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neuropsych > lesson 12 > Flashcards

lesson 12 Flashcards

1
Q

The Basal Ganglia/Nuclei

A

a group of subcortical structures found deep within the white matter of the brain

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2
Q

Consist of 5 pairs of nuclei

A

(1) Caudate nucleus, (2) Putamen, (3) Global pallidus, (4) Subthalamic nucleus, (5) Substantia nigra

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3
Q

grouped into broader clusters

A

striatum, globus pallidus, subthalamic nucleus, substantia nigra

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4
Q

striatum

A

afferent structure - dorsal stritum, ventral striatum

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5
Q

globus pallidus

A

efferent structure, with its internal segment (GPi) and external segment (GPe)

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6
Q

dorsal striatum

A

caudate nucleus and putamen

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7
Q

ventral striatum

A

(considered part of the limbic system): nucleus accumbens and olfactory tubercle

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8
Q

Afferences

A

mainly received by the striatum (=caudate + putamen) from the whole cortex, thalamus and brainstem

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9
Q

Efferences

A

sent primarily to the frontal cortex (through the thalamus) by the internal segment of the global pallidus

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10
Q

Indirect/Inhibitory Pathway (STOP)

A

through GABA; contributes to inhibit involuntary or unwanted movements

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11
Q

Indirect/Inhibitory Pathway (STOP) PATHWAY

A

cortex — GLU + —> striatum (caudate + putamen) — GABA - —> GPe — GABA - —> STN — GLU + —> GPi/SNr — GABA - —> thalamus — GLU + —> Frontal regions of cortex

Striatum also sends DA – to substantia nigra

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12
Q

Indirect/Inhibitory Pathway (STOP) dysfunction

A

hyperkinetic disorders (e.g. Huntington’s disease)

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13
Q

Direct/Excitatory Pathway (GO)

A

Through Glutamate; contributes to the starting of voluntary movements

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14
Q

Direct/Excitatory Pathway (GO) PATHWAY

A

whole cortex — GLU + —> striatum (caudate + putamen) — GABA - —> GPi/SNr — GABA - —> thalamus — GLU + —> Frontal regions of cortex

Striatum also sends DA + to substantia nigra

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15
Q

Direct/Excitatory Pathway (GO) dysfunction

A

hypokinetic disorders (e.g. Parkinson’s disease)

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16
Q

Classification of Hyperkinetic Symptoms (Motor Disorder)

A

Can be divided between rhythmic and non-rhythmic symptoms

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17
Q

Hyperkinetic Symptoms

A

rhythmic, non-rhythmic, tremors, myoclonus, hemiballism, chorea, athetosis (or slow chorea), dystonia, tics

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18
Q

Rhythmic

A

tremors at rest (e.g. Parkinson’s disease)

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19
Q

Non-rhythmic

A

slow, sustained or rapid

Non suppressible (most) and suppressible (tics, characterizing Tourette’s syndrome)

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20
Q

Tremors

A

involuntary, alternating moments involving one or more joint(s) occurring at a regular frequency resulting in rhythmic oscillations

Typical of PD

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21
Q

Myoclonus

A

involuntary, sudden and brief muscle contraction leading to shock-like movements

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22
Q

Hemiballism

A

violent flinging movements involving all the muscle controlling one limb in a coordinated way

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23
Q

when can hemiballism occur/due to what lesion

A

Can occur in the acute phase of a cerebrovascular lesion of the subthalamus nucleus

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24
Q

Chorea

A

involuntary, non-rhythmic, abrupt movements resulting in continuous flow of muscle contractions from one muscle group to another (usually contractions flow from proximal to distal segments), resulting in jerky and dance-like movements

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25
Q

what is the most distinctive feature of huntington’s disease?

A

chorea

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26
Q

what hyperkinetic symptom is typical of PD

A

tremors

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27
Q

Athetosis (or slow chorea)

A

slow twisting movements or sequences of abnormal postures involving the hand muscles

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28
Q

Dystonia

A

sustained patterned repetitive movements, often torsional, leading to abnormal postures

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29
Q

Tics

A

stereotypes, intermittent movements (motor) or sounds (vocal/phonic tics) with abrupt onset

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30
Q

what leads to diagnosis of Tourette’s syndrome?

A

tics when persistent throughout childhood

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31
Q

Gilles de la Tourette’s Syndrome (TS)

A

neurodevelopmental disorder that begins in childhood/adolescence, is characterized by multiple motor tics and at least one vocal (phonic) tic

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32
Q

what can change about TS

A

Can change location, strength and frequency

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33
Q

where in the spectrum on tic disorders is TS

A

at the most severe end of the spectrum

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34
Q

is TS most common in males or females and how common in children?

A

males, <1%

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35
Q

Huntington’s Disease

A

degenerative disease due to a progressive atrophy in caudate and putamen structures –> determines an unbalance in the indirect pathway

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36
Q

what is the most common autosomal dominant neurological disease of adulthood

A

huntington’s disease

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37
Q

what is Huntington’s Disease determined by

A

a mutation of a dominant gene on chromosome 4

Affects 5 – 10/100,000 individuals

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38
Q

at what age do most Huntington’s Disease cases occur at

A

Most cases occur between 20-40 years of age:

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39
Q

three types of symptoms of Huntington’s Disease

A

motor, cognitive, psychiatric symptoms

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40
Q

Huntington’s Disease - Motor symptoms

A

chorea, athetosis and later rigidity and dysarthria

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41
Q

Huntington’s Disease - Cognitive symptoms

A

cognitive slowing and dysexecutive deficits –> Huntington’s dementia

42
Q

Huntington’s Disease - Psychiatric symptoms

A

anxiety, irritability, aggression, psychotic behavior

43
Q

what do some Huntington’s Disease patients also exhibit versus others

A

Some patients exhibit poor judgements and socially inappropriate behaviors, others are apathic and abulic

44
Q

treating Huntington’s Disease

A

Treated with drugs that reduce chorea symptoms, but efficacy on cognitive and psychiatric symtoms is limited

45
Q

where in the indirect pathway is the issue with Huntington’s Disease

A

between striatum and GPe

46
Q

Parkinson’s disease

A

degenerative disease due to a progressive atrophy in substantia nigra (dopamine hypoactivity) –> determines an unbalance in the direct pathway

issue between substantia nigra and striatum

47
Q

parkinson’s onset is characterized by

A

specific motor deficits (‘parkinsonism’):

48
Q

‘parkinsonism’

A

Akinesia, hypokinesia and bradykinesia, muscle stiffness, resting tremor, shuffling gait, posture in flexion, reduced facial expressions, reduced blinking movements, poor speech articulation

49
Q

Akinesia

A

difficulty initiating voluntary movements

50
Q

hypokinesia and bradykinesia

A

slowness of movement

51
Q

parkinson’s disease treatment

A

Treatment: taking specific medications aimed to increase dopamine concentrations (levodopa, L-dopa)

52
Q

what does not usually benifit from usually parkinson’s disease treatment

A

So called ‘atypical parkinsonism’ disorder do not usually benefit from this treatment

53
Q

‘atypical parkinsonism’

A

Lewy Body dementia, cortico-basal degeneration, progressive supranuclear palsy

54
Q

parkinson’s neuro explanation

A

Important reduction in dopamine metabolism in the basal ganglia

55
Q

when do parkinson’s symptoms occur

A

when dopamine metabolism is >70%

56
Q

how is the reduction in dopamine activity measured and what is it proportional to in Parkinson’s disease

A

The reduction in dopamine activity (measured by the number of receptors responsible for the re-uptake of the neurotransmitter) is proportional to the motor deficits

57
Q

Basal ganglia also involved in

A

cognitive and emotional control

58
Q

Functional dysfunctions in the basal ganglia circuit also generate

A

non-motor symptoms and non-motor pathologies, as OCD

59
Q

basal ganglia non-motor disturbances

A

psychiatric symptoms, autonomous nervous system disorders, sleep disorders, others

60
Q

basal ganglia non-motor disturbances - psychiatric symptoms

A

depression, anxiety, psychosis, cognitive-behavioral problems

61
Q

basal ganglia non-motor disturbances - Autonomous nervous system disorders

A

gastroenteric disorders, orthostatic pressure, urological disorders

62
Q

basal ganglia non-motor disturbances - sleep disorders

A

insomnia, daily drowsiness, disturbances of REM sleep (nightmares)

63
Q

basal ganglia non-motor disturbances - others

A

falls, pain, respiratory disorders

64
Q

Cerebellum

A

means ‘little brain’; although the cerebellum constitutes approximately 10% of the brain mass in homosapiens, but ~ 80% of the total brain neurons

65
Q

comparison of how much the cerebellum does with neuron numbers

A

Approx 70 bill neurons compared to 16 bill in the cortex and 0.69 bill in brainstem

66
Q

cerebellum structure

A

two hemispheres, separated by the ‘vermis’ and a flocculonodular lobe

Carachterized by parallel fissures

67
Q

cerebellum structure - In the depth, surrounded by the white matter there are three cerebellar nuclei

A

The dentate nucleus

The interposed nucleus (including the emboliform and globose nuclei)

The fastigial nucleus

68
Q

what other structure does the cerebellum communicate with and through what

A

Communicates with the cerebrum through the superior, middle and inferior peduncles

69
Q

how many layers is the cerebellar cortex organized into and what are they called

A

3

Granular layer, Purkinje cell, Molecular layer

70
Q

Granular layer

A

receives afferent information

71
Q

Purkinje cell

A

efferent layer

have integrative function

72
Q

Molecular layer

A

interneurons

73
Q

Three functionally distinctive regions of cerebellum

A

The flocculonodular lobe/vestibulocerebellum

The medial zone (vermis)/spinocerebellum

The lateral zone (hemispheres)/cerebrocerebellum

74
Q

The flocculonodular lobe/vestibulocerebellum function

A

responsible for balance, posture, and orientation

75
Q

The flocculonodular lobe/vestibulocerebellum nuero connection

A

connected to the vestibular nuclei in the brainstem

76
Q

The medial zone (vermis)/spinocerebellum function

A

sends infor to the cerebral cortex and brainstem

77
Q

The medial zone (vermis)/spinocerebellum neuro connection

A

connected to the fastigium and interposed nuclei

78
Q

The lateral zone (hemispheres)/cerebrocerebellum function

A

contributes to cognitive functions

79
Q

The lateral zone (hemispheres)/cerebrocerebellum neuro connection

A

Connected to the dentate nuclei and cerebral cortex

80
Q

how does hemispheric communication work with the cerebellum

A

The left cerebral hemisphere communicates with the right cerebral hemisphere (and vice-versa)

81
Q

what happens to hemispheric communication with a double decussation

A

damage to one side of the cerebellum impairs motor activity of the same side of the body (ipsilateral)

82
Q

The Cerebellum Pathway PATHWAY

A

sensori-motor/vestibular/proprioceptive/… information reaches the cerebellum –>

purkinje cells send information to the deep cerebellar nuclei –>

information is sent to areas like brainstem and thalamus –>

influence on motor areas or descending motor tracts to modify/correct movement or make it more fluid

83
Q

The cerebellum participates in various functions associated with

A

movement due to integrating information from the brain, spinal cord and sensory organs

84
Q

what specifically does the cerebellum do with motor function

A

SPECIFICALLY facilitating movements by detecting errors and correcting them so the movement appears fluid and achieves its intended goal

85
Q

what kinds of facilitating movements by detecting errors and correcting them so the movement appears fluid and achieves its intended goal

A

Plays __leading role in learning to move__ (e.g. precise movements necessary to practice a sport)

Allows setting __posture__ to stay balanced

__Coordinates voluntary movements__, which in most cases are made possible by the simultaneous activation of multiple muscles, allowing the body, arms and legs to move fluidly

86
Q

Cerebellar ataxia

A

the pathognomonic sign (i.e. uniquely allows recognition of the disease) of a cerebellar dysfunction

87
Q

cerebellar ataxia leads to

A

discontinuity of movement, inability to coordinate balance, gait, extremity, and eye movements

so-called ’intentional tremor’

88
Q

Functional boundaries in the human cerebellum revealed by a multi-domain task battery

A

Fundamental question on whether the cerebellum is organized into distinct functional subregions —> so employed a rich task battery designed to tap into a broad range of cognitive processes with fMRI

Derived a comprehensive function parcellation of cerebellar cortex and evaluated it – identified distinct functional subregions

89
Q

The cerebellar cognitive-affective syndrome (CCAS)

A

all cerebellar dysfunctions (acquired lesions more than congenital cerebellar malformations cause motor impairments, plus… cognitive impairments and affective impapirments

90
Q

cognitive impairments of CCAS

A

executive dysfunction, visuo-spatial abnormalities, linguistic dysfunctions

91
Q

Executive dysfunction

A

working memory, planning, set-shifting, abstract reasoning, perseveration, distractibility, and inattention

92
Q

Visuo-spatial abnormalities

A

visual-memory memory and visuo-spatial disorganization

93
Q

Linguistic dysfunctions

A

dysprosody, agrammatism, mild anomia

94
Q

Affective impairments of CCAS

A

Anxiety, lethargy, depression, lack of empathy, ruminativeness, perseveration, anhedonia, aggression, disinhibited and inappropriate behavior

95
Q

what is a key structure in all high-level cognitive functions (attention, language, memory, executive functions, social cognition)

A

cerebellum

96
Q

The cerebellar cognitive affective syndrome – a meta-analysis methods

A

Ten studies; neuropsychological investigation was done within one year of diagnosis

97
Q

The cerebellar cognitive affective syndrome – a meta-analysis results

A

Cerebellar patients perform significantly worse on phonemic fluency, semantic fluency, strop test, block design test and WMS-R visual memory – have significant and relevant deficits in the visuospatial, language, and executive function domain

98
Q

Morphometric analyzes have shown that

A

the cerebellum and its connections with target cortical areas, are altered in disorders such as:

Bipolar, depression, autism, ADHD, down syndrome, schizophrenia, OCD, developmental dyslexia, fragile X syndrome

99
Q

Schizophrenia

A

suggested that there is dysfunction of the cortical-thalamo-cerebellar circuit leading to problems with emotional behaviors and cognition

100
Q

postmortem studies - schizophrenia

A

Postmortem studies have shown smaller anterior portions of the vermis and reduced density of the Purkinje cells in the vermis as well as smaller inferior vermis and less cerebellar hemispheric asymmetry

101
Q

ADHD

A

have smaller posterior inferior cerebellar lobes than a control group and the size of the vermis seems to be correlated with the severity of ADHD

102
Q

Developmental dyslexia

A

lower activation in the cerebellum during a motor task relative to a control group

neuropsych (25 decks)

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