Antipsychotic medications are probably the major cause of parkinsonism worldwide. The incidence of drug-induced parkinsonism increases with age, and affects 40–75% of all schizophrenic patients. No correlation of incidence with gender has been observed.

Drug-induced parkinsonism occurs at a greater incidence with high potency drugs than with low potency drugs¹¹. It affects 5–15% of patients receiving olanzapine¹² or risperidone¹³. Experience at our clinic indicates that olanzapine and risperidone produce similar levels of EPS.  With risperidone, these effects seem to be dose-related.

Differential diagnosis
Drug-induced parkinsonism is associated with a number of signs or symptoms that should make differential diagnosis a relatively simple task (Table 4). Yet parkinsonism appears severely under diagnosed, for a variety or reasons.
 

Sign  Tremor  Rigidity  Bradykinesia  Loss of postural reflexes Falls (caused by loss of postural reflexes)  Incidence (%)  15  90  95  20  20

Table 4. Signs that comprise a differential diagnosis for drug-induced parkinsonism.

Most non-neurologists associate parkinsonism with tremor, a relatively easy symptom to spot. However, in drug-induced parkinsonism, tremor is relatively rare, occurring with only 15% of patients.  This is possibly one reason for under-diagnosis of parkinsonism in psychiatric populations.

Rigidity is more common in patients with drug-induced parkinsonism, with up to 90% of psychiatric patients exhibiting this condition. Yet it is frequently missed because many psychiatrists, through training or preference, do not physically examine their patients. Bradykinesia is even more common, occurring in at least 95% of patients with drug-induced parkinsonism. However, bradykinesia is often not diagnosed as a neurological problem, but instead is explained as a blunted affect or other negative symptoms of schizophrenia.

Another cardinal sign of parkinsonism that psychiatrists invariably miss is loss of postural reflexes, seen in approximately 20% of cases.  Many psychiatrists never test for this sign, and others are unaware it exists.  A simple postural stability test is a practical way of determining whether drug-induced parkinsonism is involved.

Falls caused by loss of postural reflexes can cause hip fractures in older patients, and are a substantial cause of morbidity and mortality.  Such falls are estimated to result in :

• A 23% mortality rate in the first year (compared with 8% in the absence of falls)
• 50% of patients losing the capacity to walk independently, and
• 33% of patients requiring long-term care in a nursing home care.

In a similar fashion, bradykinesia or akinesia in a schizophrenic patient may be assumed to be part of the apathy and avolition associated with negative symptoms of schizophrenia.  Even the latency in responding to questions may be misdiagnosed as an alogia or a poverty of content of speech.  The patient’s sad face, lack of energy, depressive posture, and fatigue may all be wrongly attributed to depression, rather than to drug-induced parkinsonism.

A feeble posture in older patients caused by drug-induced parkinsonism may be overlooked as a result of society’s perception of the elderly.  It is curious that, in many countries, the medication of choice for older individuals is haloperidol, arguably the most potent inducer of parkinsonian symptoms.

Treatment
The most common treatments employed by psychiatrists for drug-induced parkinsonism are the anticholinergic agents, with their associated side-effects of dry mouth, blurred vision, constipation, and central nervous system (CNS)  impairments, such as confusion, disorientation, short-term memory impairment, and delirium.  The alternative, the downward titration of antipsychotic dose to a level that does not cause parkinsonism, risks taking the dose to a subtherapeutic level in terms of antipsychotic efficacy.

In a few countries, amantadine is used for the treatment of EPS.  Amantadine shows efficacy in this indication but also produces characteristic side-effects, such as subjective dizziness, and may exacerbate psychosis. Patients must also have good renal function in order to be candidates for amantadine.  Amantadine is probably underutilized in the treatment of drug-induced parkinsonism.

Quality of life
Patients and members of their families will often say that they do not like the ‘zombie-like’ appearance that anti-schizophrenic drug therapy has induced. They are, of course, describing drug-induced parkinsonism.
 

Zombie-like appearance  Decreased emotional expressiveness  Decreased physical activity  Decreased ability to function in environment  Impaired social responsiveness, possibly attributable to bradyphrenia  and/or bradykinesia

Table 5. Features of parkinsonism that affect the patient’s quality of life.

Many features of parkinsonism have a significant impact on the patient’s quality of life (see Table 5). These problems are often overlooked in a psychiatric setting because the patients look ‘normal’ in that environment.  However, the same people are very easy to spot in a shopping arcade.  The loss of the ability to smile, or to show an appropriate affect when addressed, clearly has a substantial impact on quality of life.  Drug-induced parkinsonism impairs enormously the social responsiveness of patients, and this clearly hinders integration back into the community.  Psychiatry is effectively robbing patients of important components needed for leading a normal life.

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