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Block 6 > 10.6 Hypokinetic disorders > Flashcards

10.6 Hypokinetic disorders Flashcards

1
Q

What area of the cortex is involved with motor function and what is the role of each?

A

Primary motor cortex: Execution of movements, input from SMA/PMC and basal ganglia

Supplementary motor area: innervates form distal muscle groups directly

Premotor cortex: involved in the design of movements

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2
Q

What is the effect of the direct pathway?

A

Net effect of excitatory input from the cortex will be excitation of the thalamus which will facilitate movement

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3
Q

What is the effect of the indirect pathway?

A

Ne effect of excitation of the indirect pathway will be inhibition of the thalamus, resulting in inhibition of movements

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4
Q

How does teh direct pathway work?

A

Glu from Cx - Striatum
GABA from Striatum - GPi and SNr
GABA from GPi and SNr - thalamus
Glu from thalamus - cortical motor areas

Disinhibition of the thalamus causes Glu to be released and initiation of movement from motor areas

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5
Q

How does teh indirect pathway work

A 
Glu from Cx - Striatum 
GABA from striatum - GPe 
GABA from GPe - STN 
Glu from STB - GPi and SNr 
GABA from GPi and SNr - Thalamus 
GABA from thalamus inhibits movements
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6
Q

What are the cardinal parkinson features?

A

Tremor, rigidity/stiffness, bradykinesia (slow movement), postural instability

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7
Q

What are the other motor features of parkinsons?

A 
Mask like faces 
Decreased blink rate 
Hypometric saccased 
Hypophonia 
Dysarthria 
Dysphagia 
Micographia 
Gait abnormalaties: shuffling, reduced arm swing, freezing, festination
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8
Q

What are the non motor parkinsons symptoms?

A 
Anosmia (sense of smell) 
Depression 
Dementia 
Psychosis 
Pain 
Constipation 
Fatigue 
Sleep disturbance
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9
Q

What are the red flags that it is a parkinson mimic?

A 
Symetrical onset 
Early falls 
Broad based gait 
Early cognitive dysfunction 
Dyspraxia 
Cortical sensory loss 
Early severe autonomic dysfunction 
Cerebellar signs 
UMN signs 
Suprnuclear gaze palsy 
Antecollis 
Poor response to levodopa
Rapid progression
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10
Q

What are the Parkinson mimics?

A

Secondary parkinsonism: vascular, drugs, normal pressure hydrocephalus, subdural haematoma, repeated head traums

Dementia with Lewy bodies
Corticobasal degeneration
Progressive supranuclear palsy
Multiple systems atrophy

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11
Q

What are the clinical features of vascular parkinsonism and what causes it?

A

Postural instability
Greater effect on lower body
Pyramidal signs
Early subcortical damage

due to underlying ischaemic cerebrovascular disease

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12
Q

What is the triad of normal pressure hydrocephalus?

A

Cognitive impairment, incontinence and gait apraxia

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13
Q

What drugs can induce parkinsons?

A

Typical Antipsychotics: haloperidol, flupenthixol, chlorpromazine
Atypical antipsychotics: Risperidone
Antiemetics: metoclopramide

Avoid these in parkinsons patients

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14
Q

What are the drugs used to treat psychosis in parkinson patients?

A

Quetiapine and clozapine

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15
Q

What is the presentation of demetia with lewy bodies and what are the core and suggestive features?

A

Cognitive impairment preceding or early after onset of parkinsonian motor symptoms

Core features: recurrent well formed visual hallucinations
Suggestive features: REM sleep disorder, sensitivity to neuroleptics

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16
Q

What will you see in corticobasal degeneration?

A 
Apraxia 
Cognitive decline 
Dystonia/rigidity 
Myoclonus 
Alien hand phenomenon 
Poor response to levodopa
17
Q

What will you see in progressive supranuclear palsy?

A

Deficit in downgaze
Frequent falls
Executive dysfunction
Poor response to levodopa

18
Q

What will you see in multisystem atrophy?

A

Autonomic dysfunction
Parkinsonian or cerebellar dysfunction
+/- pyramidal signs
Poor response to levodopa

19
Q

What causes parkinsons disease, when will symptoms occur?

A

Destruction of the dopaminergic neurons in the substantia nigra, brainstem, olfactory tract and GIT
Symptoms will occur after 60-80% loss

20
Q

What are the genes involved in PD and what do they encode?

A

PARK 1 - 16

Encode: SNCA (alpha synuclein), LRRK2 (leucine rich repeat kinase)

21
Q

What is the pharmacological treatment for parkinsons?

A 
Levodopa 
Dopamine antagonists 
COMT inhibitors 
MAOB inhibitors 
Amantadine
22
Q

What is levodopa, what does it do and what is it effective with and wha should you give it with?

A

Precursor to dopamine which compensates for the loss of dopaminergic neurons

Most effective drug for the motor symptoms - bradykinesia and rigidity (less effective for tremor)

Should be given with peripheral DOPA decarboxylase inhibitor

23
Q

What are dopamine agonists, when are they preferable, what are the side effects?

A

Direct agonist at D2 receptors
May be preferable as first line therapy in younger patients
SE: sleepiness, impulse control disorders and hallucinations

24
Q

What is a COMT inhibitor

A

Catechol-O-methyltransferase inhibitor - increases the availability of dopamine at the synapse
Given with l-dopa to increase ‘on’ time

25
Q

What is a MAOB inhibitor?

A

Monoamine oxidase B inhibitor which acts to increase the availability of dopamine at the synapse

26
Q

What is the role of amantadine?

A

Increases dopamine release, blocks cholinergic receptors (NMDA)
mainly used in adjunctive therapy to reduce drug induced dyskinesia

27
Q

What should you do when there are motor fluctuations?

A

Add adjunctive medications
Parenteral dopamine agonist
Intstinal levodopa

28
Q

What are the surgical targets in PD surgery and what symptoms is it effective for?

A

GPi - interrupts inhibitory input to the thalamus

STN: reduced excitatory input to GPi

29
Q

What are the clinical findings of stiff person syndrome?

A 
Rock hard muscles in symptomatic regions 
Hyperlordosi, paraspinal muscle spasm 
Stiff gait 
Hyperreflexia 
Head retraction reflex 
Autonomic dysfunction
30
Q

What is the diagnosis of stiff person syndrome?

A
  1. Insidious onset of muscular rigidity with difficulty turning or bending, with rigidity most prominent in limbs and axial muscles
  2. Co-contraction of agonist and antagonist muscles (clinical and electrophysiological)
  3. Episodic spasms superimposed on the underlying rigidity precipitated by noise, tactile stimuli and emotional upset
  4. Absence of other neurological or systemic disease that could explain the symptoms
31
Q

What is the tetrad of neuroleptic malignant syndrome?

A

Altered mental state
Muscle rigidity
Fever (>38)
Autonomic instability

32
Q

What is the proposed mechanism for neuroleptic malignant syndrome?

A

Central dopamine receptor blockade

Block 6 (48 decks)

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