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Motor side effects emerging from the use of neuroleptics have been recognised since their first use in the 1950s. There is however an increasing awareness that other drug classes (in particular other psychotropic drugs and calcium channel blockers) are also implicated in the genesis of parkinsonism and other abnormal involuntary movements. Second-generation antipsychotics have a reduced propensity to lead to these side effects but may still cause problems in high-risk groups like people with dementia. Treatments for the various movement problems (parkinsonism, dyskinesia and dystonias) vary dependent upon the symptoms that predominate, given the differential balance between dopaminergic and cholinergic dysfunction between these three side effect clusters. Though stopping or switching the offending drug is always the first option, newer drugs for the treatment of Alzheimer’s disease whose effects are upon cholinergic transmission are showing some promise as an adjunct to treatments for motor side effects.

From their launch in the 1950s, it was widely recognised that the beneficial effects of antipsychotic drugs were being severely hampered by their propensity to create movement disorders in patients. This led to research (led principally by the pharmaceutical industry) into the biological basis of these side effects with a view to creating new, equally efficacious drugs for psychosis, which were less likely to cause motor side effects. These ‘atypical’ or ‘second-generation’ antipsychotics have had a major impact on the management of psychosis over the last 20 years.

Iatrogenic parkinsonism and other abnormal involuntary movements can undoubtedly be severely disabling for patients. These side effects have an indirect impact on compliance thereby reducing the efficacy of the offending drug, as well as more broadly on quality of life. Moreover, the injudicious use of treatments for these iatrogenic movement disorders can in themselves have deleterious effects on the patient’s mental state.

The clinical features of these side effects will be discussed, which will be followed by a review of what is currently known regarding the biological basis of these symptoms.

This will lead to a description of the drugs most commonly associated with the generation of movement disorders and the patient groups most at risk. Finally, a concluding comment is made upon treatment options.

The motor symptoms of parkinsonism are characterised by four cardinal features namely tremor, bradykinesia, postural instability and hypertonicity. Dystonias also commonly arise in Parkinson’s disease but will be discussed separately below.

The tremor is characteristically at a frequency of approximately 4–6 Hz and can affect any voluntary muscle group in the body. It is most clearly observable though in the fingers and hands leading to the characteristic pill rolling tremor. The tremor can be improved by activity which helps to differentiate it from benign essential tremor which is made worse upon activation.

Bradykinesia (literally slow movement) also can have an impact on all muscle groups. It is particularly observable when it affects the muscles of facial expression giving rise to the characteristic ‘mask-like facies’ and truncal muscles leading to decreased arm swing, stooping and festinant gait.

Postural instability leads to impaired balance and falls. It tends to occur more frequently in elderly patients, and therefore it is a particular problem when using antipsychotic drugs in this patient group.

Hypertonicity of skeletal muscles can be very problematic for patients, and when superimposed on tremor gives rise to the characteristic cogwheel rigidity noted in clinical examination. Without tremor, the hypertonicity may give rise (if severe) to ‘lead pipe rigidity’.

Iatrogenic parkinsonism can be distinguished from idiopathic parkinsonism, as the former tends to cause symmetrical motor symptoms (though up to one third of patients with drug-induced parkinsonism have been reported to have unilateral symptoms [1, 2]), has a subacute onset and is often associated with dyskinesia and akathisia. Drug-induced parkinsonism is also associated with the so-called ‘rabbit syndrome’ which is a low-frequency, high-amplitude jaw tremor [3, 4]. This is an important distinction to make as correct diagnosis will avoid the use of inappropriate dopaminergic therapy. It is also worth considering that whilst neuroleptic drugs are most likely to cause this side effect, they may also be caused by other classes of drugs (table 1).

Dyskinetic movements are distinguished from the tremor seen in Parkinson’s disease because they are irregular in rhythm. These side effects may emerge suddenly (acute dyskinesia) or after chronic exposure to antipsychotics (chronic or tardive dyskinesia). It is important to distinguish parkinsonian tremor from dyskinesia as the treatments vary, with (for instance) anticholinergic treatments being likely to make dyskinetic symptoms worse.

Table 1.
Drugs associated with the development of parkinsonian symptoms (updated from Van Gelder [53])
graphic
graphic

Chorea (which is Greek for ‘dance’ as in choreography) is a particular subtype of dyskinetic movement that is both irregular and non-repetitive. It can appear that the choreic movements travel from muscle group to muscle group causing the characteristic dance-like presentation.

There are many different aetiologies to dystonias which include both genetic and iatrogenic causes. Iatrogenic dystonias can be either acute or chronic and may or may not be related to other features of parkinsonism. Acute dystonic reactions include the oculogyric crisis, where muscles of the eye and neck contract violently very soon after administration of a dopamine-blocking drug, though a wide range of other drugs have also been associated with this condition. Chronic dystonias can be particularly disfiguring and stigmatising especially when they affect shoulder, neck (torticollis) and facial muscles including eye lids (blepharospasm).

The biological basis of the movement disorders is complex. However, those listed above as secondary to medication are characterised by the action of drugs on central nuclei and in particular pathways and nuclei associated with the basal ganglia, a functional unit located at the base of the forebrain.

The basal ganglia have principal connections to the cortices and thalamus. Although involved in multiple functions including cognition and emotional function, it is their role in the control of involuntary movements that is relevant to this chapter. The other functions, though, are clinically important and discussed elsewhere in this book. At rest, the structures of the basal ganglia can be considered to provide a tonic inhibition of motor activity. This inhibition is released through conscious activity via an increased release of dopamine from (in particular) the substantia nigra, thereby allowing voluntary control of motor activity in the necessary area.

The basal ganglia’s key nuclei with regard to movement disorders are the striatum (caudate, putamen and globus pallidus), substantia nigra and the subthalamic nucleus. In Parkinson’s disease, α-synucleinopathy leads to neurodegeneration of the melanin-pigmented dopaminergic neurones of the substantia nigra pars compacta. When activity in the pathways between the substantia nigra and striatum drop by 80%, parkinsonism will develop [5]. It follows that the treatment of Parkinson’s disease is principally through dopamine replacement. Drugs, therefore, that inhibit dopaminergic receptors in the basal ganglia are associated with parkinsonian symptoms. As there is usually functional reserve in this system, people with reduced albeit asymptomatic reductions in dopaminergic function of the basal ganglia will be more sensitive to the effects of dopamine receptor blockers.

There are several centrally expressed subtypes of dopamine receptors. These include the D2 receptors that were originally considered important in the symptoms observed in schizophrenia and other psychotic disorders through their presence and possible dysfunction in the dopaminergic mesolimbic (positive symptoms) and mesocortical (negative symptoms) pathways. The dopaminergic hypothesis of schizophrenia was developed from the accidental discovery of effective dopamine receptor blocking drugs and subsequently motivated drug development in the 1950s and 1960s to generate new dopamine antagonists. However, early antipsychotics (e.g. chlorpromazine) lacked specificity for this receptor, affecting other dopamine receptors, as well as serotonergic, histaminergic and noradrenergic receptors, and led to multiple side effects. The desired blockade of mesolimbic dopaminergic pathways led to concurrent inhibition of D2 receptors in the substantia nigra resulting in parkinsonism.

Cholinergic interneurons within the basal ganglia balance the dopaminergic activity here. Accordingly, in Parkinson’s disease, when the equilibrium is upset through degeneration of dopaminergic neurones, there is a relative predominance of cholinergic activity. The genesis of the abnormal movements in Parkinson’s disease can therefore be considered as both a deficiency of dopaminergic activity as well as a relative increase in cholinergic activity. Accordingly, as well as dopamine augmentation as a therapy for Parkinson’s disease, anticholinergic medication may also be of some benefit to help reset the equilibrium.

However, cholinergic pathways elsewhere are involved in cognition, vigilance and emotional modulation and degenerate in Parkinson’s disease – while anticholinergic medication may therefore be associated with an improvement in movements, it is at the expense of deterioration in cognition in this disease, as well as in patients with psychosis, where anticholinergic medication may additionally mediate confusion and psychotic symptoms.

As the neurotransmitter basis of parkinsonism is due to dopamine deficiency or iatrogenic blockade with a resultant excess of cholinergic activity in the basal ganglia, dyskinesias may be due to dopaminergic hypersensitivity and cholinergic hypofunction. It has also been proposed that tardive dyskinesia may emerge due to free radical damage of relevant basal ganglia neurones. Long-term antipsychotic use is associated with the genesis of free radicals emerging from increased catecholamine metabolism [6]. Mitigating such oxidative damage to susceptible neurones has formed the basis of anti-oxidant treatments for tardive dyskinesia.

While parkinsonian side effects emerge from pathology and drug interactions in the substantia nigra, dyskinetic symptoms may be more closely associated with problems in the striatum – in particular with the caudate nucleus.

Whilst dystonias may emerge as part of a general parkinsonian reaction to medication, they may also arise acutely without other cardinal features of parkinsonism. Patients who developed an oculogyric crisis often do so after only a matter of hours after ingesting the medication responsible. Whilst associated with juvenile parkinsonism, there are also suggestions that acute dystonia may be related to abnormalities in the putamen, thalamus, substantia nigra or globus pallidus. Research into myoclonus and other dystonias has tended to focus on lesions of the pallidum within the basal ganglia. However, it is most likely that the vast majority of patients who develop acute dystonic reactions after ingesting medications known to cause these problem have no pathology in any of these or other brain nuclei.

In summary, lesions in any of the structures of the basal ganglia may be associated with the development of parkinsonism, dyskinesias or dystonias. Parkinsonism tends to be associated with problems of the substantia nigra, dyskinesia with the caudate, and dystonias with the globus pallidus (although there is no complete specificity). Furthermore, any of these symptom clusters can be caused by acute and chronic exposure to anti-dopaminergic drugs, but dyskinesias are also associated with cholinergic hypofunction which has important implications for treatment.

There are numerous drugs and drug classes that are associated with the development of parkinsonism (table 1) and other abnormal involuntary movements. Drug-induced parkinsonism is often not recognised, especially in the non-psychiatric patient [7], The side effect often develops within 1 month of the start of treatment, with 60% of patients developing it by this time point and 90% within 3 months [8].The potency of antipsychotics is defined by their ability to block the D2 receptors. Therefore, high-potency neuroleptics tend to have a greater propensity to cause extra-pyramidal side effects. However, some high-potency neuroleptics that also have anticholinergic properties are associated with fewer motor side effects. Atypical antipsychotics tend to have broader pharmacodynamic effects, and it is thought that their activity at 5HT2a receptors mediate efficacy with less need for blocking of the D2 receptors in the mesolimbic pathways and therefore in the substantia nigra.

The evidence surrounding iatrogenic dystonias is less well developed. Conventional neuroleptics are clearly implicated as are (from case reports) calcium channel blockers. Additionally, there are several case reports noting an association with olanzapine, carbamzaepine, lithium, imipramine, gabapentin and ziprasidone. Other dystonias (e.g. cervical dystonia) are less clearly associated with iatrogenic causes.

Iatrogenic parkinsonism is common in the elderly [9] with rates as high as 2.7% from community samples, with idiopathic parkinsonism being present in another 3% [10]. Moreover, the presence of cognitive impairment, female gender and HIV disease have all been cited as increasing the risk of developing parkinsonism.

Certain types of drugs (table 1), after prolonged exposure and high doses, have also been associated with increasing the risk of iatrogenic parkinsonism.

The interaction between dementia, neuroleptic medication and parkinsonism is well established. The risk of postural instability and falls has been of concern [11] and has motivated national public health strategies to reduce the use of neuroleptics in people with dementia [12]. Patients with Parkinson’s disease dementia and Lewy body dementia are particularly prone to autonomic instability [1315], because of pre-existing α-synucleinopathy affecting dopaminergic pathways and autonomic nuclei in the brain stem. Patients with Alzheimer’s dementia are also at greater risk of parkinsonism and are also (perhaps through different mechanisms) more prone to orthostatic hypotension [13]. In vascular dementia, white matter lesion (WML) volume has been associated with falls in a well-controlled prospective study [16], though it was not clear from this study whether parkinsonism mediated this association. Moreover, WML burden in idiopathic Parkinson’s disease is associated with more motor symptoms [for review see 17].

It is known that smokers are less likely to develop Parkinson’s disease. Despite the fact that smokers with schizophrenia tend to receive more antipsychotic medication than non-smokers [18], there is consistent evidence that the former are less likely to develop parkinsonism [19]. This is in conflict with the observation that parkinsonism is treated with anticholinergic drugs, and may be due to the fact that chronic exposure to nicotine leads to receptor desensitisation and upregulation of some (α4β2) but not other (α7) nicotinic receptors [for review see 20]. While this may drive dependence on nicotine in smokers, it may also result in a functional reduction in cholinergic activity in the basal ganglia, helping to reduce the risk of parkinsonism. This hypothesis would predict that smoking leads to increased rates of dyskinesia associated with hypofunction of cholinergic activity. This has in fact been demonstrated [21, 22], especially with regard to patients on conventional neuroleptics as compared with clozapine [22]. Despite earlier reports of a reduced risk of dystonias in smokers [23], later evidence suggests that blepharospasm is not associated with smoking status [24, 25], though it may be associated with coffee consumption [25] and anxiety [24]. Other dystonias have been less well characterised in this regard, but there may be a protective effect of smoking [23].

The first step in managing drug-induced abnormal involuntary movements is to recognise the syndrome and that one of the patient’s medications may be its cause. If the culprit can be identified (see table 1), then the next logical step is to discontinue this drug, and if necessary replace it with another drug with similar efficacy but a reduced propensity to cause the same side effect. The advent of atypical antipsychotics with evidence of reduced abnormal movements in controlled trials [26], including in the elderly [27, 28], led to a dramatic change away from conventional neuroleptics. If symptoms do persist, idiopathic parkinsonism may actually cause the observed movement disorder. Tardive dyskinesia may be more resilient to change, with a reduced likelihood of improvement despite discontinuation of the offending therapy. This suggests that it may be related to eventual structural damage to the basal ganglia after chronic exposure.

In cases where there is not a clear relationship between drug exposure and parkinsonism, single-photon emission tomography with 123Iodine labelled 123I-N-w-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl)nortropane will be conclusive, as this dopamine transporter scan will be normal in patients with iatrogenic parkinsonism compared with the reduced uptake of tracer in the putamen of patients with idiopathic parkinsonism [29].

In Alzheimer’s disease, the use of antipsychotics to manage behavioural symptoms remains commonplace, despite the association with mortality especially with conventional (5-fold increase in risk) compared with atypical (double the risk) neuroleptics [30]. A more precise diagnosis of psychotic symptoms may lead to a more judicious use of antipsychotics, although other drug classes may also be useful: SSRIs for depression associated with dementia have proved disappointing [e.g. 31], but have proved valuable for agitation [32]. Trazodone is indicated for agitation [32] and insomnia [33]. Memantine would appear to have a particular propensity to manage symptoms of agitation [34]. The cholinesterase inhibitors appear to have benefit for broadly defined neuropsychiatric symptoms, including psychotic phenomena [e.g. 35, 36]. Many psychotic symptoms in Alzheimer’s disease and Lewy body dementia respond to treatment with cholinesterase inhibitors, with empirical evidence for the use of rivastigmine to treat hallucinations in Alzheimer’s disease [37] and Lewy body dementia [38, 39]. There is a genetic linkage between delusions in Alzheimer’s dementia with haplotypic variation in the α7 nicotinic receptor gene [40]. This supports the hypothesis that psychotic symptoms in dementia are a manifestation of the well-documented cholinergic deficits in the disease.

Where switching is either not possible or fails to manage the symptoms effectively, various pharmacological interventions have been tested.

For parkinsonism, the use of anticholinergic drugs like benztropine may be efficacious [41], although use should be limited to short-term, especially in the elderly where there is a clear risk of iatrogenic confusion and worsening psychosis [42]. Moreover, though their use for idiopathic Parkinson’s disease is well supported [42], their use for iatrogenic parkinsonism is not. Anticholinergics are useful also in dystonic symptoms but should be avoided in dyskinesia as they are likely to make symptoms worse.

Trials of drugs for the management of persistent dyskinesia have largely been disappointing. Acetylcholinesterase inhibitors, despite hypothetically addressing the hypocholinergic function in dyskinesia, have shown little benefit in small studies of donepezil [43, 44] and galanthamine [45], despite an earlier promising Cochrane Review [46]. However, recent evidence from a small study suggested that donepezil did reduce the frequency of falls in patients with idiopathic Parkinson’s disease [47]. As tardive dyskinesia may be a consequence of synaptotoxic and eventually neurotoxic oxidative stress due to chronic neuroleptic use [6], anti-oxidant strategies may ameliorate symptoms. A recent Cochrane review noted that although far from conclusive, vitamin E tended to reduce the severity of established tardive dyskinesia and merited further study [48].

For cervical dystonia (torticollis) and other dystonias, patients can initially be offered physiotherapy or occupational therapy. Failing these conservative interventions, pharmacotherapy, botulinum toxin or surgery can be undertaken. While the evidence for the use of botulinum in primary cervical dystonia is robust, its efficacy in secondary (iatrogenic) dystonia is less certain [49, 50]. Drug treatments include anticholinergic, dopaminergic, antidopaminergic and benzodiazepine therapies, though these are less well studied than local injection of botulinum [51, 52]. Of various drug classes, gradually uptitrated anticholinergics are the most likely to show benefit [52].

Iatrogenic parkinsonism and other abnormal involuntary movements have detrimental effects on compliance and thereby the efficacy of the drugs concerned. They are also associated with reduced quality of life and can be extremely disabling and stigmatising. Recognising that they may arise in other drug classes apart from neuroleptics is crucial.

The advent of new antipsychotics with a reduced propensity to parkinsonian side effects has caused a reduced acceptance of such side effects by patients and clinicians. However, where switching to an atypical antipsychotic is not possible or acceptable, low and carefully monitored use of anticholinergic medication may be helpful for parkinsonism and dystonias, but harmful for dyskinesias.

Chronic or tardive dyskinesia would appear to be secondary to neurodegeneration perhaps secondary to oxidative damage to key basal ganglia nuclei, and has proven to be more resistant to switching therapies. Prevention through avoidance of drugs linked to their genesis and (perhaps) prophylaxis with vitamin E may be indicated.

The evidence supporting the use of pharmacotherapy for dystonias is patchy; there is a robust evidence for the use of botulinum toxin for primary dystonia, and the evidence for this intervention for secondary dystonia is less complete.

In conclusion, early recognition and monitoring of patients for abnormal movements and a much lower threshold for what is acceptable as a side effect to psychotropic and other medications will improve the patient’s prognosis.

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