Neuroscience Block 3

Front 1

Cerebellum lesion associated w/ what clincal symptoms?

Back 1

Ataxia, no balance, coordination

Front 2

Basal ganglia lesion associated w/?

Back 2

movement disorders and usually involuntary movements

Front 3

Area of the brain for planning activity of body?

Back 3

Dentate nucleus in cerebellum

Front 4

Basal ganglia caudate nucleus

Back 4

Huntington's Disease

Front 5

Putamen

Back 5

dystonia, Wilson's Disease

Front 6

Globus Pallidus

Back 6

carbon monoxide

Front 7

Subthalamic nucleus

Back 7

hemiballismus

Front 8

Substantia Nigra

Back 8

Parkinson's Disease

Front 9

Striatum composed of?

Back 9

caudate and putamen; very similar histologically

Front 10

Putamen controls?

Back 10

motor

Front 11

Caudate controls?

Back 11

cognitive, behavioral control of eye movements

Front 12

Lentiform nucleus composed of?

Back 12

putamen and globus pallidus

Front 13

Corpus striatum composed of?

Back 13

caudate, putamen, globus pallidus

Front 14

Addiction center of brain?

Back 14

nucleus accumbens

Front 15

Wilson's Disease due to?

Back 15

Cu excess; results in dystonia

Front 16

Where are the neurons located that die in Parkinson's pts?

Back 16

substantia nigra pars compacta and substantia nigra pars reticulata

Front 17

Where is the subthalamic nucleus located?

Back 17

under the thalamus

Front 18

Does an abcess in subthalamic nucleus cause ipsilateral or contralateral problems?

Back 18

contralateral problems

Front 19

What is the output center of the basal ganglia?

Back 19

GPI

Front 20

The three basal ganglia excitatory pathways are?

Back 20

1)cortex to striatum
2)STN to GPI
3)thalamus to cortex

Front 21

Inhibitory neurotransmitter is?

Back 21

GABA

Front 22

Excitatory neurotransmitter is?

Back 22

Glutamate

Front 23

Hypokinetic movement disorder is?

Back 23

Parkinson's

Front 24

Hypokinetic movement disorders are due to overactivity or underactivity of GPI?

Back 24

overactivity

Front 25

Hyperkinetic movement disorders are?

Back 25

chorea, ballismus, dystonia

Front 26

GPI does what in its normal state?

Back 26

inhibit thalamus

Front 27

How does overactivity of GPI cause hypokinetic movements disorders?

Back 27

more than usual amounts of GPI inhibtion of thalamus; thalamus has less excitation of cortex; results in less movement

Front 28

Hyperkinetic movement disorders are due to overactivity or underactivity of GPI?

Back 28

underactivity

Front 29

How does underactivity of GPI cause hyperkinetic movement disorders?

Back 29

GPI normally inhibits thalamus, but with that inhibition gone, there is more excitation of the cortex which results in extra movement

Front 30

Main clinical features of Parkinson's disease?

Back 30

tremor, bradykinesia, rigidity, postural instability

Front 31

Main features of Parkinson's Disease?

Back 31

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)

Front 32

neurochemical abnormality in Parkinson's disease

Back 32

dopamine deficiency

Front 33

Pathology of Parkinson's disease is?

Back 33

loss of dopamine producing neurons in the substantia nigra

Front 34

Remaining neurons of Parkinson's pts contain?

Back 34

lewy bodies - eosinophilic cytoplasmic inclusions

Front 35

Dopamine deficiency leads to overactivity of the GPI by?

Back 35

decreasing inhibitory influence of direct pathway and increasing excitatory effects of indirect pathway

Front 36

Rate-limiting step for dopmaine synthesis?

Back 36

tyrosine hydroxylase

Front 37

What enzyme takes L-DOPA to dopamine?

Back 37

aromatic amino acid decarboxylase

Front 38

What are the catecholamine neurotransmitters?

Back 38

dopamine, epi, norepi

Front 39

Why is Carbidopa given?

Back 39

is an aromatic amino acid decarboxylase; given w/ Levadopa so that there is minimal peripheral conversion; saves the DOPA for the brain

Front 40

The top number of the Sinemet dosage is?

Back 40

mg of carbidopa

Front 41

The bottom number of the Sinemet dosage is?

Back 41

mg of levadopa

Front 42

Dopamine is brokendown by what enzyme?

Back 42

MAO-B and COMT

Front 43

What are the products of dopamine breakdown?

Back 43

DOPAC and HVA

Front 44

COMT converts Levadopa into?

Back 44

3-OMD; a substance of no value; COMT is bad in this way

Front 45

Why are COMT inhibitors given to pts w/ Parkinson's?

Back 45

Entacapone (COMTAN) is a COMT inhibitor; allows more Levadopa to get into CNS

Front 46

Main thing for Parkinson's pts is to?

Back 46

increase dopamine or decrease Ach

Front 47

3 components of Parkinson's treatment

Back 47

agents that increase brain dopamine activity, anticholinergic agents, or surgery

Front 48

Agents that increase brain dopamine activity are?

Back 48

Sinemet, dopamine agonists, COMT inhibitors, MAO-B inhibitors

Front 49

What type of surgery would you perform on a Parkinson's pt?

Back 49

thalamotomy (helpful for tremor) and/or bilateral GPI or STN deep brain stimulator (blocks overactive output)

Front 50

Other clincal problems that develop w/ Parkinson's pts?

Back 50

depression, dementia, psychosis, involuntary movements (chorea)

Front 51

Chorea is also known as?

Back 51

dyskinesia

Front 52

What can cause chorea?

Back 52

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.

Front 53

Important test for inherited Parkinson's disease

Back 53

dardarin

Front 54

Proteosome booster treatment may help treat neurodegenerative diseases because?

Back 54

Lewy bodies seen in Parkinson's pts are full of proteins; other diseases my be based on the absence of abnormal protein degradation

Front 55

What is dystonia?

Back 55

repetitive, sterotyped involuntary movements; hyperkinetic

Front 56

Dystonia caused by a lesion in?

Back 56

putamen

Front 57

GPI output in dystonia is?

Back 57

reduced

Front 58

focal dystonia

Back 58

typically begins in adulthood and involves only one part of the body; usually idiopathic

Front 59

Examples of focal dystonia are?

Back 59

blepharospasm, spasmodic dystonia, writer's cramp

Front 60

generalized dystonia

Back 60

affects entire body and is often debilitating; usually onset in childhood and caused by genetic disorder

Front 61

What can you do for pts w/ dystonia?

Back 61

treat w/ drugs, or surgery by bilateral GPI lesioning or bilateral GPI stimulation

Front 62

hemiballismus

Back 62

large amplitude, throwing, ballistic motions

Front 63

Hemiballismus results from a lesion in the?

Back 63

subthalamic nucleus

Front 64

What is located near the subthalamic nucleus?

Back 64

ansa lenticularis

Front 65

What is Huntington's disease?

Back 65

basal ganglia neurodegenerative disease that causes chorea

Front 66

What is chorea?

Back 66

brief involuntary movements that flit from one part of the body to another

Front 67

Inheritance of Huntington's?

Back 67

AD; each child has a 50% risk of inheriting the disease

Front 68

Other effects of Huntington's?

Back 68

emotional disorders and cognitive disturbances

Front 69

Suicide risk for HD pts?

Back 69

10-15%

Front 70

What are the components of the motor disorder aspect of Huntington's?

Back 70

chorea, dysarthria, abnormal eye movements, motor impersistance, dysphagia, poor coordination, abnormal walking, poor balance

Front 71

What is dysarthria?

Back 71

slurred speech

Front 72

age of onset for HD

Back 72

39

Front 73

What kind of triplet repeat disease is HD?

Back 73

expansion of trinucleotide repeat CAG

Front 74

normal CAG range

Back 74

17-30

Front 75

A person who has ___ repeats will develop HD if they live to be 70?

Back 75

>40

Front 76

HD caused by a mutation?

Back 76

in the coding region of the IT15 gene on chromosome 4

Front 77

What is anticipation?

Back 77

greater disease severity in
future generations

Front 78

When are CAG repeat numbers likely to increase?

Back 78

during gametogenesis; especially in men w/ HD; explains why pts w/ juvenille onset inherit disease from their father

Front 79

treatable symptoms of HD

Back 79

depression, anxiety, chorea

Front 80

Tardive dyskinesia syndromes are?

Back 80

variety of persistant abnormal involuntary movements caused by drugs that block dopamine receptors; neuroleptics

Front 81

When does tardive dyskinesia appear?

Back 81

usually after many yrs of treatment w/ dopamine blocking agents; can be permanent

Front 82

Classical tardive dyskinesia includes?

Back 82

abnormal movements of the mouth and tongue

Front 83

How could neuroleptics cause tardive dyskinesis?

Back 83

possibly caused by dopamine receptor supersensitivity

Front 84

What causes TICS and/or Tourette's syndrome?

Back 84

too many dopamine receptors, or the receptors are too sensitive (in striatum)

Front 85

What treatment can help tics?

Back 85

haldol

Front 86

Tics are?

Back 86

intermittent sterotyped movements and sounds; can be motor and vocal tics

Front 87

What is dysmetria?

Back 87

pt can't approximate areas of body

Front 88

Midline lesions of the cerebellum would be in?

Back 88

vermis (spinocerebellar) or flocculonodular lobes

Front 89

What do you test for in lateral lesions of the cerebellum?

Back 89

action or intention tremor, asynergia, dysmetria, dysrhythmia, dysdiadochokinesia

Front 90

What is found in the epithalamus?

Back 90

parts of pretectum and the pineal body

Front 91

How many APs are fired per second with the combined firing for the purkinje cells?

Back 91

51

Front 92

VPM receives sensory input from?

Back 92

head

Front 93

Mamillary bodies are important for?

Back 93

memory

Front 94

Experience causes cerebellar circuits to be?

Back 94

modified...this is learning

Front 95

How do you test for truncal ataxia?

Back 95

Romberg test - Ask pt to close their eyes and stand still; if they wobble or move, there is a problem

Front 96

Relay nuclei in the thalamus receive inputs from ______ and project to?

Back 96

numerous pathways; cerebral cortex

Front 97

What causes long-term depression?

Back 97

AP on parallel fiber and AP on climbing fiber occurring simultaneously

Front 98

MGN receives sensory input from?

Back 98

cochlea

Front 99

A decrease in APs from the purkinje cells causes _____ of the deep cerebellar nuclei

Back 99

disinhibition

Front 100

Sensory from middle ear for balance travels to what relay nuclei?

Back 100

VPL

Front 101

What is asynergia?

Back 101

unregulated movements that are non-functional

Front 102

Cerebellar lesions cause ataxia on what side of the lesion?

Back 102

ipsilateral

Front 103

Midline lesions of the cerebellum cause?

Back 103

truncal ataxia - unsteady gait, and eye movements abnormalities accompanied by intense vertigo, nausea, and vomiting

Front 104

VPL receives sensory from?

Back 104

body

Front 105

What will parallel fiber synapses display following a paired firing of the synapse with a climbing fiber?

Back 105

depressed (smaller) EPSP for up to one hr

Front 106

What happens to the number of simple spikes during the learning process?

Back 106

gradually decreases and remains depressed after the task is learned

Front 107

What is dysdiadochokinesia?

Back 107

pt unable to perform rapid alternating movements

Front 108

What are the 4 major components of the midbrain?

Back 108

epithalamus, thalamus, hypothalamus, subthalamus

Front 109

The direct (AMPA) channel allows?

Back 109

a rise in intracellular Na+ in the purkinje cell which causes further depolarization

Front 110

LGN receives sensory input from?

Back 110

eyes through the optic tract

Front 111

Which fiber fires more frequently during learning?

Back 111

climbing

Front 112

What happens to the deep cerebellar nuclei with motor learning?

Back 112

disinhibition

Front 113

What does the presynaptic terminal of the parallel fiber release?

Back 113

glutamate

Front 114

The rise in intracelluar ionic calcium in the purkinje cell causes an increase in? Now what?

Back 114

protein kinase C; further release of stored calcium for the SR

Front 115

What is the main second messenger that causes LTD?

Back 115

calcium