4a. Parkinson (subcortical dementia) Flashcards

1
Q

Subcortical dementia in general

Which 3 areas are associated with the cognitive, emotional, and behavioral part of the fronto-subcortical circuits?

A
  1. Dorsolateral prefrontal cortex
  2. Lateral orbital cortex
  3. Anterior cingulate cortex
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2
Q

Which triad of symptoms are distinguished in PD?

A
  1. Bradykinesia = slowing of movements

And at least 1 of:

  1. Rigidity
  2. Tremor: during rest, in the extremities or the tongue
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3
Q

What is the characteristic posture of PD patients? (8x)

A
  1. Bend forward
  2. Blank facial expression
    3, Slow
  3. Monotonous speech
  4. Reduced arm swinging
  5. Rigidiy
  6. Tremor
  7. Short, shuffling gait
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4
Q

What are 3 risk factors of PD?

And what is a protective factor?

A
  1. Age
  2. Male gender
  3. 2 rare dominant mutations and several recessive mutations

Protective: smoking

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5
Q

What are non-motor symptoms in PD? (6x)

A
  1. Olfactory dysfunction (early): loss of smell and taste
  2. Changes in personality and mood: apathy, anxiety, depression
  3. Sleep: excessive daytime sleepiness & REM sleep behavior disorder
  4. Autonomic dysfunction: sweating, hypotension
  5. Psychotic symptoms: visual hallucinations
  6. Additional: pain, cognitive impairment, dementia
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6
Q

When can we distinguish a definite diagnosis of PD? (2x)

A
  1. When post-mortem there is depigmentation of the substantia nigra: in PD there is a loss of the (black) dopamine producing cells > leading to motor dysfunction
  2. Reacton to levodopa: when a patient reacts on this medication, you know it’s a dopamine problem and thus probably PD
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7
Q

What is the neuropathology of PD?

A

There are different pathological stages of PD which begins in the brain stem and spreads throughout the brain in 6 stages (low is the olfactory nucleus > that’s why you have loss of taste/smell early on)

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8
Q

Which neurotransmitters are also involved in PD, besides dopamine? (3x)

A
  1. (Nor)adrenaline
  2. Serotonine
  3. Choline
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9
Q

Explain the ‘dog’ figure in normal people and in PD patients.

A

Normal: the thalamus is a station that serves as a filter for the cortex. It has an excitatory effect on the (motor)cortex, but it is inhibited by the globus pallidus and substantia nigra, so it’s never too active (=dog on the leech).

PD: loss of dopamine > too much inhibition of the thalamus > loss of excitation to the cortex > lack of motor activity (=dog is doing nothing)

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10
Q

Which 3 clinical subtypes of PD can be distinguished?

A
  1. Tremor-dominant: you can see their tremors really easy on the outside, but they have a mild disease progression (not fast and little cognitive complaints
  2. Akinetic-rigid: they hardly move (more severe cognitive impairment)
  3. Postural instability & gait difficulty: falling a lot, more severe fom (more cognitive impairment and faster progression)
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11
Q

Which 3 domains are mostly impaired in NPA of PD patients?

A
  1. EF: initiation, planning, concept formation, rule finding, set shifting, attention, bradyphrenia (=slowing)
  2. Memory: retrieval inefficiencies, relative intact recognition (compared to AD)
  3. Micrographia: abnormally small or cramped handwriting
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12
Q

What are 2 core features of PD-dementia?

A
  1. Diagnosis of PD

2. Dementia syndrome (>1 cognitive domain affected, decline from premorbid functioning, and impairment in daily life

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13
Q

What are 2 associated clinical features of PD-dementia?

A
  1. Cognitive: fluctuating attention, EF, visuospatial, memory, language is preserved
  2. Behavior: apathy, delusions, sleepiness, changes in personality/mood
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14
Q

What 2 features give an uncertain diagnosis of PD-dementia (but no exclusion)?

A
  1. Co-existence of abnormalities that can cause cognitive impairment
  2. Time interval of cognitive and motor symptoms are unknown
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15
Q

What 2 features give an impossible reliable diagnosis of PD-dementia?

A
  1. Cognitive/behavioral symptoms solely in the context of other conditions (depression/medication)
  2. Features of possible vascular dementia
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16
Q

Treatment

Which medication is used in PD?

A

L-Dopa = a dopamine precursur that replaces the diminished dopamine. Especially motor functioning can be improved. It can give some side-effects: hallucinations, too much involuntary movements.

17
Q

Treatment

What is DBS?

A

Deep Brain Stimulation = with an electrode 2 parts of the basal ganglia (Gb & Sn) are stimulated, leading to more dopamine. The electrodes go to the skull and then to a battery on the clavicula.

  • You can’t have a lot of cognitive impairments for this surgery.
  • The patient is awake during the surgery.
  • The patient still gets Levodopa besides DBS.
18
Q

What 2 Parkinsonian disorders can be distinguished?

A
  1. Corticobasal Denegeration (CBD)

2. Progressive Supranuclear Palsy (PSP)

19
Q

What is Corticobasal Denegeration?

And what 2 symptoms can be distinguished?

A

A Parkinsonian disorder > a combination of degeneration of the basal ganglia and asymmetric atrophy of the frontal and parietal lobes.

Symptoms:

  1. Dementia: there are features of dementia in the beginning of the disease, especially apraxia (=difficulties with making unvoluntary movements)
  2. Alien hand syndrome: the patient is not aware of the movements of his arm
20
Q

What is Progressive Supranuclear Palsy?

And what symptom can be distinguished?

A

A Parkinsonian disorder > especially bradykinesia, but also dementia from the fronto-subcortical pattern, and a lot of falling as initial symptom.

Symptom:
1. Vertical supranuclear palsy: difficulties in moving the eyes (they can’t look downward anymore)