Neuro drugs

Question 1

Madopar/ Sinemet
use?
mechanism? 
SE? 
interactions?

Answer 1

L-dopa/peripheral decarboxylase inhibitors.

Used in PD (and secondary parkinsonism)
In PD there is a deficiency of dopamine in the nigrostriatal pathway leading to greater inhibition on thalamus and reduced excitory input to the motor cortex - increased bradykinesia and rigidity. opamine does not cross blood-brain barrier but levodopa is a precursor which can enter the brain. Dopa decarboxylase inhibitors prevents peripheral conversion of levodopa to dopamine (increasing concentration and decreasing side effects)

SEs: nausea, drowsiness, confusion, hallucinations and hypotension. Wearing off effect as therapy goes on – can increase dose but !may get excessive & involuntary movement! – dyskinesia (the on-off effect)
Interactions: Don’t combine w/ anti-psychotics or metoclopramide

Question 2

Anti-convulsants for epilepsy, name 4

Answer 2

Phenytoin, Carbamazepine,
Sodium valproate,
Lamotrigine

Question 3

Phenytoin - specific use and mechanism?

SE>?

Answer 3

To control seizures in status epilepticus (when benzodiazepines ineffective) to reduce frequency of generalised/focal seizures in epilepsy (although not first line)
Mechanism not completely known – reduces neuronal excitability by binding to neuronal Na+ channels. (also has a similar effect in cardiac purkinje fibres - antiarrhythmic and cardiotoxic)

SEs: change in appearance (skin coarsening, acne, hirsutism and gum hypertrophy. Neurological effects e.g. nystagmus, ataxia, haematological disorders, osteomalacia. Hypersensitivity (mild rash - antiepileptic hypersensitivity syndrome). Phenytoin toxicity - cardiovascular collapse/respiratory depression.

Question 4

Sodium valproate - specific uses?
Mechanism
Avoid in who?

Answer 4

first choice for epilepsy (reduce freq of seizures) and for acute treatment & prophylaxis of mania in bipolar disorder
Mechanism not fully understood – inhibitor of neuronal sodium channels reducing neuronal excitability and increases γ-aminobutyric acid (GABA).

First choice for epilepsy (reduce freq of seizures) and for acute treatment & prophylaxis of mania in bipolar disorder

Mechanism not fully understood – inhibitor of neuronal sodium channels reducing neuronal excitability and increases γ-aminobutyric acid (GABA).

Avoid in women of child-bearing age – foetal abnormalities (epilepsy drug w/ greatest risks – if necessary contraception). Avoid in hepatic and dose reduction w/ renal impairment.
Interactions: Anything metabolised by cytP450 has increased toxicity. Inhibitors of CytP450 increase SEs and inducers reduce conc of valproate + drugs that displace binding site (aspirin) and drugs that lower seizure threshold (anti-depressents/ psychotics)

Question 5

Driving rules for epilepsy?

Answer 5

Driving, for all epilepsy drugs: Advise not to drive unless seizure free for 1 year or only seizure when asleep for 3 years, don’t drive for 6 months after changing medication.