CPT26 - Neurological Disorders

Question 1

4 general features of idiopathic Parkinson’s Disease

Non-motor Symptoms x5
Pathological Features x4
Diagnosis x4
Treatment

Answer 1

1.) Non-Motor Symptoms - mood and cognitive changes, pain, urinary symptoms, sleep disorder, sweating

2. ) Pathological Features
   - neurodegeneration, Lewy bodies, reduced dopamine
   - loss of pigment (>50% loss –> symptoms)
3. ) Diagnosis - using clinical features (motor/non-motor)
   - exclude other causes of Parkinsonism
   - response to treatment
   - structural and functional neuro imaging: SPECT, PET, DAT scan looks at dopamine recycling (↓ in PD)
4. ) Treatment - drugs, surgery
   - surgery is only for severe motor complications

Question 2

5 features of using levodopa (L-DOPA) to treat Parkinson’s Disease

Examples x2
Mechanism
Usage
Additional Side Effects x3
Drug Interactions x3

Answer 2

1. ) Examples - co-careldopa, co-beneldopa (both oral)
   - contain levodopa + DOPA decarboxylase inhibitor
2. ) Mechanism - ↑dopamine in the brain
   - using carbidopa ↓dose required, and ↓side effects
3. ) Usage - first-line
   - for patients with motor symptoms affecting QoL
   - considered w/ others if QoL not affected
4. ) Additional Side Effects
   - N/V, hypotension, tachycardia
5. ) Drug Interactions
   - vitB6 (pyridoxine) ↑peripheral breakdown of L-DOPA
   - high dose MAOi –> hypertensive crisis
   - other antipsychotics: can block dopamine receptors

Question 3

3 features of using monoamine oxidase (MAO)-B inhibitors to treat parkinson’s disease

Examples x2
Mechanism
Usage

Answer 3

1.) Examples - rasagiline, selegiline

2. ) Mechanism - ↑dopamine in brain
   - inhibits MAO-B which metabolises dopamine
   - ↑activity in dopamine containing regions in the brain
3. ) Usage - first line if symptoms aren’t affecting QoL
   - can be added w/ levidopa (prolongs action)

Question 4

4 features of using dopamine agonists to treat Parkinson’s Disease

Examples x3
Mechanism
Usage
Additional Side Effects x3

Answer 4

1. ) Examples - ropinirole (non-ergot), rotigotine (patch) apomorphine (SC)
2. ) Mechanism - mimics effect of dopamine
3. ) Usage - first line if symptoms aren’t affecting QoL
   - can be added w/ levidopa if treatment not working
   - apomorphine is only used for patients with severe motor fluctuations
4. ) Additional Side Effects
   - N/V, hypotension, confusion

Question 5

Comparing levidopa, MAO-Bi, and dopamine agonists

Effect on Motor Symptoms
Motor Complications
Other Side Effects x3

Answer 5

1. ) Effect on Motor Symptoms
   - levidopa improves motor symptoms the best
   - MAO-Bi and dopamine agonists have lower impact
2. ) Motor Complications
   - levidopa has more motor complications
   - MAO-Bi and dopamine agonists have fewer
3. ) Other Side Effects - excessive sleepiness, hallucinations, impulse control disorders
   - levidopa has lowest risk of these side effects
   - MAO-Bi and dopamine agonists has highest risk

Question 6

5 examples of impulse control disorders (dopamine dysregulation syndrome)

Answer 6

Pathological Gambling
Hypersexuality
Compulsive Shopping
Desire to Increase Dosage
Punding - collecting and organising

Question 7

3 other drug types used to treat Parkinson’s Disease

COMT Inhibitors
Anticholinergics x2
Amantidine

Answer 7

1. ) COMT Inhibitors - entacapone
   - ↓peripheral breakdown of L-DOPA to 3-o-methyldopa
   - only combined w/ levodopa, prolongs effect of DOPA (reduces symptoms ‘wearing off’)
2. ) Anticholinergics - orphenadrine, procyclidine
   - ↓antagonistic effects of ACh on dopamine
   - useful for tremors but no effect on bradykinesia
   - has the usual side effects e.g. confusion, drowsiness
3. ) Amantidine - mechanism uncertain
   - not that effective but few side effects

Question 8

4 general features of myasthenia gravis (MG)

Pathophysiology
Symptoms x4
Exacerbating Drugs x5
Complications

Answer 8

1.) Pathophysiology - autoimmune IgG blocks the ACh receptors in the NMJ, preventing muscle stimulation

2. ) Symptoms - fluctuating and fatiguable weakness
   - extraocular muscles: commonest presentation
   - bulbar involvement: dysphagia, dysphonia, dysarthria
   - limb weakness: proximal symmetric
   - respiratory muscle: type 2 respiratory failure
3. ) Exacerbating Drugs - caution using these drugs
   - ACEi, ß-blockers, CCB, aminoglycosides, magnesium
4. ) Complications x2
   - acute exacerbation is a myasthenic crisis
   - overtreatment leads to a cholinergic crisis

Question 9

4 features of using AChE inhibitors to treat myasthenia gravis

Examples x2
Mechanism
Dosing
Side Effects

Answer 9

1. ) Examples - pyridostigmine and neostigmine
   - neostigmine can be IV but greater side effects
2. ) Mechanism - ↑ACh in the synaptic cleft
   - prevents the breakdown of ACh
3. ) Dosing - interval and timing is crucial
   - onset is 30min so should be taken before meals to prevent aspiration
   - duration is 3-6hrs
4. ) Side Effects - overdose –> ↑parasympathetics
   - SLUDGE

Question 10

4 other ways of managing myasthenia gravis

Answer 10

1.) Corticosteroids - decrease immune response

2. ) Steroid Sparing - azathioprine
   - ↓production of autoantibodies in the first place

3.) IV Immunoglobulin - in acute decline or crisis

4. ) Plasmapheresis - provides short term improvement
   - removes AChR antibodies