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152 Cards in this Set

  • Front
  • Back
hyperkinetic movement disorders of the basal ganglia
Huntington's-uncontrolled involuntary movements produce a random pattern of jerks and twists
hypokinetic movement disorders of the basal ganglia
Parkinson's-rigidity, slowness, and marked difficulty initiating movements
fxns of basal ganglia
movement, emotional control, cognition, and eye movements
where are the basal ganglia located
deep within white matter of cerebral hemispheres
main components of the basal ganglia
caudate nucleus, putamen, globus pallidus, subthalamic nucleus, and substantia nigra (sometimes nucleus accumbens and ventral pallidum included; amygdala primarily limbic system)
neostriatum (or striatum)
caudate and putamen thought of as single nucleus (histo and embryologically closely related); receives all inputs to the basal ganglia
what separates the putamen and caudate
penetrating fibers of internal capsule-remain joined in some places by cellular bridges
caudate nucleus relationships
C-shaped; constant relationship with lateral ventricles (like corpus callosum and fornix); 3 parts (head, body, tail)
location of amygdala
anterior to tip of caudate tail in temporal lobe
putamen specs
large nucleus forming lateral portion of basal ganglia; fuses with head of caudate anteriorly and ventrally
most of central striatum consists of
nucleus accumbebs
globus pallidus (pallidum)
pale globe' named due to many myelinated fibers traversing the region; medial to putamen
lenticular (lentiform nucleus)
putamen and globus pallidus together (resemble ice cream cone lying on side; putamen=icecream and globus pallidus = cone)
internal capsule
V-shaped collection of fibers going to and from the cortex
what does the anterior limb of the internal capsule pass btwn
lentiform nucleus (lateral) and head of caudate (medial)
what does the posterior limb of the internal capsule pass btwn
lentiform nucleus (lateral) and thalamus (medial)
where in the internal capsule are the corticobulbar and corticospinal tracts
posterior limb
what is visible just dorsal to the cerebral peduncles
substantia nigra
what separates the internal segment of the globus pallidus and the substantia nigra pars reticulata
internal capsule (similar to caudate and putamen separation)
what does the substantia nigra pars reticulata contain
cells very similar to internal segment of the globus pallidus
substantia nigra pars compacta (dorsal) contains
darkly pigmented dopaminergic neurons; degeneration important mechanism of Parkinson's
what lies under the thalamus
spindle/cigar-shaped subthalamic nucleus
what is the subthalamic nucleus derived from
midbrain (thalamus is from forebrain)
blood supply to striatum and globus pallidus
mainly from lenticulostriate branches of the MCA; medial globus pallidus often supplied by anterior choroidal artery (branch of internal carotid) and head of caudate and anterior portions of lentiform nucleus bu recurrent artery of Heubner (branch of ACA)
outputs leave basal ganglia via
internal segment of globus pallidus and closely related substantia nigra pars reticulata
inputs to basal ganglia come from
massive projections from cerebral cortex to striatum; substantia nigra pars compactal intralaminar nuclei; raphe nuclei of brainstem
most important nucleus for motor control pathways in basal ganglia
putamen
neurotransmitter used in most cortical inputs to striatum
excitatory glutamate
neurotransmitter used in substantia nigra pars compacta inputs to striatum
dopaminergic nigrostriatal pathway excitatory to some and inhibitory to others
neurotransmitter used in intralaminar nuclei (within internal medullary lamina of the thalamus) inputs to striatum
excitatory glutamatergic; especially centromedian and parafascicular nuclei
neurotransmitter used in raphe nuclei of brainstem inputs to striatum
serotonergic
where do basal ganlia outputs arise
from internal segment of globus pallidus and substantia nigra pars reticulata
motor outputs for head and neck in basal ganglia
substantia nigra pars reticulata (inhibitory via GABA)
motor output for rest of body from basal ganglia
internal segment of globus pallidus (inhibitory via GABA)
where do the main outputs from basal ganglia go
to the ventral lateral (VL) and ventral anterior (VA) nuclei of the thalamus via thalamic fasciculus (anterior portion)
posterior parts of thalamic fasciculus carry what
cerebellar outputs to posterior VL (Caudal part of VL receives inputs from Cerebellum)
information from basal ganglia is relayed mainly to where from thalamus
entire frontal lobe-mainly premotor cortex, supplementary motor area, and primary motor cortex
intralaminar nuclei (in thalamus) receive input from basal ganglia and project where
back to striatum
where does mediodorsal nucleus of thalamus project inputs from basal ganglia
primarily limbic pathways
where do internal segment of gobus pallidus and substantia nigra pars reticulata project to
pontomedullary reticular formation-influence descending reticulospinal tract
whre else does the substantia nigra pars reticulata project
superior colliculus-influences tectospinal pathways
two predominant pathways from input to output nuclei through the basal ganglia
1) direct 2) indirect
direct pathway
travels from striatum directly to internal segment of globus pallidus or substantia nigra pars reticulata
indirect pathway
detour from striatum-first to external segment of globus pallidus and then to subthalamic nucleus before reaching internal segment of globus pallidus or substantia nigra pars reticulata
net effect of excitatory input from cortex via direct pathway
excitation of thalamus-which then facilitates mavements through connections with motor and premotor cortex
net effect of excitatory input from cortex via indirect pathway
inhibition of thalamus-inhibition of movements through connections back to cortex (INdirect INhibits)
direct pathway neutrotransmitters
GABA and substance P
indirect pathway neutotransmitters
GABA and enkephalin (Enkephalin to External pallidum)
Parkinson's cause
dopamine-containing neurons in substantia nigra pars compacta degenerate
dopamine affects on direct and indirect pathways
excitatory on striatal neurons of direct; inhibitory on striatal neurons of indirect
loss of dopamine net affect on thalamus
net inhibition via both direct and indirect pathways = paucity of mvmnt in Parkinson's
aspiny neurons
large interneurons in striatum which contain acetylcholine; excitatory synapses onto striatal neurons of indirect pathway
result of removal of cholinergic excitation of indirect pathway
net decrease in inhibition of thalamus
hemiballismus
unilateral wild flinging movements of extremities contralateral to a lesion in the basal ganglia, typically with subthalamic nucleus
how does damage to subthalamic nucleus cause hemiballismus
decrease excitation of internal segment of globus pallidus, resulting in less inhibition of the thalamus casuing the hyperkinertic movement disorder
Huntington's
striatal neurons in caudate and putamen degenerate; initially enkephalin-containing striatal neurons most severely affected
what does disruption of enkephalin-containing striatal neurons cause
removal of inhibition from external segment of globus pallidus allowing it to inhibit the subthalamic nucleus
advanced Huntington's
both direct and indirect degenerate resulting in rigid hypokinetic parkinsonian state
oculomotor channel of basal ganglia
regulation of eye movements; input mainly via body of caudate and output to frontal eye fields and supplementary eye fields of frontal lobes
prefrontal channel of basal ganglia
important in cognitive processes involving frontal lobes; input from head of caudate and output reaches prefrontal cortex
limbic channel of basal ganglia
ventral pathway through basal ganglia involved in limbic regulation of emotion and motivational drives; inputs from major areas for limbic system and project to nucleus accumbens and other regions of ventral striatum
two pathways the internal segment of the globus pallidus sends outputs to the thalamus through
1) ansa lenticularis 2) lenticular fasciculus
ansa lenticularis path
looping course ventrally under internal capsule b4 passing dorsally to reach thalamus
lenticular fasciculus path
penetrate straight through internal capsule, then pass dorsal to subthalamic nucleus and ventral to zona incerta b4 turning superiorly and laterally to enter thalamus
zona incerta
inferior extension of reticular nucleus of the thalamus
thalamic fasciculus is formed by
fibers of ansa lenticularis and lenticular fasciculus join together
H1 field of Forel
thalamic fasciculus
H2 field of Forel
lenticular fasciculus-lies dorsal to subthalamic nucleus
prerubal field (H field of Forel)
region where ansa lenticularis and lenticular fasciculus join together
subthalamic fasciculus
carries fibers of indirect pathway from external segment of globus pallidus to subthalamic nucleus and from subthalamic nucleus to internal segment of globus pallidus
movement disorders often refer to
abnormal movements caused by basal ganglia pathology
spasticity
slow, clumsy, stiff movements and hyperreflexia resulting from corticospinal, upper motor neuron lesions
ataxia
irregular, uncoordinated movements caused by lesions of cerebellar circuitry
dyskinesia
abnormal movements caused by basal ganglia dysfunction; means 'abnormal movement'
conversion disorder and abnormal movements
occasionally occurs; psychological condition
basal ganglia disorders often reffered to as
extrapyrimidal syndromes (due to historical misguidance)
unilateral movement disorders caused by focal basal ganglia lesions like infarct, hemorrhage, abscess, tumor or degeneration are
contralateral to basal ganglia lesion
what movement disorders do not cease during sleep
palatal myoclonus and some tic disorders; although some aspects may persist
bradykinesia vs hypokinesia
slowed vs decreased amount of movement; terms only used for lesions higher than upper motor neurons
what can cause bradykinesia
increased inhibitory basal ganglia outflow to thalamus; loss of fxn of dopaminergic nigrostriatal system, loss of inhibitory pathways from striatum to substantia nigra and internal pallidum, or loss of inhibitory neurons projecting from the external pallidum to the subthalamic nucleus; in parkinson's along with hypokinesia
decrease spontaneous movements without coma can be seen in
diffuse lesions of frontal lobes, subcortical white matter, thalami, or brainstem reticular formation; psych disorders (advanced schizophrenia and depression)
rigidity
increase resistence to passive movement of a limb; often present with bradykinesia or dystonia
rigidity along with spasiticty (upper motor neuron lesion)
velocity dependent
rigidity and corticospinal disorders
initially increases as muscles stretched, but may then decrease; clasp-knife rigidity
rigidity and basal ganglia disorders
more continuous; called plastic, waxy, lead pipe rigidity
cogwheel rigidity
ratchetlike interruptions in tone that can be felt as limb bent; seen inparkinsonian disorders
paratonia or gegenhalten
actively resist movement of limbs
dystonia
assume abnormal, often distorted positions of limbs/trunk/face that are more sustained or slower than in athetosis; generalized, unilateral, or focal
focal dystonias
torticollis-neck muscles; blepharospasm-facial muscles around eyes; spasmodic dysphonia-laryngeal muscles; writer's cramp; presumed to be caused by basal ganglia dysfunction
botulinum toxin MOA
interferes with presynaptic acetylcholine release at NM jxn
Primary idiopathic torsion dystonia
uncommon hereditary disorder causing generalized dystonia
when are dystonias or faster dyskinesias (athetosis or chorea) commonly seen
acutely and after long term use of dopaminergic antagonists
what are often used prophylactically with antipsychotic and anti-emetic dopaminergic antagonists
antocholinergic medications to prevent tardive dyskinesia
Wilson's disease
autosomal recessive disorder of biliary copper excretion; progressive degeneration of liver and basal ganglia; 'wing beating' tremor=arms abducted with elbows flexed; wry smile (risus sardonicus)
athetosis
twisting movements of limbs, face, and trunk that sometimes merge with faster choreic movements = choreoathetosis
chorea
nearly continuous involuntary movements that have fluid or jerky, constantly varying quality
major cause of chorea
huntington's-autosomal dominant
benign familial chorea
autosomal dominant; chorea nonprogressive and not accompanied by cognitive or emotional decline
sydenham's chorea or rheumatic chorea
rare; onset adolescence, more common in females; 4 months after strep infection dvlp increased fidgetiness and emotional lability; apparent over weeks and gradually declines, but recurs in 1/5
rheumatic fever and sydenham's
up to 1/3 with sydenham's dvlp rheumatic fever
Sydenham's vs lupus
positive ANA or other positive rheumatilogic blood tests in SLE
chorea as a side effect is common with
levodopa use in parkinson's; early/delayed (tardive) in patients taking antipsychotic or anti-emetic meds
ballismus
movements of proximal limb muscles with larger-amplitude, more rotary or flinging quality than chorea; hemiballismus most common-contralateral to lesion
classic cause of ballismus
lacunar infarct of subthalamic nucleus-leads to decreased pallidal inhibition of thalamus
what can imprive ballismus
dopaminergic antagonists like haloperidol
tics
sudden brief action preceded by an urge to perform it and is followed by a sense of relief
Tourette's syndrome
persistent motor and vocal tics; autosomal dominant with incomplete penetrance; boys>girls; late childhood onset
myoclonus
sudden rapid muscular jerk that can be focal, unilateral, or bilateral
palatal myoclonus
persistence during sleep, rhythmicity; generally caused by lesions of central tegmental tract (brainstem infarcts can cause)
asterixis ('lack of fixed position') or flapping tremor
brief rapid movement that is often seen in toxic or metabolic encephalopathies (hepatic failure=liver flap)
how does an examiner cause asterixis
have patient hold out arms straight in front of chest with palms facing forward and wrists extended ('stopping traffic'); positive which brief flexion movements bilaterally as patient attempts to hold pose
what causes asterixis
not caused by muscle contractions, but brief interruptions in contraction of wrist extensors
tremor
rhythmic or semirhythmic oscillating movements; agonist and antagonist muscles activated resulting in bidirectional movement
resting tremor
most prominent when limbs relaxed; important feature of parkinson's; often asymmetric-mostly hands and upper limbs; aka pill-rolling tremor; 3-5 Hz frequency
postural tremor
most prominent when limbs actively held in a position and disappears at rest
essential tremor frequency and what can help it
5-8 Hz; beta-adrenergic antagonists like propranolol, also alcohol briefly
intention tremor aka ataxic tremor
feature of appendicular ataxia associated with cerebellar disorders; occurs as attempt to move limb toward a target-irregular, oscillating movement in multiple planes throughout trajectory; frequency 2-4 Hz
action tremor
either postural or intension tremor
terminal tremor
tremor increases toward the end of a movement
rubral tremor
caused by lesion of superior cerebellar peduncle or other cerebellar circuitry (not red nucleus); frequency 2-4 Hz; low amplitude at rest; MS or brainstem infarcts
physiologic tremor
frequency 8-13 Hz; enhanced with caffeine
Parkinson's specs
common idiopathic neurodegenerative condition caused by loss od dopaminergic neurons in the substantia nigra pars compacta; charcterized by asymmetrical resting tremen, bradykinesia, rigidity, and postural instability; onset 40-70; generally no familial tendency
characteristics of remaining dopaminergic neruons in Parkinson's
often contain Lewy bodies (eosinophilic cytoplasmic inclusions), which contain alpha-synuclein and ubiquitin and have a faint halo
classic triad of parkinson's
resting tremor, bradykinesia, and cogwheel rigidity (accompanied by postural instability that causes an unsteady gait)
masked facies or hypomimia
decrease in spontaneous blink rate and in facial expression
hypophonic
speech is hurried, with muttering quality
retropulsion
if pulled back slightly, person takes several steps backward to regain balance or they may fall
festinating gait
walk with small shuffling steps
anteropulsion
appear continually falling and ahuffling forward
en bloc turning
turns are executed without normal twists of the torso
Myerson's sign
inability to suppress blinking when center of glabella is tapped repeatedly; seen in neurodegenerative conditions
dementia and Parkinson's
not an early feature; later in course 15-40% or higher
bradyphrenia
responses to questions are slowed but may be accurate if enough time is allowed
carbidopa
decarboxylase inhibitor that cannot cross the blood-brain barrier; inhibits breakdown of lecodopa to dopamine in peripheral tissues
most common peripheral side effects of dopamine
GI disturbances and orthostatic hypotension-substantially reduced by carbidopa
what can help on-off phenomena
sustained release formulations and catechol O-methyltransferase (COMT) inhibitors
Parkinson's and thalamus
decreased dopaminergic input to striatum results in increased inhibition of the thalamus by basal ganglia outputs causing a hypokinetic movement disorder
what meds can induce parkinsonian signs like rigidity, hypokinesia, and even resting tremor
antipsychotic and anti-emetic sopaminergic antagonists like haloperidol and prochlorperazine; onset abrupt and symmetrical
multisystem atropy examples
striatonigral degeneration, Shy-Drager syndrome, and olivopontocerebellar atrophy; degeneration of striatal neurons projecting to globus pallidus and substantia nigra pars reticulata; insensitive to levodopa therapy
Shy-Drager syndrome
marked atrophy of intermediolateral cell colum of spinal cord plus parkinsonism; autonomic disturbances like marked orthostatic hypotension, impotence, and urinary incontinence
Olivopontocerebellar atrophy
parkinsonism with ataxia
Progressive supranuclear palsy (PSP) aka Steele-Richardson-Olszewski syndrome
degeneration of multiple structures around midbrain-diencephalic jxn (superior colliculus, red nucleus, dentate nucleus, subthalamic nucleus, globis pallidus)
eye movements and PSP
vertical eye movement markedly limited (upward and downward saccades) early in illness
PSP vs Parkinsons
wide-eyed stare; rigidity early in course and tends to be more proximal (neck not limbs) in PSP
Dementia with Lewy bodies
lewy bodies in substantia nigra and throughout cerebral cortex; prominent psychiatric symptoms early-episodic
cortical basal ganglionic degeneration
parkinsonism-asymmetric with marked cortical features like apraxia and corticospinal abnormalities
Machado-Joseph disease and dentatorubropallidoluysian atrophy
rare; both autosomal dominant via trinucleotide repeats
Huntington's
trinucleotide repeat disorder; onset childhood/early adult; autosomal dominant; progressive, choreiform movement, demenia, and psychiatric disturbances
hallmark of huntington's
progressive atrophy of striatum, especially caudate nucleus, putamen also involved and nucleus accumbens to a lesser extent
what can make ventricles appear enlarged in huntington's
atrophy of caudate and putamen-look for bulge of caudate on walls of lateral ventricles in coronal sections to distinguish from hydrocephalus
pallidotomy location for parkinsons
ventral posterior portion of globus pallidus-interupts inhibitory output pathway carried by the ansa lenticularis from medial globus pallidus to ventral lateral nucleus of thalamus (16.7 and 16.9)
thalamotomy for debilitating tremor location
posterior portion of ventral lateral nucleus of thalamus; mechanism for improvement unknown