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25 Cards in this Set
- Front
- Back
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How is the basal ganglia involved in motor function?
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It modulates motor output: in essence it decides which movement will be performed given a range of stimuli.
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What five structures make up the basal ganglia?
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1.Caudate
2.Putamen 3.Globus pallidus 4.Subthalamus 5.Substantia nigra |
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Other than motor signals from the cortex, what are three kinds of information the basal ganglia receives?
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1.Sensory information
2.Motivational state 3.Emotional state |
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What are the major outputs from the globus pallidus? What neurotransmitter dominates these pathways?
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*to the thalamus and subthalamus
*GABA |
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What are the major outputs from the caudate and putamen? What neurotransmitter dominates these pathways?
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*to the globus pallidus and substantia nigra
*GABA |
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What are the major inputs to the caudate and putamen? What neurotransmitters dominate these pathways?
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*from the cerebral cortex and substantia nigra to the caudate and putamen
*from the substantia nigra - dopamine *from the cortex - glutamate |
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What three neurotransmitters dominate basal ganglia circuits? Are they inhibitory or excitatory?
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1.GABA - inhibitory
2.Dopamine - excitatory 3.Glutamate - excitatory |
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How is output from the basal ganglia similar to output from the cerebellar cortex?
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They both are all inhibitory
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Name the 4 dyskinesias seen with damage to the basal ganglia.
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1.Bradykinesia
2.Resting tremor 3.Chorea 4.Rigidity |
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What is the incidence of PD in the general population? In adults over age 70? What percentage of PD patients are under age 50?
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*1:1000
*1:100 *4% |
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Are men and women equally affected by PD?
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No - men are twice as likely to have PD than women.
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Give 4 of the characteristic symptoms of PD.
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1.Bradykinesia
2.Resting tremor 3.Rigidity 4.Masking 5.Characteristic gait - short steps, stooped posture, little arm movement 6.Dementia |
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What neurons degenerate in PD?
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The dopaminergic neurons of the substantia nigra.
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What is the cause of the majority of PD cases? Name some environmental factors postulated to be at play. With what lifestyle has PD been associated?
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*most cases have an idiopathic etiology
*exposure to carbon monoxide, carbon disulfide, cyanide, manganese *farming and well water |
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Two classes of medication are used to alleviate the symptoms of PD. What are these and what symptoms does each alleviate?
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1.Dopaminergic agonists - alleviate bradykinesia, slow gait, rigidity
2.Cholinergic antagonists - alleviate resting tremor |
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Why is the effectiveness of medication limited in PD patients?
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Patients develop tolerance and require larger and larger doses. Eventually the size of the dose eclipses the margin of safety. Also there are significant side effects associated with these drugs.
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Name two surgical techniques aimed at alleviating the symptoms of PD.
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1.Specific lesioning of the globus pallidus (pallidotomy)
2.Transplant of fetal or stem cell dopaminergic neurons. |
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MPTP has been shown to destroy dopaminergic neurons in the substantia nigra and cause a syndrome almost identical to PD. In what way is this condition different from PD?
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Rather than the gradual onset seen in PD patients, individuals who have been administered MPTP show sudden destruction of neurons and dramatic onset of symptoms.
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Typically, what are the first signs of HD? How does this frequently lead to misdiagnosis?
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*emotional lability and disorders in mood
*often misdiagnosed as a psychiatric illness |
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What are the motor symptoms of HD? How do these symptoms contribute to the death of these patients?
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*chorea
*progressive inability to walk, speak, and swallow *bacterial pneumonia secondary to aspiration |
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What is the incidence of HD? Are men and women equally affected?
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*5-10:100,000
*men are twice as likely to have HD than women |
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What is "anticipation" as seen in HD? How was this phenomenon explained biochemically?
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*age of onset decreases and severity of symptoms increases with successive generations
*the number of CAG triplet repeats increases with successive generations |
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Though HD patients eventually show widespread degeneration of brain tissue, where does this pathology generally begin?
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With destruction of GABA-nergic (medium spiny neurons) in the caudate and putamen.
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Is the genetic mutation that causes HD recessive or dominant? How is this mutation expressed in the affected genome?
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*autosomal dominant
*expansion of CAG triplet repeats in the huntingtin gene from 10-35 to 40-100 |
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It is known that the genetic mutation in HD causes an accumulation of an insoluble polyprotein, but why does this fail to explain the pathology seen in the disease?
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The effects of polyglutamine on neurons is not known. Also, this gene is expressed throughout the body but only the GABA-nergic neurons in the caudate and putamen are affected.
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