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Neuro Block 8 > Basal Nuclei: Parkinsons And Huntingtons > Flashcards

Basal Nuclei: Parkinsons And Huntingtons Flashcards

1
Q

Absence of movement

A

Akinesia

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2
Q

Decreased amount of movements

A

Hypokinesia

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3
Q

Slowed movements

A

Bradykinesia

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4
Q

What terms are not used for corticospinal, corticobulbar, LMN, or muscular disorders

A

Akinesia
Hypokinesia
Bradykinesia

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5
Q

What are bradykinetic movements caused by

A

Increases inhibitory basal ganglia outflow to the thalamus

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6
Q

What do basal nuclei dysfunctions affect

A

Body movements, eye movements, cognition, and emotional regulation

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7
Q

What disorder is bradykinesia, hypokinesia, and akinesia seen with

A

Parkinson’s

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8
Q

If you have too much dopamine

A

Psychological disorders

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9
Q

If you have too little dopamine

A

Parkinson’s

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10
Q

Decreases spontaneous movements, without coma, can be seen in

A

Diffuse lesions of the frontal lobes, subcortical white matter, thalami, or brainstem reticular formation

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11
Q

Depression and advances schizophrenia

A

Can also causes marked psychomotor retardation, which in the extreme is called Catatonia
-mimics basal nuclei disorders

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12
Q

If you give someone too many anti-psychotics, what is the effect

A

Parkinson’s like symptoms

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13
Q

Types of rigidity

A

Spasticity

Cogwheel

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14
Q

What kind of rigidity is seen in corticospinal disoriders

A

Spasticity

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15
Q

Spastic rigidity

A

Spasticity

  • strokes
  • results from UMN damage
  • tone initially increases and then decreases (clasp-knife) rigidity in corticospinal disorders
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16
Q

Cogwheel rigidity

A
  • Parkinson’s
  • caused by basal ganglia disorders
  • continuous throughout attempts to bend the limb
  • rigidity with a superimposed tremor
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17
Q

What kind of rigidity is seen in Parkinson’s

A

Cogwheel

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18
Q

__________ is a common idiopathic neurodegenerative condition caused by loss of dopaminergic neuron in the substantia nigra pars compacta

A

Parkinson’s

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19
Q

What is Parkinson’s caused by

A

Loss of dopaminergic neurons in the substantia nigra pars compacta

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20
Q

What is Parkinson’s characterized by

A
  • bradykinesia
  • rigidity
  • instability
  • tremor (at rest)

BRIT

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21
Q

Why is there a tenor at rest with Parkinson’s

A

Basal nuclei are what allow you to sit still without random movements, this is disrupted

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22
Q

Age of onset for Parkinson’s

A

40-70

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23
Q

How many people affected with Parkinson’s

A

1% of individuals over 65

24
Q

Familial tendency and Parkinson’s

A

There is verbally no familial tendency, except in rare cases of familial Parkinson’s

25
Q

Pathological cause of Parkinson’s

A

There is a loss of pigmented dopaminergic neurons in the substantia nigra pars compacta, causing the substantia nigra to appear pale to the eye on cross section

26
Q

Are Lewy bodies pathognomonic for Parkinson’s

A

No

27
Q

What is diagnosis of Parkinson’s disease is based on what

A

Almost ONLY on clinical features

28
Q

Common manifestations of bradykinesia and hypokinesia in Parkinson’s disease

A
  • micorgraphia
  • masked fancies or hypomimia
  • posture is stooped
  • postural instability
  • festinating gait
  • armswing is dimnishied
29
Q

What is often the 1st symptom of Parkinson’s

A

Micrographia, writing becomes small

30
Q

Characteristic decrease in spontaneous blink rate and in facial expression

A

Marked facies or hypomimia

31
Q

Festinating gait in Parkinson’s

A

Once they have started, they tend to walk with small shuffling steps

32
Q

Late symptoms of Parkinson’s

A
  • depression and anxiety
  • Dementia
  • diffuse Lewy bodies diseas
  • bradyphrenia (slow response to Qs)
  • seborrhea (oily skin) and hypersalivation
  • impaired smell is an earlier symptom
33
Q

When should a diagnosis other than idiopathic Parkinson’s should be suspected

A
  • patient does not respond to levodopa
  • symmetrical symptoms
  • absence of resting tremor
  • rapid progression of symptoms
34
Q

Shy-Crager syndrome

A

Parkinson’s + orthostatic hypotension

35
Q

Parkinson’s like diseases

A

Dementia with Lewy bodies

36
Q

Main mode of treatment for Parkinson’s

A

Levodopa

37
Q

A progressive, untreatable disorder which patients lose their ability to function and experience increasing dementia

A

Huntington’s disease

38
Q

The initial symptoms indicative of this disease generally being to appear ______ years of age

A

45-44

39
Q

What kind of disease Huntington’s

A

Genetic disorders inherited in autosomal dominant fashion

40
Q

What is the Huntington disease due to

A

Mutation on the short arm of chromosome 4

41
Q

Huntington’s disease at the molecular level

A

Mutated gene has multiple copies of the DNA sequence CAG, which codes for glutamate

42
Q

What do the CAG repeated in huntingtons result in

A

Addition of glutamate residues inside the gen coding for the protein. Huntington

43
Q

Dysfunction Huntington does what

A

Leads to premature death of neurons in the striatum

44
Q

When is Huntington’s more severe

A

Patients with larger numbers of repeats have a more severe illness with an earlier onset

45
Q

Trinucleotide repeat disorders

A
  • DNA replication error
  • abnormal amplification of sequence of 3 nucleotides. This may prevent normal expression of the gene or encode a dysfunctional protein
  • will worsen with each generation
  • most repeats contain guanine and or cytosine
46
Q

What is the trinucleotide repeat in huntingtons disease

A

CAG

47
Q

What is the primary responsibility for huntingtons

A

Glutamate exitotoxicity especially at caudate nucleus

48
Q

What happens when glutamate binds its receptor

A

Opens calcium channels

49
Q

Glutamate binding receptors in huntingtons

A

An unknown mechanism causes glutamate to persist at the NMDA receptor, which opens calcium ion channels, the resulting influx of Ca causes an increase in intracellular calcium, which triggers a cascade that leads to cell death

50
Q

Signs and symptoms of huntingtons

A

Initial symptoms are susally subtle chorea and behavioral disturbances
-subtly eye abenormalities such as slow saccades, impaired smooth pursuit, sluggish nystagmus

51
Q

Early movement abnormalities of huntingtons

A

Clumsiness and subtle chorea, such as mild jerking, fidgety movements

52
Q

Psychiatric manifestations of huntingtons

A
  • affective disorders such as depression and anxiety
  • OCD
  • impulsive or destructive behavior
  • psychosis
53
Q

Cognitive impairments with huntingtons

A
  • decreases attention
  • memory disorder that affects both recent and remote memories
  • atomic aphasia
  • impaired executive functions
54
Q

Advanced huntingtons

A

Patients are profoundly demented and lose the ability to make nearly all purposeful movement, they are bedbound, cannot speak, and usually die of respiratory infection

55
Q

Median survival from onset of huntingtons

A

15 years

56
Q

Huntington’s and MRI

A

Flattening of the head of the caudate nucleus

57
Q

MRI of huntingtons more advanced

A

Milder atrophy of the cerebral cortex also occurs

Neuro Block 8 (11 decks)

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