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Brain and Behavior > Lectures 34-36, 38, Basal Ganglia and OCD > Flashcards

Lectures 34-36, 38, Basal Ganglia and OCD Flashcards

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The Brain flashcards
1
Q

Basic basal ganglia connectivity

A

Cerebral cortex–> striatum –> globus pallidus / substantia nigra –> thalamus –> cortex

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2
Q

Inputs to BG and corresponding NTs

A

Cortex (glu), thalamus (glu), midbrain (DA), raphe nuclei (5-HT), locus coeruleus (NE)

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3
Q

Major cortical input to BG is from which lobe?

A

Frontal lobe

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4
Q

Thalamic inputs to BG (3)

A

Ventral, intralaminar, medial dorsal

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5
Q

Two parts of the SN and their NTs

A

SN pars compacta = DA; SN pars reticulata = GABA

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6
Q

LC and Raphe are located in which brainstem region?

A

Pons

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7
Q

Parts of the striatum. Basic function?

A

Dorsal (C + P); Ventra (NAS, olfactory tubercle); receives most extrinsic projections

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8
Q

Where is the nucleus accumbens located? What NT?

A

Leans on septum pellucidum in the ventral portion of the striatum; GABA

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9
Q

Where is the olfactory tubercle located? What NT?

A

Medially, below the anterior commissure; GABA

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10
Q

Where is the subthalamic nucleus located?

A

Medially to BG, caudal to thalamus

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11
Q

What cell type in the striatum receives inputs and projects outputs? What NT?

A

Medium spiny neurons; GABA

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12
Q

Two types of medium spiny neurons (organize via their respective NTs and receptors)

A
  1. substance P, D1 (excitatory via adenylyl cyclase); 2. enkephalin, D2 (inhibitory via adenylyl cyclase)
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13
Q

Where does the dorsal striatum project to? (2)

A

Globus pallidus (internal and external segments); Substanti nigra (pars reticulata and compacta)

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14
Q

Where does the ventral striatum project to? (2)

A

Ventral pallidum and VTA

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15
Q

More likely to visualize which segment of GP in cross section?

A

GPe

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16
Q

Where is the ventral pallidum?

A

Ventral to the GP (beneath anterior commissure)

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17
Q

The major outputs from the BG are all ________ and arise from? (3)

A

GABAergic; GPi, SNpr, VP

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18
Q

Where do the major outputs from BG system project to? What do you notice about this?

A

Mostly thalamus: Ventral groups, MD, ILN; same areas as major inputs!

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19
Q

Fiber bundles from BG to thalamus…combine with what?

A

Thalamic fasciculus w/ cerebellar efferents

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20
Q

Then where does the thalamus project?

A

The same frontal lobe structures that input into BG (mostly motor)

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21
Q

Inputs to BG are mostly what? Outputs are mostly what?

A

Excitatory, inhibitory

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22
Q

What are the functions of the five loops of the BG

A

Motor, oculomotor, cognitive (2), limbic

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23
Q

Model of BG function states…Which family of medium spiny neurons?

A

Direct (striatonigral) Path facilitates movement through disinhibition of thalamocortical activity; substance P/D1

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24
Q

The end of the direct path stimulates where, which loops back to where? And who projects DA to where?

A

VA/VL –> cortex; SNpc to striatum

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25
Q

How is the indirect pathway different?

A

SNpc projects to D2 receptors in striatum, which is inhibitory –> GPe –> disinhibits STN –> excites GPi/SNpr –> inhibits thalamus and cortex

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26
Q

What does the indirect pathway result in?

A

Inhibits BG output by increasing inhibition of thalamocortical pathway

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27
Q

What is the hyperdirect pathway? Describe the path.

A

Fast way to repress undesired behaviors (because indirect would be slower); Ctx –> STN –> (+) output structures of thalamus (GPi/SNpr)

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28
Q

What happens to the direct pathway in PD, broadly and specifically.

A

DECREASED, SNpc is damaged, so striatum is less active, so it does NOT disinhibit output structures, leading to inhibited thalamus/cortex

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29
Q

What happens to the indirect pathway in PD?

A

INCREASED, SNpc is damaged, so striatum is MORE active, suppressing GPe, disinhibiting STN, more activity in output structures, suppressing activity of thalamus and cortex

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30
Q

Huntington’s Disease is characterized by what change to the BG?

A

Atrophy of medium spiny neurons in dorsal striatum

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31
Q

HD is primarily thought to affect what pathway? How?

A

Indirect pathway; loss of striatum leads to overactive GPe, an inhibited STN, so no excitation to the output structures, so no inhibition of the thalamus/cortex

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32
Q

Hemiballismus is characterized by what symptom and what nucleus damage?

A

Wild, flailing muscles; STN

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33
Q

Describe the pathway in Hemiballismus

A

No STN in indirect pathway means no excitation of the output structures, so overactive thalamus and and cortex

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34
Q

Parkinson symptom constellation (4)

A

Bradykinesia, rigidity, postural instability, tremor

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35
Q

Parkinson ancillary features (3)

A

Freezing, hypophonia, bradyphrenia (slow thinking)

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36
Q

Parkinsonian Tremor

A

Asymmetrical onset, pill rolling, 3-5 Hz, postural re-emergent tremor, resting, chin/tongue, disappears in sleep

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37
Q

What other disease has a postural re-emergent tremor?

A

None!

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38
Q

Parkinsonian bradykinesia

A

Poor dexterity with decrementing (worsening) rapid alternating movements, micrographia, hypomimia, infrequent blinking

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39
Q

Rigidity (definition)

A

Increased resistance to passive movement (ratcheting)

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40
Q

Parkinsonian gait

A

Short strides, multipivot turn, loss of postural reflexes (>2 steps to recover from push = impaired)

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41
Q

Cardinal feature of PD? (and 4 related symptoms)

A

Asymmetric: rigidity, tremor, slowness, postural instability

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42
Q

Supportive features for PD diagnosis

A

Proressive and marked improvement with levadopa

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43
Q

Name and describe the major pathological finding of PD

A

Lewy body! Eosinophilic inclusion in neuron containing ubiquinated protein, alpha synuclein and neurofilament; forms due to misfolded alpha synuclein that cannot be cleared

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44
Q

What do misfolded alpha synuclein proteins form into?

A

Amyloid fibrils

45
Q

Is the Lewy Body itself pathogenic?

A

No! Attempt to deal with oxidative stress, etc caused by amyloid fibrils

46
Q

T/F: Lewy Bodies can be transferred between neurons?

A

True!

47
Q

Genes related to PD are in which organelles? Early or late onset?

A

Mitochondria and degradation system; early

48
Q

T/F: All PD patients have Lew Bodies

A

False! Those w/ mitochondrial-related genetic factors do not

49
Q

What medications are first given? And SEs…

A

Levodopa (motor fluctuations, dyskinesia), dopamine agonists (sedation, impulse control issues, hallucinations), MAOB inhibitors

50
Q

Why don’t we give young patients levodopa right away?

A

Can cause motor issues with increased use. Also cycle through periods where it works, periods of ON (dyskinesia) and periods of OFF time.

51
Q

Older patients will get what drug “up-front”

A

Levodopa

52
Q

What regions are targeted with deep brain stimulation for PD? How much can tremor be decreased? What is NOT improved by DBS?

A

GPi or STN; 75-90%; freezing/postural issues/cognitive issues

53
Q

Prodromal (non-motor) symptoms (4)

A

Constipation, anosmia, REM behavioral disorder, psych

54
Q

Lewy Body/PD Dementia symptomology (4); Lewy Bodies are where?

A
  1. Visual hallucinations; 2. Dementia; 3. Fluctuations of attention/arousal; 4. Parkinsonism that begin ~1 year of dementia; cortical regions
55
Q

Define Multiple System Atrophy

A

Autonomic Dysfunction (orthostatic hypotension, incontinence, impotence) w/ PD or Cerebellar symptoms

56
Q

Age of onset of MSA

A

40-60s

57
Q

Parkinson’s signs of MSA

A

Asymmetric w/ major gait disorder

58
Q

Cerebellar signs of MSA

A

Gait disorder, limb ataxia, nystagmus

59
Q

Pathology of MSA

A

Alpha synuclein inclusions in oligodendrocytes

60
Q

Define Progressive Supranuclear Palsy and onset (one big difference from PD). What are the other PD-like symptoms? What’s missing?

A

SYMMETRICAL bradykinesia; 70s; early balance problems (falls w/in a year); no tremor

61
Q

Eye movement signs of PSP

A

Supranuclear vertical palsy (cannot look up)

62
Q

Cognitive signs of PSP

A

Frontal lobe dementia

63
Q

Pathology of PSP

A

Accumulation of tau

64
Q

Define Corticobasal Degeneration, PD-ike symptoms, and onset

A

Asymmetric bradykinesia and rigidity in one limb (useless, alien limb); gait/postural instability; 60s-70s

65
Q

Is CBD responsive to levodopa?

A

No

66
Q

Cortical signs of CBD

A

Apraxia (cannot perform purposeful actions), cortical sensory loss (cannot identify objects by touch), dementia

67
Q

PSP imaging

A

“Humming-Bird Sign” (atrophy of midbrain, flat tectum)

68
Q

MSA imaging

A

“Hot cross bun” in pons and “hyperintense putaminal rim”

69
Q

CBD imaging

A

Asymmetric cortical atrophy (opposite to symptomatic side)

70
Q

Secondary etiologies in PD and some examples

A

Meds (neuroleptics, anti-seizure), toxins (MO, CO, CN, pesticides), structural (tumor), infection (HIV, syphilis)

71
Q

T/F: Removing exposure to secondary etiologies always removes symptoms?

A

Sometimes, depending on the cause; often NOT with toxins

72
Q

Define tremor

A

Rhythmic, oscillatory mov’t of a body part

73
Q

Define essential tremor; what happens when they drink?

A

Kinetic tremor condition = tremor during tasks, various frequencies; tremor attenuates w/ ETOH

74
Q

Name 3 other tremor conditions

A

Enhanced physiological tremor (postural); Cerebellar Tremor (slow, kinetic tremor); PD tremor (pill rolling, primarily at rest)

75
Q

Define dystonia

A

Involuntary, sustained muscle contractions causing twisting/repetitive movements

76
Q

What are some variations in dystonia?

A

Age of onset, focal (tend to be adult), generalized (tend to be child), hemidystonia (pallidal injury), etiology (genetic, degenerative, secondary)

77
Q

Is dystonia associated with rigidity of muscles?

A

Nope

78
Q

Define chorea

A

Involuntary, irregular flitting movements flowing across body movements

79
Q

Huntington’s Disease is…(cause and threshold)

A

Autosomal dominant repeat in HTT gene on chromosome 4, threshold number of repeats is 40

80
Q

What’s the association b/t repeat number and age of onset?

A

More repeats, younger onset

81
Q

Treatment for HD

A

Tetrabenazine, neuroleptics, benzodiazepines

82
Q

What’s an important co-morbidity for HD?

A

Neuropsychiatric problems, including irritability, psychosis, suicide

83
Q

Besides chorea, what kind of movement disorders do you see with HD?

A

Parkinsonism (early onset), dystonia

84
Q

How does someone with HD die?

A

Respiratory complications

85
Q

HD pathology

A

Atrophy of spiny neurons in striatum (atrophy of caudate)

86
Q

Define tic disorder. What is special about tic disorder?

A

Quick, stereotype movements/vocalizations that can be temporarily suppressed; only mov’t disorder that persists through sleep

87
Q

Define myoclonus and how is it different from tic disorder

A

Involuntary, very brief muscle jerks that interrupts voluntary movements generated anywhere in CNS but NOT suppressible

88
Q

Two sources of physiological myoclonus

A

Hiccups, hypnic jerks

89
Q

What’s an important pathological etiology of myoclonus?

A

Epilepsy

90
Q

Define Wilson’s Disease. Age of onset?

A

Copper accumulation disorder related to AR disorder on chromosome 13; 20s - 30s

91
Q

Describe the common neurological feature of Wilson’s

A

Tremor (80%): if child presents w/ essential tremor, screen for Wilson’s

92
Q

How do you test for Wilson’s?

A

Low serum cerulosplasmin, very high 24hr urine copper, low normal total serum copper and genetic testing

93
Q

OCD is filed where in the DSM-5?

A

Obsessive-compulsive & related disorders

94
Q

What is the time consuming threshold for OCD?

A

1 hour

95
Q

When does OCD typically onset?

A

Childhood (50% before age 14)

96
Q

Obsessions; contrast to hallucinations

A

Recurrent, intrusive, disturbing thoughts; recognized as own thoughts

97
Q

Compulsions; what can a compulsion NOT be in the book of OCD?

A

Repetitive, obsessive acts often driven by obsessions; pleasurable

98
Q

What proportion of patients with Tourette’s develop OCD symptoms? What about the converse (OCD patients w/ tics)

A

50%; 10-20%

99
Q

Two predominant theories of OCD

A

NT-based (5-HT/Glutamate) and Cortico-striato-thalamo-cortical loops

100
Q

Serotonin Hypothesis

A

Some role for 5-HT in OCD, based on the fact that SSRIs are helpful for OCD

101
Q

Role of glutamatergic involvement in OCD

A

Genetic, animal models of OCD, elevated glutamate, but no data for glutamate treatment efficacy

102
Q

Abnormal OCD circuits

A

Increased activity in OFC, striatum, ACC

103
Q

OCD animal model

A

SAPAP3 scaffolding protein at excitatory synapse in striatum deleted –> OCD that responds to SSRIs

104
Q

Main treatments for OCD

A

SSRIs (other classes ineffective) or CBT (exposure and response prevention)

105
Q

For OCD non-responders

A

Different SSRI, add an antipsychotic, neurosurgery

106
Q

Describe ablation surgical OCD treatment

A

For severely impaired patients, ablated anterior capsulotomy/anterior cingulotomy

107
Q

Where do the leads go in DBS for OCD?

A

Stimulate anterior limb of internal capsule (ventral capsule), deepest point on NA/ventral striatum

108
Q

Currently, what does research say about success rate for DBS and OCD? What about AEs?

A

About two-thirds; generally well-tolerated, but stimulation-specific adverse effects (hypomania), especially during programming

Brain and Behavior (56 decks)

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