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115 Cards in this Set

  • Front
  • Back
Cerebellum lesion associated w/ what clincal symptoms?
Ataxia, no balance, coordination
Basal ganglia lesion associated w/?
movement disorders and usually involuntary movements
Area of the brain for planning activity of body?
Dentate nucleus in cerebellum
Basal ganglia caudate nucleus
Huntington's Disease
dystonia, Wilson's Disease
Globus Pallidus
carbon monoxide
Subthalamic nucleus
Substantia Nigra
Parkinson's Disease
Striatum composed of?
caudate and putamen; very similar histologically
Putamen controls?
Caudate controls?
cognitive, behavioral control of eye movements
Lentiform nucleus composed of?
putamen and globus pallidus
Corpus striatum composed of?
caudate, putamen, globus pallidus
Addiction center of brain?
nucleus accumbens
Wilson's Disease due to?
Cu excess; results in dystonia
Where are the neurons located that die in Parkinson's pts?
substantia nigra pars compacta and substantia nigra pars reticulata
Where is the subthalamic nucleus located?
under the thalamus
Does an abcess in subthalamic nucleus cause ipsilateral or contralateral problems?
contralateral problems
What is the output center of the basal ganglia?
The three basal ganglia excitatory pathways are?
1)cortex to striatum
2)STN to GPI
3)thalamus to cortex
Inhibitory neurotransmitter is?
Excitatory neurotransmitter is?
Hypokinetic movement disorder is?
Hypokinetic movement disorders are due to overactivity or underactivity of GPI?
Hyperkinetic movement disorders are?
chorea, ballismus, dystonia
GPI does what in its normal state?
inhibit thalamus
How does overactivity of GPI cause hypokinetic movements disorders?
more than usual amounts of GPI inhibtion of thalamus; thalamus has less excitation of cortex; results in less movement
Hyperkinetic movement disorders are due to overactivity or underactivity of GPI?
How does underactivity of GPI cause hyperkinetic movement disorders?
GPI normally inhibits thalamus, but with that inhibition gone, there is more excitation of the cortex which results in extra movement
Main clinical features of Parkinson's disease?
tremor, bradykinesia, rigidity, postural instability
Main features of Parkinson's Disease?
shaking in one hand (tremor), slowness, reduced facial expression and blink rate, leaning forward when walking, often losing balance and falling forward, small handwriting (micrographia)
neurochemical abnormality in Parkinson's disease
dopamine deficiency
Pathology of Parkinson's disease is?
loss of dopamine producing neurons in the substantia nigra
Remaining neurons of Parkinson's pts contain?
lewy bodies - eosinophilic cytoplasmic inclusions
Dopamine deficiency leads to overactivity of the GPI by?
decreasing inhibitory influence of direct pathway and increasing excitatory effects of indirect pathway
Rate-limiting step for dopmaine synthesis?
tyrosine hydroxylase
What enzyme takes L-DOPA to dopamine?
aromatic amino acid decarboxylase
What are the catecholamine neurotransmitters?
dopamine, epi, norepi
Why is Carbidopa given?
is an aromatic amino acid decarboxylase; given w/ Levadopa so that there is minimal peripheral conversion; saves the DOPA for the brain
The top number of the Sinemet dosage is?
mg of carbidopa
The bottom number of the Sinemet dosage is?
mg of levadopa
Dopamine is brokendown by what enzyme?
What are the products of dopamine breakdown?
COMT converts Levadopa into?
3-OMD; a substance of no value; COMT is bad in this way
Why are COMT inhibitors given to pts w/ Parkinson's?
Entacapone (COMTAN) is a COMT inhibitor; allows more Levadopa to get into CNS
Main thing for Parkinson's pts is to?
increase dopamine or decrease Ach
3 components of Parkinson's treatment
agents that increase brain dopamine activity, anticholinergic agents, or surgery
Agents that increase brain dopamine activity are?
Sinemet, dopamine agonists, COMT inhibitors, MAO-B inhibitors
What type of surgery would you perform on a Parkinson's pt?
thalamotomy (helpful for tremor) and/or bilateral GPI or STN deep brain stimulator (blocks overactive output)
Other clincal problems that develop w/ Parkinson's pts?
depression, dementia, psychosis, involuntary movements (chorea)
Chorea is also known as?
What can cause chorea?
Once pt starts on treatment of Sinemet, the receptors see dopamine for the first time in a long time. They only get dopamine for about 90 minutes and then it is gone. After that, they become super-sensitive and do what they want to do.
Important test for inherited Parkinson's disease
Proteosome booster treatment may help treat neurodegenerative diseases because?
Lewy bodies seen in Parkinson's pts are full of proteins; other diseases my be based on the absence of abnormal protein degradation
What is dystonia?
repetitive, sterotyped involuntary movements; hyperkinetic
Dystonia caused by a lesion in?
GPI output in dystonia is?
focal dystonia
typically begins in adulthood and involves only one part of the body; usually idiopathic
Examples of focal dystonia are?
blepharospasm, spasmodic dystonia, writer's cramp
generalized dystonia
affects entire body and is often debilitating; usually onset in childhood and caused by genetic disorder
What can you do for pts w/ dystonia?
treat w/ drugs, or surgery by bilateral GPI lesioning or bilateral GPI stimulation
large amplitude, throwing, ballistic motions
Hemiballismus results from a lesion in the?
subthalamic nucleus
What is located near the subthalamic nucleus?
ansa lenticularis
What is Huntington's disease?
basal ganglia neurodegenerative disease that causes chorea
What is chorea?
brief involuntary movements that flit from one part of the body to another
Inheritance of Huntington's?
AD; each child has a 50% risk of inheriting the disease
Other effects of Huntington's?
emotional disorders and cognitive disturbances
Suicide risk for HD pts?
What are the components of the motor disorder aspect of Huntington's?
chorea, dysarthria, abnormal eye movements, motor impersistance, dysphagia, poor coordination, abnormal walking, poor balance
What is dysarthria?
slurred speech
age of onset for HD
What kind of triplet repeat disease is HD?
expansion of trinucleotide repeat CAG
normal CAG range
A person who has ___ repeats will develop HD if they live to be 70?
HD caused by a mutation?
in the coding region of the IT15 gene on chromosome 4
What is anticipation?
greater disease severity in
future generations
When are CAG repeat numbers likely to increase?
during gametogenesis; especially in men w/ HD; explains why pts w/ juvenille onset inherit disease from their father
treatable symptoms of HD
depression, anxiety, chorea
Tardive dyskinesia syndromes are?
variety of persistant abnormal involuntary movements caused by drugs that block dopamine receptors; neuroleptics
When does tardive dyskinesia appear?
usually after many yrs of treatment w/ dopamine blocking agents; can be permanent
Classical tardive dyskinesia includes?
abnormal movements of the mouth and tongue
How could neuroleptics cause tardive dyskinesis?
possibly caused by dopamine receptor supersensitivity
What causes TICS and/or Tourette's syndrome?
too many dopamine receptors, or the receptors are too sensitive (in striatum)
What treatment can help tics?
Tics are?
intermittent sterotyped movements and sounds; can be motor and vocal tics
What is dysmetria?
pt can't approximate areas of body
Midline lesions of the cerebellum would be in?
vermis (spinocerebellar) or flocculonodular lobes
What do you test for in lateral lesions of the cerebellum?
action or intention tremor, asynergia, dysmetria, dysrhythmia, dysdiadochokinesia
What is found in the epithalamus?
parts of pretectum and the pineal body
How many APs are fired per second with the combined firing for the purkinje cells?
VPM receives sensory input from?
Mamillary bodies are important for?
Experience causes cerebellar circuits to be?
modified...this is learning
How do you test for truncal ataxia?
Romberg test - Ask pt to close their eyes and stand still; if they wobble or move, there is a problem
Relay nuclei in the thalamus receive inputs from ______ and project to?
numerous pathways; cerebral cortex
What causes long-term depression?
AP on parallel fiber and AP on climbing fiber occurring simultaneously
MGN receives sensory input from?
A decrease in APs from the purkinje cells causes _____ of the deep cerebellar nuclei
Sensory from middle ear for balance travels to what relay nuclei?
What is asynergia?
unregulated movements that are non-functional
Cerebellar lesions cause ataxia on what side of the lesion?
Midline lesions of the cerebellum cause?
truncal ataxia - unsteady gait, and eye movements abnormalities accompanied by intense vertigo, nausea, and vomiting
VPL receives sensory from?
What will parallel fiber synapses display following a paired firing of the synapse with a climbing fiber?
depressed (smaller) EPSP for up to one hr
What happens to the number of simple spikes during the learning process?
gradually decreases and remains depressed after the task is learned
What is dysdiadochokinesia?
pt unable to perform rapid alternating movements
What are the 4 major components of the midbrain?
epithalamus, thalamus, hypothalamus, subthalamus
The direct (AMPA) channel allows?
a rise in intracellular Na+ in the purkinje cell which causes further depolarization
LGN receives sensory input from?
eyes through the optic tract
Which fiber fires more frequently during learning?
What happens to the deep cerebellar nuclei with motor learning?
What does the presynaptic terminal of the parallel fiber release?
The rise in intracelluar ionic calcium in the purkinje cell causes an increase in? Now what?
protein kinase C; further release of stored calcium for the SR
What is the main second messenger that causes LTD?