Striatonigral fibers (excite/inhib?, NT) |
inhib
GABA |
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Striatal outputs
Striatopallidal fibers (project to) |
massive fiber system projects to:
GPi GPe |
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Striatal outputs
Striatopallidal fibers (NTs, disease correlation) |
GABA
enkephalin to GPe substance P to GPi signif reductions in enkephalin and substance P in the GP in patients with Huntington's |
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GP
(physical appearance and why?) |
paler appearance than putamen in fresh tissue
bundles of myelinated fibers traverse it (globus pallidus means "pale globe") |
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GP
(divisions, NT) |
GPi (internal division)
GPe (external division) GP mainly GABAergic |
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GP
(major inputs from what structures) |
striatum: (striatopallidal fibers are principal afferents)
subthalamic nucleus |
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Does the GP receive inputs from the cerebral cortex?
|
NO NO NO
Unlike the striatum, the GP does NOT NOT NOT receive afferents from the cerebral cortex |
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Does the GP receive inputs from the thalamus?
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NO NO NO
Unlike the striatum, the GP does NOT NOT NOT receive afferents from the thalamus (subthalamus is NOT part of thalamus) |
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GP
Other inputs |
receives dense DA projections from SNc
|
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GP inputs
Striatopallidal fibers (projection, NT, disease correlation) |
Striatum to GPi and GPe
GABA enkephalin to GPe substance P to GPi signif reductions in enkephalin and substance P in GP in Huntington's |
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GP inputs
Subthalamopallidal fibers (project to, excite and/or inhib?) |
project to:
GPe GPi excitatory |
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Major GP outputs
GPi projects to _ _ |
thalamus
pedunculopontine nucleus |
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Major GP outputs
GPe projects to _ |
subthalamic nucleus
|
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Major GP outputs
(name the 4 efferent pathways from pallidum) |
Ansa lenticularis
Lenticular fasciculus Pallidotegmental fibers Pallidosubthalamic projection |
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Efferent pathways from GP
Initial pathways taken on way to thalamus |
Ansa lenticularis
Lenticular fasciculus (output fibers initially take one of these two pathways from GPi either thru or around the internal capsule on the way to the thalamus |
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Efferent pathways from GP
How to thalamus? |
from GPi
thru or around internal capsule using either: ansa lenticularis or lenticular fasciculus They come together as thalamic fasciculus and project to ventral thalamus (thus, GP linked to motor cortex) |
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Efferent pathways from pallidum
Pallidotegmental fibers (from _ to _) |
from GPi descend and terminate in
pedunculopontine nucleus (PPN) of brainstem |
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Efferent pathways from pallidum
Pallidotegmental fibers (feedback connection, excite and or inhib, NT) |
PPN provides feedback to GPi
excite ACh |
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Efferent pathways from pallidum
Pallidosubthalamic projection (projection from _ to _ via _) |
GPe to subthalamic nucleus
via subthalamic fasciculus |
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Subthalamic Nucleus
(major inputs from) |
GPe
cerebral cortex (particularly frontal lobe) |
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Subthalamic Nucleus
(major outputs) |
are excitatory connections
back to GPe and to GPi and SNr |
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Ventral Thalamus (VA, VLo)
(input from) |
GPi
SNr |
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Ventral Thalamus (VA, VLo)
(project reciprocally to) |
cerebral cortex (excitatory)
striatum |
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Functional organization of BG
(organization each circuit engages separate regions of _ _ _, output of each circuit centered on _) |
organized in parallel but remain segregated in structure and function
each circuit engages separate regions of BG, thalamus, cortex output of each centered on different part of frontal lobe |
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Functional Organization of BG
(how many circuits (loops)) |
At least 5 basal ganglia-thalamocortical circuits (loops)
|
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Name 5 basal ganglia-thalamocortical circuits (loops)
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"Motor" circuit
"Oculomotor" circuit (links cortical eye fields to BG) 2 "Prefrontal" circuits "Limbic" circuit (links ant cingulate and medial orbitofrontal cortex to BG) **Organization suggests a functional specificity of info processing in BG** |
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Functional Organization of BG
(organization suggests _) |
functional specificity of info processing in the BG
|
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"Motor" Circuit
(strongly implicated in pathophys of _) |
movement disorders
|
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"Motor" Circuit
(putamen receives somatotopic projections from) |
primary motor cortex and from
premotor areas including supplementary motor area (M2) also from somatosensory cortex (motor and sensory somatotopic maps are in register such that "arm" regions of putamen receive input from "arm" regions of motor and somatosensory cortex) |
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"Motor" Circuit
(putamen projects somatotopically to specific regions of _ _ _, these regions then send projections to specific nuclei in _, this motor loop completed by _ projections back to _ _ _) |
GPe
GPi SNr ventral thalamus motor loop completed by thalamocortical projections back to: primary motor cx premotor cx supplementary motor cx |
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"Motor" Circuit
(There are _ and _ pathways) |
"direct"
"indirect" |
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"Motor" Circuit
"Direct" pathway (primary function) |
facilitate movement by allowing
disinhibition of the thalamocortical neurons by GPi/SNr |
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"Motor" Circuit
"Indirect" pathway (role) |
inhibit movement by increasing the
inhibition of thalamocortical neurons |
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"Motor" Circuit
"Direct" and "Indirect" pathways (how the two pathways are differentially affected is thought to lead to _ and _) |
hypokinetic and
hyperkinetic movement disorders |
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Pathophys Model of Parkinson's based on Motor circuit
It is thought that the direct and indirect pathways are differently affected by dopamine loss direct pathway becomes _ resulting in _ indirect pathway becomes _ resulting in _ Overall result is _ |
direct pathway:
**underactive** resulting in reduced disinhibition and increased inhib of thalamocortical neurons Indirect: **overactive** resulting in increased inhib of thalamocortical neurons Overall result is increased activity in GPi and increased inhibition to ventral thalamus |
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Parkinson's
(Overall result of direct pathway underactive and indirect pathway overactive, this is thought to cause _ _ _ which are associated with the disease, Which nucleus plays a key role and why) |
overall result is increased activity in GPi and
increased inhib to ventral thalamus akinesia rigidity tremor subthalamic nucleus b/c symptoms ameliorated by blockage of activity or stimulation of this nucleus |
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Disorders of BG
(spectrum of movement abnormalities ranging from _ to _, give an example of each) |
hypokinetic (Parkinson's) to
hyperkinetic (Huntington's) |
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Hypokinetic disorders
(characterized by _ _) |
akinesia = absence of movement
bradykinesia = slowness of voluntary movements |
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Hypokinetic disorders
(2 symptoms are _ _) |
***resting tremor***
muscle rigidity |
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Hyperkinetic disorders
(characterized by _) |
dyskinesia = excessive involuntary motor activity
|
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Types of Dyskinesia
(associated with lesions of _) |
corpus striatum
|
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Types of Dyskinesia
(name) |
tremor
athetosis chorea ballismus |
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Dyskinesias
Tremor (what, involves what body parts in Parkinson's and occurs at _) |
most common form
rhythmical involuntary movement Parkinson's: involves primarily the digits, hands, head, lips occurs at rest at 4-8 Hz |
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Dyskinesias
Athetosis (what) |
slow, twisting movements involving limbs, face, or trunk
movements blend together into continuous spasm |
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Dyskinesias
Chorea (what, seen in what disease) |
(means dance)
brisk series of successive involuntary movements that resemble fragments of purposeful voluntary movement often involve distal extremities, muscles of facial expression and tongue example is Huntington's disease (chorea) |
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Huntington's disease
|
inherited
adult-onset progressive involves choreiform activity of the face and hands and eventually severe behavioral disturbances with dementia patient's generally die about 15 years after onset genetic screening available |
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Dyskinesias
Ballismus (what, most common type, *usually associated with discrete lesions of _, side affected*) |
violent forceful flinging movement of the arms or legs caused by contractions of the proximal muscles
the most violent form of dyskinesia **hemiballismus** is the most common ***usually associated with discrete lesions of subthalamic nucleus or its connections effects are contralateral*** |
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Ballismus
(usually associate with _, side affected) |
***usually associated with discrete lesions of subthalamic nucleus or its connections
effects contralateral |
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Parkinson's Disease
(a _ disorder, *caused by _) |
hypokinetic disorder
caused by: loss of dopamine containing neurons in SNc (pars compacta of SN) |
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Parkinson's Disease
(symptoms) |
mask-like face
infrequent eyeblinks slow dysarthric speech stooped posture slow shuffling gait loss of associated movements like swinging the arms during walking slowness and general poverty of movement 4-8 Hz resting tremor |
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Parkinson's Disease
levodopa (aka, positive effects, problems, does not stop _, current research) |
L-dopa, a precursor to DA
exerts antirigidity and antikinesia Problems: large amounts = choreiform movements L-dopa effects only transitory does not stop cell death (the cause of the disease) neural tissue transplants |
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MPTA story
|
accidentally formed in illegal drug lab
individuals on it showed classic signs Parkinson's found to induce pathological hallmark of Parkinson's - loss of DA containing SNc neurons provided the much-needed animal model |
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Neurosurgical approaches to treating Parkinson's disease
(name 2) |
Ablative
Deep brain stimulation (DBS) |
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Neurosurgical approaches to treating Parkinson's Disease
Ablative (types) |
thalamotomy (not common)
pallidotomy (most common) |
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Neurosurgical approaches to treating Parkinson's Disease
DBS (what do they stimulate) |
thalamic (Vim)
GPi subthalamic nucleus (most common) |
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Treatment of choice for Parkinson's
|
DBS but pallidotomy continues to be performed worldwide
|
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DBS
(long term _ benefits, decline in _) |
long term motor benefits
decline in: oral and visuomotor info processing verbal fluency verbal recognition memory |