The drug is matched to the individual patient and the type of epileptic seizures. Between 70 and 80% of epileptic patients will become seizure free with the appropriate medication.

The aim is to treat the patient without causing side effects and using a single drug. Sodium valproate is usually the drug of choice. Carbamazepine (Tegretol or Carbatrol; see Figure 33.5) and phenytoin (Dilantin or Phenytek) can be used in its place, but are considered alternatives.

Lamotrigine is now rapidly becoming a drug of choice, as it does not need constant monitoring and has relatively few side-effects.

Carbamazepine is the drug of choice for partial seizures. It is a tricyclic antidepressant derivative and is thought to work by blocking the calcium and sodium channels on the neurons (see Chapter 31 ‘The nervous system’, p. 237). Because of this, it has been used in neuralgias and certain types of dystonia. Because it induces its own metabolism (it is an enzyme inducer) its half-life can fall dramatically during chronic administration. It is therefore started at a low dose, which is gradually increased.

Ethosuximide is used instead of sodium valproate for absence (petit mal) seizures.

Phenobarbital is now only used when other treatments fail; it is an inexpensive medication.

Anticonvulsants tend to have interactions with a wide range of drugs, but particularly those that bind to the plasma proteins (see Chapter 16 ‘How do drugs get into cells?’, p. 126) or those metabolized by the liver (see Chapter 17 ‘Metabolism’, p. 129).

One of the problems is that they can increase the chances of toxicity without increasing the antiepileptic effect. Supplements or herbal treatment do, therefore, have the potential to interact with these powerful drugs. Valproate and newer antiepileptic drugs do not require such careful monitoring of the plasma levels, but the newer drugs are expensive and tend to be used not in isolation but with other drugs that have reached their optimum dosage and are not having the required effect.

A third of patients will need more than one drug to keep the condition under control.

The substantia nigra deteriorates. This is the area of the brain that sends signals down the spinal cord to control the muscles of the body. Dopamine, the main neurotransmitter, is made by the cells of the substantia nigra.

The basal ganglia, the red nucleus, the substantia nigra, the reticular formation and the cerebellum are all part of the extrapyramidal system, which controls gross autonomic motor movement (Figure 33.1). The basal ganglia inhibit the rapid firing of the motor neurons. This control is reduced when the inhibitory function of dopamine is lessened; hence the increase in tremors through lack of inhibition.

Figure 33.1 The basal nuclei and their linkage to motor tracts.

Dopamine cannot cross the blood–brain barrier and therefore cannot be used as therapy. However, its precursor, levodopa, can cross the barrier and enter the brain. Once in the brain, it is converted to dopamine (Figure 33.2), thereby increasing the levels and helping to reduce symptoms. Dopamine agonists are used largely in an effort to maintain the dopamine levels in the body.

Figure 33.2 The conversion of levodopa to dopamine.

These are extensive:

These are used in patients in whom Parkinson’s has been induced by antipsychotic drugs or recreational drugs. They reduce the effects of the cholinergic excess in the CNS, which occurs as a result of dopamine deficiency (Figure 33.3).

Figure 33.3 Chemical structures of the neurotransmitter acetylcholine, benztropine (an antimuscarinic used to counteract cholinergic symptoms) and other types of muscarinic blocker, demonstrating the similarities between the structures.