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60 Cards in this Set
- Front
- Back
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BG components
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caudate, putamen, GP, subthalamic nucleus, and SN
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striatum
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caudate and putamen, receives virtually all BG inputs. separated by penetrating fibers of internal capsule but connected by cellular bridges. putamen more lateral, and is fused w/ caudate at ventral head (called ventral striatum), most of which is nucleus accumbens
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lentiform nucleus
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putamen + globus pallidus
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BG outputs
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substantia nigra pars reticulata and globus pallidua
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substantia nigra
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2 components: pars reticulata and pars compacta. ventral pars reticulata connected to GP. pars compacta has darkly pigmented dopamenergic neurons that degenerate in PD
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inputs: striatum
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putamen most important input nucleus for motor control pathways. most inputs are excitatory and use glutamate. SN pars compacta input to striatum and is dopaminergic (+ and -). intralaminar nuclei of thal provides + inputs, serotenergic inputs from raphe nucleus in BS
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outputs: BG
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GP and SN pars reticulata, SN for motor control of head and neck and GP for rest of body. outputs are - and use GABA; main pathways to VL and VA of thalamus and other areas. also to reticular formation and superior colliculus. affects both lateral and medial motor systems
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direct pathway of striatum
indirect pathway |
from cortex to striatum to GPinternal or SN pars reticulata (net effect is excitatory on thalamus)
from cortex to striatum to GPexternal to subthalamic nucleus to GPinternal or SN pars reticulata (net effect is inhibitory on thalamus) |
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PD pathway
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degeneration of DA neurons in SNpc. loss of DA causes net inhibition of thalamus, which may account for paucity of mvmt. anticholinergic drugs may reduce inhibition, in addition to using DA agonists. model does not account for tremor.
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hemiballismus
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unilateral wild flinging movement of extremities caused by BG lesion, usu subthalamic nucleus- caused decreased excitation of GP, resulting in less inhibition of thalamus, leading to hyperkinetic d/o.
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HD model
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loss of inhibitory output of basal ganglia to thalamus, particularly indirect pathway, leading to disinhibition of descending motor systems. in late stages, both direct and indirect degenerate, causing hypokinetic rigid parkinsonian state. Striatal degeneration in HD, particularly the caudate.
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name 4 parallel channels in BG
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motor, oculomotor, prefrontal channel (all dorsal striatal pathways) and limbic channel (ventral striatal)
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motor channel
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cortical inputs to putamen, outputs from GP and SNpr to VL and VA of thalamus to supp motor area, premotor and primary motor cortex
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oculomotor channel
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regulates eye mvmt, input from body of caudaye, output to VA, MD of thalamus to frontal eye fields and supplementary eye fields in FL
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prefrontal channel
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most important for cog processing in FL, input from posterior parietal cortex, premotor cortex to head of caudate; output to VA, MD of thalamus to prefrontal cortex
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limbic channel
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involved in regulation of emotion and motivational drives. input from TL, hippocampus, amygdala to nucleus accumbens, ventral caudate, ventral putamen; output to MD, VA of thalamus to anterior cingulate and orbital frontal cortex
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dyskinesia
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abnormal mvmt from BG dysfx
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bradykinesia
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SLOWED MVMTS
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hypokinesia
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decreased amount of movement
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akinesia
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absence of movement
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rigidity
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increased resistance to passive movement of a limb, oft present in d/o that cause bradykinesia or dystonia
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clasp-knife rigidity
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initial increase resistive tone as limb is stretched, then decreased tone (in spasticity, not BG d/o)
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plastic, waxy, or lead pipe rigidity
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continuous resistance to the stretch of a limb muscle (w/o clasp-knife release)
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cogwheel rigidity
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ratchet-like interruptions in tone as limb is bent, seen in PD. thought to be rigidity with superimposed tremor
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paratonia or gegenhalten
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pts with FL dysfx often actively resist movement of their limbs. has active, inconsistent voluntary quality
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dystonia
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abnormal, distorted position of limbs, trunk or face. can be generalized, unilateral of focal.
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torticollis
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focal dystonia of neck muscles
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blepharospasm
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focal dystonia of facial muscles around the eyes- rapid involuntary blinking
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spasmodic dysphonia
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focal dystonia of laryngeal muscles. voice disorder dysregulation of vocal cords
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tx for dystonia
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botox
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Wilson's disease sxs
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gradual onset of dysarthria, dystonia, rigidity, tremor, choreoathetosis, prominent psychiatric disturbance. st has "wing-beating tremor" with arms abducted, elbows flexed and facial dystonia (risus sardonicus -wry smile). degeneration of liver and BG
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athetosis
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writhing, twisting movement of limbs, face, trunk that st merge w/ faster choreic movements (choreoathetosis). causes: perinatal hypoxia w/ BG involvement, antipsychotic meds, HD, WD, PD from meds
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chorea
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continuous involuntary mvmts that are fluid or jerky, vary in scope, can involve proximal and distal muscles, trunk, neck, face and respiratory muscles. can occur as L-dopa side effect, in SLE, CO2 poisoning, toxins, perinatal anoxia, electrolyte and glucose abnormalities, toxins, etc.
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ballismus
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movement of proximal limb muscles with larger-amp, more rotatory or flinging quality, can be hemiballismus in BG lesion
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myoclonus
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rapid muscle jerk, can be focal, unilat or bilat. mult causes (BG, cortical, cerebellar, BS, SC lesions, anoxia, encephalitis, epilepsy, paraneoplastic, cortical-basal degeneration, CJD, LBD, AD)
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asterixis
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flapping tremor. causes include toxic/met enceph, part in liver failure.
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resting tremor
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when hands are relaxed. best observed when pt's hands on lap and they are distracted. important feature of PD, ala Parkinson's tremor. oft assymetrical and usu upper extremities but can be legs or mouth
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postural tremor
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most prominent when pts limbs actively held in a position (e.g., parallel to floor).
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essential tremor
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most common type of postural tremor, aka benign, semile or familial. usu hands/ars but can be in jaw, tongue, lips, vocal cords, head, legs, trunk
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physiologic tremor
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present in all individuals but not usu visiblw w/o equipment.
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intention tremor
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aka ataxic tremor, usu a feature of appendicular ataxia, occurs when pt moves towards a target and has irregular, oscillating movements
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PD
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loss of dopaminergic neurons in SN pars compacta; char by assymetrical resting tremor, bradykinesia, rigidity, postural instability. generally no family tendency, rare familial PD
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suspicious sxs of PD that may require alt dx
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rapid progression, absence of resting tremor (altho it happens 30% of time), postural instability early in course
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pathology of PD
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loss of pigmented DA neuons in SNpc, remaining DA neurons have lewy body inclusions in cytoplasm, loss of pigmented neurons in other parts of NS
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retropulsion
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if pt pulled backward, will take a few steps backward to regain balance (seen in PD)
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festinating gait
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small, shuffling steps
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anteropulsion
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gait that appears to be falling and shuffling forward
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en bloc turning
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turn which include numerous small steps and no torso turn
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Myerson's sign
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inabiloty to suppress blinking when the center of the brow ridge is tapped repeatedly. seen in PD and other neurodegen cond
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associated features of PD
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depression, anx common. impaired smell very early, seborrhea (itchy, flaky skin and scalp), hypersalivation
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off-on phenomena
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fluctuation b/w dyskenesias and immobility (freezing) between dosing, caused by abnormal regulation of DA in response to intermittent exogenous dosing
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parkinsonism plus syndromes
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neurodegerative conditions assoc w/ parkinsonism; have atypical parkinsonism, relatively symmetric sxs, ansence of resting tremor, early postural instability and poor response to DA agents
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multisystem atrophy
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a group of d/o falling under atypical parkinsonism; includes striatonigral degeneration, Shy-Drager, olivopontocerebellar atrophy. loss of DA neurons in SNpc, but also striatal projections to GPand SNpr
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PSP
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degeneration of multiple structures around midbrain-diencephalic junction (sup colliculus, red nucleus, dentate nucleus, subthalamic nucleus, and GP). limited range of vertical eye mvmt early in illness, waxy rigidity, bradykinesia, falls, wide-eyed stare
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DLB
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parkinsonism, dementia w/ lewy body inclusions in SN and cerebral cortex, prominent early psychiatric sxs, visual hallu, w/ episodic exacerbations.
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cortical basal degeneration
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parkinsonism, ll PD w/ asymetry, w/ limb dystonia, cortical features such as apraxia, wandering or alien limb syndrome, corticospinal abnormalities
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HD
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progressive atrophy of striatum, esp caudate nucleus. all 4 BG fxs impaired. onset b/w 30-50, initial sxs subtle chorea and behavioral sxs (dep, anx, OCD, impulsivity, mania, occ psychosis)
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4 fxs of basal ganglia
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body movement, eye movement, emotions, cognition
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motor circuit
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cortical projections from supp motor, arcuate premotor, motor cortex and somatosensory cortex project to putamen, to internal/external GP and SN, to thalamus (VL) back to supp motor area
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hyperkinetic movement disorders
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OFTEN CAUSED BY DYSFX OF CONTRALATERAL SUBTHALAMIC NUCLEUS, OR OF INDIRECT PATHWAY NEURONS IN THE STRIATUM
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