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NEURO (Neurology) > Movement Disorders > Flashcards

Movement Disorders Flashcards

1
Q

Parkinson’s Disease Tremor vs. Benign Essential Tremor (6).

A
  1. Parkinson’s = Asymmetrical; BET = Symmetrical.
  2. Parkinson’s = Frequency of 4-6Hz; BET = Frequency of 5-8Hz.
  3. Parkinson’s = Worsens with Rest; BET = Improves with Rest.
  4. Parkinson’s = Improves on Intentional Movement; BET = Worsens with Intentional Movement (e.g. Outstretched Arms).
  5. Parkinson’s = No Change with Alcohol; BET = Improves with Alcohol.
  6. To distinguish, NICE recommend I-FP-CIT SPECT Scans.
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2
Q

Differential Diagnosis of Tremor (7).

A
  1. Benign Essential Tremor.
  2. Parkinson’s Disease.
  3. Hyperthyroidism.
  4. Multiple Sclerosis.
  5. Huntington’s Disease.
  6. Fever.
  7. Medications e.g. Antipsychotics, Lithium.
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3
Q

Types of Tremor (4).

A
  1. Resting = abolished on voluntary movement, usually Parkinson’s.
  2. Intention = large amplitude and irregular tremors worse at the end of purposeful acts, usually Cerebellar Damage.
  3. Postural = absent at rest and present on maintained posture and movement, usually BET, Thyrotoxicosis, Anxiety, B-Agonists.
  4. Re-Emergent = postural tremor that develops after a delay around 10 seconds, usually Parkinson’s.
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4
Q

What is Benign Essential Tremor?

How is it diagnosed?

A

An autosomal dominant condition that usually affects the upper limbs. It is the commonest cause of titubation (head tremor).

It is a clinical diagnosis (after excluding differentials).

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5
Q

Management of Benign Essential Tremor (2).

A
  1. No definitive treatment unless psychological or functional symptoms.
  2. Pharmacological : Propanolol (Non-Selective B-Blocker) or Primidone (Barbiturate Anti-Epileptic).
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6
Q

Structure of Basal Ganglia (4).

A

On both sides of the brain :

  1. Caudate Nucleus.
  2. Globus Pallidus.
  3. Substantia Nigra.
  4. Sub-Thalamic Nucleus.
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7
Q

What is the function of the Basal Ganglia?

A

Helps plan and control complex patterns of movement, by controlling the relative intensities, directions and sequencing of multiple successive and parallel movements to achieve specific complicated motor goals. It is an accessory motor system.

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8
Q

What are the two sections of the Basal Ganglia? (2)

A
  1. Pars Reticulata - receives signals from the Striatum (Caudate Nucleus + Putamen) and relays signals to the Thalamus via GABAergic neurones.
  2. Pars Compacta - forms the Nigrostriatal Pathway by sending messages to the Striatum (Caudate Nucleus + Putamen) via Dopaminergic Neurones.
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9
Q

What are the three cardinal clinical features of Parkinson’s Disease?

A
  1. Bradykinesia.
  2. Rigidity.
  3. Tremor.
    BRT.
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10
Q

Give 5 characteristics of the Tremor in Parkinson’s Disease.

A
  1. Resting Tremor (more pronounced when resting).
  2. Pill-Rolling Tremor.
  3. Frequency of 4-6 Hz.
  4. Improvement on Voluntary Movement.
  5. Exacerbation on Distraction, Stress and Fatigue.
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11
Q

Give 4 characteristics of the Rigidity in Parkinson’s DIsease.

A
  1. Resistance due to passive movement in a joint.
  2. Cogwheel Rigidity : passive flexion against tension in their limb gives way to movement in small increments - little jerks.
  3. This is due to a super-imposed tremor.
  4. Can be lead-pipe rigidity.
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12
Q

Give 2 characteristics of the Bradykinesia in Parkinson’s Disease.

A
  1. Progressively slower and smaller nature of patient’s movements.
  2. Can be seen with hypokinesia (poverty of movement).
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13
Q

Give 4 manifestations of Bradykinesia.

A
  1. Micrographia (Smaller Handwriting).
  2. Shuffling Gait (Smaller Steps).
  3. Difficulty Initiating Movement/Turning Around.
  4. Hypomimia/Mask-Like Facies (Reduced Facial Movements and Facial Expression).
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14
Q

Epidemiology of Parkinson’s Disease (2).

A
  1. 2x commoner in men.

2. Mean age of diagnosis = 65 years.

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15
Q

Aetiology of Parkinson’s Disease (3).

A
  1. Substantia Nigra of Basal Ganglia produces Dopamine (responsible for correct functioning of Basal Ganglia).
  2. Gradual progressive fall in the production of Dopamine (due to loss of neurones from the Substantia Nigra).
  3. Dopamine produced in the Striatum (Caudate Nucleus + Putamen) is inhibitory - so in Parkinson’s, the Striatum will become overly active to cause a continuous output of excitatory signals to the corticospinal tracts, overly exciting muscles of the body.
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16
Q

Investigations of Parkinson’s Disease (2).

A
  1. Clinical Diagnosis by a Specialist (2/3 symptoms needed).

2. NICE recommend using UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria.

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17
Q

Management of Parkinson’s Disease (2).

A
  1. If symptoms affect quality of life, 1st line = Levodopa.

2. If symptoms don’t affect quality of life = non-Ergot derived Dopamine agonists, Levodopa, MAO-B Inhibitors.

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18
Q

Parkinson’s Plus Syndromes (5).

A
  1. Multiple System Atrophy.
  2. Dementia with Lewy Bodies.
  3. Progressive Supranuclear Palsy : ophthalmoplegia (CN III, IV, VI) and no tremor.
  4. Corticobasal Degeneration : dysphagia, dysarthria and aphasia (cortical cell death).
  5. Steele-Richardson-Olszweski Syndrome : difficulty moving downstairs.
19
Q

Features of Multiple System Atrophy (6).

A

Any sign of Autonomic Dysfunction :

  1. Postural Hypotension.
  2. Constipation.
  3. Abnormal Sweating.
  4. Sexual Dysfunction.
  5. Cerebellar Dysfunction.
  6. Atonic Bladder.
20
Q

Features of Dementia with Lewy Bodies (5).

A

Dementia with :

  1. Parkinsonian Symptoms.
  2. Delusions.
  3. Visual Hallucinations.
  4. REM Sleep.
  5. Fluctuating Consciousness.
21
Q

Mechanism of Action of Levodopa (3).

A
  1. Synthetic Dopamine that is given orally to boost Dopamine levels.
  2. Administered with a peripheral Decarboxylase inhibitor e.g. Carbidopa (Co-Careldopa) and Benserazide (Co-Benyldopa).
  3. Once inside the remaining nigrostriatal neurone, it will be converted by DOPA-Decarboxylase.
22
Q

Indication of Levodopa.

A

Most effective Parkinson’s Disease Drug but efficacy decreases over time so it’s reserved for when other treatments cannot manage symptoms.

23
Q

Caution of Levodopa.

A

If a patient cannot take Levodopa orally or is admitted to hospital, give a Dopamine agonist patch as rescue medication to prevent acute dystonia.

24
Q

Adverse Effect of Levodopa.

A

Dyskinesias.

25
Q

Examples of MAO-Inhibitors (2).

A
  1. Selegiline.

2. Rasagiline.

26
Q

Mechanism of Action of MAO-Inhibitors (3).

A
  1. MAO Enzymes break down neurotransmitters such as Dopamine, Serotonin and Adrenaline.
  2. MAO-B is more specific to Dopamine and does not act on Serotonin or Adrenaline.
  3. MAO-B Inhibitors therefore block the enzyme and increase the circulating Dopamine.
27
Q

Indications of Other Parkinson’s Drugs (not Levodopa).

A

Delay the use of and reduce the dose required of Levodopa.

28
Q

Examples of COMT Inhibitors (2).

A
  1. Entacapone.

2. Tolcapone.

29
Q

Mechanism of Action of COMT Inhibitors (2).

A
  1. Inhibitor of Catechol-O-Methyltransferase Enzyme (COMT).

2. COMT usually metabolises Levodopa in both the body and the brain.

30
Q

Examples of Dopamine Agonists (4).

A

CabBroPerRop

  • Cabergoline (Ergot-Derived);
  • Bromocriptine (Ergot-Derived);
  • Pergolide (Ergot-Derived);
  • Ropinirole.
31
Q

Mechanism of Action of Dopamine Agonists.

A

Mimic the action of Dopamine in the basal ganglia and stimulate the Dopamine receptors (less effective than Levodopa).

32
Q

Adverse Effects of Dopamine Agonists (6).

A
  1. Impulse Control Disorders.
  2. Excessive Daytime Somnolence.
  3. Hallucinations.
  4. Confusion.
  5. Compulsive Behaviours.
  6. Ergot-Derived : Pulmonary, Retroperitoneal, Cardiac Fibrosis (monitoring + investigations before treatment).
33
Q

Other Parkinson’s Disease Drugs (4).

A

AAAD.

  1. Amantadine - weak Dopamine agonist.
  2. Anti-Muscarinics e.g. Procyclidine, Benzotropine - more useful in Drug-induced Parkinsonism.
  3. Apomorphine - subcutaneous injection of Dopamine agonist (single injection when required).
  4. Duodopa - a gel version of Levodopa, continuously pumped into gut through abdomen, only prescribed if severe on-off fluctuations.
34
Q

Parkinson’s Disease Surgery (2).

A
  1. Deep Brain Stimulation - surgically implanting a pulse generator (like a pacemaker) into specific areas of the brain to produce a tiny electric current. Not curative - only symptomatic.
  2. Surgical Ablation of Overactive Basal Ganglia Circuits e.g. Sub-thalamic Nuclei.
35
Q

Causes of Parkinsonism (8).

A
  1. Parkinson’s Disease.
  2. Vascular/Lower-Limb Parkinsonism = Diabetic/Hypertensive Patient with Postural Instability and Falls.
  3. Drug-Induced e.g. Antipsychotics, Antiemetics = motor symptoms are usually bilateral and of rapid onset and rigidity and rest tremors are uncommon.
  4. Parkinson’s Plus Syndromes.
  5. Wilson’s Disease.
  6. Post-Encephalitis.
  7. Dementia Puglistica (secondary to chronic head trauma e.g. boxing).
  8. Toxins e.g. CO, MPTP.
36
Q

Epidemiology of Huntington’s Disease.

A

Asymptomatic until the age of 35-50.

37
Q

Genetics of Huntington’s Disease.

A
  1. Type : Autosomal Dominant.
  2. Mutation : HTT Gene on Chromosome 4 - Trinucleotide Repeat Disorder. Usually CAG godes for Glutamine and is repeated 10-35x in good health but in Huntington’s, it is repeated more than 36x = polyglutamine disease.
  3. Anticipation : Successive generations have more repeats in the gene - this causes an earlier age of onset and increased severity of disease across generations. This is due to DNA Polymerase errors during gamete (especially sperm) synthesis, causing more repeats to be added, making it more unstable.
  4. Penetrance : 100% if 40+ repeats (definitely shows symptoms) and reduced penetrance if between 36-39 repeats.
38
Q

Pathophysiology of Huntington’s Disease (5).

A
  1. Mutated protein aggregates within neuronal cells of the caudate and putamen.
  2. Neuronal cell death and excitotoxicity.
  3. Excessive signalling increases Calcium levels.
  4. Degeneration of cholinergic and GABAergic neurones in the striatum of the basal ganglia. Axon terminals of GABAergic neurones normally inhibit portions of the Globus Pallidus and Substantia Nigra - loss of these neurones allows spontaneous outbursts of activity in these structures, causing distortional movements.
  5. Tissue loss in dorsal striatum (caudate and putamen) leading to expansion of lateral ventricles.
39
Q

Clinical Features of Huntington’s Disease (5).

A

Insidious and progressive worsening, typically beginning with cognitive/psychiatric/mood problems followed by movement disorders :

  1. Chorea.
  2. Eye Movement (Saccadic) Disorders.
  3. Dysarthria.
  4. Dysphasia.
  5. Personality Changes.
40
Q

Management of Huntington’s Disease.

A

Medications to suppress disordered movements e.g. antipsychotics, benzodiazepines, Dopamine-depleting agents.

41
Q

Prognosis of Huntington’s Disease (3).

A
  1. Life expectancy is at 15-20 years after the onset of symptoms.
  2. Death is often due to respiratory disease e.g. Pneumonia.
  3. Higher rates of Depression - suicide is a commoner cause of death than in the general population.
42
Q

Definition and Aetiology of Dyskinesia.

A

Definition : Abnormal involuntary movement associated with excessive motor activity.
Aetiology : Dose of Dopamine is too high.

43
Q

Clinical Features of Dyskinesias (3).

A
  • Dystonia (abnormal postures of exaggerated movements).
  • Chorea (abnormal involuntary movements that can be jerking and random e.g. facial grimacing, raising shoulders, flexing/extending fingers - putamen).
  • Athetosis (slow, sinuous, confluent, involuntary twisting/writhing movements, usually in the hands/feet - globus pallidus).

NEURO (Neurology) (54 decks)

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