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Parkinsonism may rarely occur on a familial basis, and the parkinsonian phenotype may result from mutations of several different genes Postencephalitic parkinsonism is becoming increasingly rare Exposure to certain toxins (eg, manganese dust, carbon disulfide) and severe carbon monoxide poisoning may lead to parkinsonism Typical parkinsonism has occurred in individuals who have taken 1-methyl-4-phenyl1,2,5,6-tetrahydropyridine (MPTP) for recreational purposes This compound is converted in the body to a neurotoxin that selectively destroys dopaminergic neurons in the substantia nigra Reversible parkinsonism may develop in patients receiving neuroleptic drugs (see 25), reserpine, or metoclopramide Only rarely is hemiparkinsonism the presenting feature of a progressive space-occupying lesion In idiopathic parkinsonism, dopamine depletion due to degeneration of the dopaminergic nigrostriatal system leads to an imbalance of dopamine and acetylcholine, which are neurotransmitters normally present in the corpus striatum Treatment is directed at redressing this imbalance by blocking the effect of acetylcholine with anticholinergic drugs or by the administration of levodopa, the precursor of dopamine

Treatment is often unnecessary When it is required because of disability, propranolol may be helpful but will need to be continued indefinitely in daily doses of 60 240 mg However, intermittent therapy is sometimes useful in patients whose tremor becomes exacerbated in specific predictable situations Primidone may be helpful when propranolol is ineffective, but patients with essential tremor are often very sensitive to it Therefore, the starting dose is 50 mg daily, and the daily dose is increased by 50 mg every 2 weeks depending on the patient s response; a maintenance dose of 125 mg three times daily is commonly effective Occasional patients do not respond to these measures but are helped by alprazolam (up to 3 mg daily in divided doses), clozapine (30 50 mg twice daily), or mirtazapine (15 or 30 mg at night) Benefit has been reported with topiramate titrated up to a dose of 400 mg daily over about 8 weeks Other antiepileptic agents including gabapentin, levetiracetam, and zonisamide are reported to be effective sometimes Disabling tremor unresponsive to medical treatment may be helped by contralateral thalamotomy Unilateral highfrequency thalamic stimulation is an alternative approach that is equally effective, is associated with only mild and transient side effects, and is therefore preferred Bilateral thalamotomy

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Tremor, rigidity, bradykinesia, and postural instability are the cardinal features of parkinsonism and may be present in any combination There may also be a mild decline in intellectual function The tremor of about four to six cycles per second is

clear palsy, bradykinesia and rigidity are accompanied by a supranuclear disorder of eye movements, pseudobulbar palsy, and axial dystonia Creutzfeldt-Jakob disease may be accompanied by features of parkinsonism, but dementia is usual, myoclonic jerking is common, ataxia and pyramidal signs may be conspicuous, and the electroencephalographic findings are usually characteristic In cortical-basal ganglionic degeneration, parkinsonism is accompanied by conspicuous signs of cortical dysfunction (eg, apraxia, sensory inattention, dementia, aphasia)

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most conspicuous at rest, is enhanced by emotional stress, and is often less severe during voluntary activity Although it may ultimately be present in all limbs, the tremor is commonly confined to one limb or to the limbs on one side for months or years before it becomes more generalized In some patients, tremor is absent Rigidity (an increase in resistance to passive movement) is responsible for the characteristically flexed posture seen in many patients, but the most disabling symptoms of parkinsonism are due to bradykinesia, manifested as a slowness of voluntary movement and a reduction in automatic movements such as swinging of the arms while walking Curiously, however, effective voluntary activity may briefly be regained during an emergency (eg, the patient is able to leap aside to avoid an oncoming motor vehicle) Clinical diagnosis of the well-developed syndrome is usually simple The patient has a relatively immobile face with widened palpebral fissures, infrequent blinking, and a certain fixity of facial expression Seborrhea of the scalp and face is common There is often mild blepharoclonus, and a tremor may be present about the mouth and lips Repetitive tapping (about twice per second) over the bridge of the nose produces a sustained blink response (Myerson s sign) Other findings may include saliva drooling from the mouth, perhaps due to impairment of swallowing; soft and poorly modulated voice; a variable rest tremor and rigidity in some or all of the limbs; slowness of voluntary movements; impairment of fine or rapidly alternating movements; and micrographia There is typically no muscle weakness (provided that sufficient time is allowed for power to be developed) and no alteration in the tendon reflexes or plantar responses It is difficult for the patient to arise from a sitting position and begin walking The gait itself is characterized by small shuffling steps and a loss of the normal automatic arm swing; there may be unsteadiness on turning, difficulty in stopping, and a tendency to fall.

FIGURE 7-13

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