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73 Cards in this Set
- Front
- Back
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diseases of the basal ganglia
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movement disorders
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characteristics of movement disorders
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not weak
chorea dyskinesias akinesia |
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parts of striatum
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caudate
putamen |
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striatum receives afferents from where
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motor cortex
substanctia nigra (pars compacta) centromedian nucleus of thalamus |
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local processing within the striatum involves which neurotransmitter
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ACh
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output from the striatum goes where
via what |
internal segment of GP and pars reticulata of SN (GABA and Substance P)
external segment of GP (GABA and enkephalin) |
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inputs to the striatum from the pars compact use which neurotransmitter
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Dopamine
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what do D1 and D2 receptors due respectively
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D1 - stimulated by dopamine, increases cAMP
D2 - inhibited by dopamine, decreases cAMP |
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primary output nucleus of the basal ganglia back to the thalamus (ventral anterior)
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internal segment of GP
substantia nigra (pars reticulata) |
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internal segment of GP and pars reticulata receive info via what two structures
which neurotransmitters |
striatum - GABA and Sub P
Subthalamic nucleus- glutamate |
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what is the direct pathway
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efferents from the striatum to the internal segment of GP and pars reticulata
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indirect pathway
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efferents from the stratium to the external segment of GP
because info first travels through Subthalamic nucleus |
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step by step of the indirect pathway
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Striatum -> GPe (GABA and ENK) -> STN (GABA) -> GPi and SNpr (Glutamate)
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serves as a relay between the GPe and GPi
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subthalamic nucleus
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due to degeneration of the pars compacta
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Parkinson's disease
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degeneration of the pars compacta results in what physiological problem
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less dopamine production
less dopamine being sent from substantia nigra to striatum |
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characteristics of Parkinson's disease
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T - tremor
R - rigidity A - akinesia P - postural instability |
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differentiate rigidity and spasticity
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spasticity - increased tone that is velocity dependent, hyperreflexia
rigidity - increased tone is constant and independent of velocity, normal reflexes |
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asymmetrical arm swing
asymmetrical tremor finger tapping of small amplitude shuffled steps loss of facial expression difficult with fine motor task normal reflexes |
Parkinson's disease
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other common signs of parkison's disease patients
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depression
dementia dyskinesias constipation sensory symptoms sweating seborrheic dermatitis dystonia hyposmia REM sleep behavior disorder |
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a neurological movement disorder, in which sustained muscle contractions cause twisting and repetitive movements or abnormal postures
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dystonia
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manifestations that would suggest patients doesn't have parkinson's disease
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lack of response to dopamine therapy
symmetrical exam findings early falling |
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normal pathway from pars compacta of SN to the Cortex with neurotransmitters
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SNpc activates D1 and deactivates D2 receptors in striatum.
D1 - activated D1 sends GABA and SP to the GPi and SNpr D2 - inactivated D2 sends GABA and ENK to GPe which in turns sends GABA to STN which sends Glutamate to GPi and SNpr GPi and SNpr sends GABA to the VA nucleus of thalamus VA nucleus of thalamus sends glutamate to the cortex |
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anti-viral agent which provides symptomatic improvement in parkinson's disease
what is the mechanism |
Amantadine
augmentation of dopamine release and blocking re-uptake |
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drugs that block cholinergic interneuron's in the striatum. Most effective for tremor.
Side Effects |
Trihexyphenydyl
Benztropine muscarinic antagonists effects: confusion, blurred vison, dry mouth, urinary retention, constipation |
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What is the drug of choice in a patient with parkinson's that is young or with mild to moderate symptoms
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dopamine receptor agonists
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drug of choice with older patients with parkinson's or have cognitive difficulties
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levodopa
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Dopamine agonists
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Pramipexole
Ropinirole |
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Characteristics of Levodopa
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precursor of dopamine that can cross the BBB, is converted to dopamine in the striatum.
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Caribidopa
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taken in conjunction with levodopa to inhibit peripheral decaroxylation of levodopa to dopamine to decrease peripheral side effects such as nausea and hypotension
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differentiate mechanism of dopamine agonists with levodopa
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dopamine agonists do not require enzymatic conversion in the striatum and are therefore indepdendent on intact nigrostriatal neurons.
Longer half-life than levodopa |
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Sinemet
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Levodopa and Carbidopa
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what does a lack of response to levodopa suggest
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that the patient probably doesn't have parkinson's disease
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what helps prolong the effects of levodopa
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entacapone
COMT inhibitor |
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Side effects of dopamine agonists
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nausea
compulsive behavior (gambling or sexual) sudden attacks of sleep confusion |
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side effects of levodopa
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nausea
hallucinations hypotension dyskinesias |
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what competes with levodopa for absorption in the duodenum and BBB
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protein
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surgical pallidotomy should be done on which side of the brain in parkinson's patients
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opposite hemisphere of the effected side
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two diseases that can be confused with parkinsons
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Progressive supranuclear palsy
multisystem atrophy |
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characteristics of progressive supranuclear palsy that differentiate from parkinsons
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early falling
vertical supranuclear gaze palsy pseudobulbar palsy early onset of dementia |
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characteristics of multisystem atrophy that differentiate from parkinsons
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early falling
rapid progression anterocollis autonomic instability ataxia pseudobulbar palsy |
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two common drugs that present with parkinson symptoms
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metoclopromide
prochlorperazine |
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toxin that can present with parkinson symptoms and respond to Sinemet therapy
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MPTP - methyl-phenyl-tetrahydropyridine
develop symptoms within days |
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differentiate the brain pathway from striatum to cortex in patient with parkinson's disease
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decrease dopamine production in SNpc decreases action on D1 and D2
D1 - decreases GABA and SP to GPi and SNpr D2 - increases GABA and ENK to GPe which decreases GABA to STN which increases glutamate to GPi and SNpr GPi and SNpr sends more GABA to VA nucleus of thalamus which decreases Glutamate to the cortex |
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what happens when the GPi and SNpr is more activated with glutamate from the STN and less inhibited by GABA and SP from the striatum
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It is more activated to sends more GABA to the VA nucleus of the thalamus
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what happens with the VA nucleus of the thalatmus receives more inhibitory GABA from the GPi and SNpr
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it sends less glutamate to the cortex
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slowness or poverty of movement
common complaints are difficult getting out a chair/sofa, loss of facial expression, softer voice, drooling, difficulty with fine motor tasks |
bradykinesia involved with parkinson's disease
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early onset of dementia is associated with what disease
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progressive supranuclear palsy
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putaminal and midbrain atrophy respectively
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putaminal - multisystem atrophy
midbrain without affecting the pons - progressive supranuclear palsy |
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hot cross buns sign
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signal changes in the pons and middle cerebellar peduncle seen in multisystem atrophy
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disorders classified as hyperkinetic movement disorders
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essential tremor
dystonias wilson's huntington's hemiballismus tourette's |
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hypokinetic movement disorder
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parkinson's disease
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most common movement disorder
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essential tremor
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assymetric tremor that worsens when try to do tasks, symptoms improve with alcohol intake, autosomal dominant
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essential tremor
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List of dystonias
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blepharospasm
torticollis spasmodic dysphonia writer's cramp |
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characteristic of dystonias and treatment
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sustained muscle contraction
botulinum toxin is the treatment of choice |
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task specific dystonia
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writer's cramp
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most common dystonia
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torticollis
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what can briefly help dystonias
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sensory tricks
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site of copper deposit in wilson's disease
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liver
basal ganglia cornea |
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any young patient (<40) with a movement disorder should be checked for which disease
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Wilson's
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patient presents with proximal tremor, dysarthria, psychiatric symptoms. what lab findings are present
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Kaiser-Fleischer ring
low serum ceruloplasmin high urine copper level |
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Autosomal dominant progressive neurodegenerative disease with CAG trinucleotide repeats on chromosome 4
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Huntington's disease
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Dementia
Choreiform movements and family history of these traits |
Huntington's disease
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progression of disease in huntington's patients
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early on have irritability, anxiety, and loss of interest - this progresses to depression and clear memory loss
at first there is hyperkinetic choreiform movements - this progresses to bradykinesia features like parkinson's |
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multiple motor or vocal tics
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tourette's syndrome
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onset of tourette's and associated characteristics
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onset before age 21
obsessive-compulsive disorder seen in most |
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due to a stroke in the subthalamic nucleus
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hemiballismus
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patients develop acute onset of wild, flinging movement in the contralateral arm and leg
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hemiballismus
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how does a stroke in the subthalamic nucleus affect glutamate to the cortex
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decreased glutamate from STN to the GPi and SNpr which decreases GABA to the VA nucleus of thalamus which increases glutamate to the cortex
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tardive dyskinesia
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chronic treatment with dopamine blockers can present with repetitive sterotypic movements particularly of the lower face
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COMT inhibitor used for the wearing off phenomenon
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entacapone
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associated with degeneration of caudate nucleus
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Huntington's disease
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