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Parkinsonism in the Psychiatric Setting: an Update on Clinical Differentiation and Management

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Parkinsonism in the Psychiatric Setting: an Update on Clinical Differentiation and Management Open access Review BMJ Neurol Open: first published as 10.1136/bmjno-2019-000034 on 27 January 2020. Downloaded from Parkinsonism in the psychiatric setting: an update on clinical differentiation and management Alice Powell ,1,2 Lara Gallur,3,4 Leslie Koopowitz,4,5 Michael William Hayes1 To cite: Powell A, Gallur ABSTRACT of subcortical grey matter nuclei including L, Koopowitz L, et al. Parkinsonism is seen frequently in patients with the substantia nigra, globus pallidus, subtha- Parkinsonism in the psychiatric psychiatric conditions. Drug- induced parkinsonism (DIP) lamic nucleus and the striatum comprising setting: an update on clinical is the second most common cause of parkinsonism in differentiation and management. the putamen and caudate nucleus), thalamus the general population after Parkinson’s disease (PD) but 3 4 BMJ Neurology Open and motor cortex governing motor output. a range of rarer aetiologies, some of them reversible, 2020;2:e000034. doi:10.1136/ Dopamine usually has an excitatory influence bmjno-2019-000034 should also be considered in patients of all ages. DIP is more common in older patients, as are neurodegenerative on the direct pathway via D1 receptors to facil- Received 21 December 2019 diseases that may produce parkinsonism and it is itate cortically initiated movements and an Revised 07 January 2020 relatively more likely that drug exposure could be inhibitory influence on the indirect pathway Accepted 07 January 2020 unmasking an underlying process in this population. There via D2 receptors, which usually impedes volun- is an extensive literature on differentiating DIP from PD tary movement through thalamic inhibition.3 but clinical features can be indistinguishable and many This pathway is summarised in figure 1. proposed investigations are not readily available. Aside In the case of PD, gradual degeneration of from cessation of the responsible medication, there is dopaminergic substantia nigra pars compacta no clear consensus on treatment strategies or duration neurons and their projections to the striatum of treatment. Practically, a delicate balance must be 3 copyright. achieved between ameliorating parkinsonism and avoiding leads to motor symptoms. A range of dopami- recurrent psychosis. Long- term prognosis in the setting nergic medications that either increase dopa- of DIP remains unclear. We review the features that may mine levels through a variety of mechanisms differentiate DIP from other causes of parkinsonism or stimulate dopamine receptors are used in patients with psychiatric illness, provide an update to address these symptoms. Conversely, any on relevant investigations and discuss management medication that either blocks dopamine D2 strategies. The use of atypical antipsychotics for a broad http://neurologyopen.bmj.com/ © Author(s) (or their receptors or reduces dopamine release may employer(s)) 2020. Re- use range of indications highlights the ongoing relevance of result in parkinsonism.5 Other aetiologies of DIP. permitted under CC BY- NC. No parkinsonism typically produce motor symp- commercial re- use. See rights and permissions. Published by toms through damage to the basal ganglia, BMJ. INTRODUCTION for example, through vascular injury in the 1 Department of Neurology, Parkinsonism, defined as bradykinesia in case of vascular parkinsonism or normal pres- Concord Repatriation General sure hydrocephalus. Hospital, Sydney, New South combination with either rest tremor, rigidity 1 A degree of parkinsonism is frequent Wales, Australia or both, classically arises in the context 2Brain and Mind Centre, The of Parkinson’s disease (PD). The major in the elderly and may be due to an age- University of Sydney, Sydney, pathology is represented by Lewy bodies related decline in the number of nigrostri- 6 7 on September 29, 2021 by guest. Protected New South Wales, Australia containing alpha- synuclein and associated atal neurons. However, neurodegenerative 3Department of Psychiatry, dopamine cell loss in the substantia nigra pathologies also accumulate with age. A recent Northern Adelaide Local Health study of over 1400 patients followed up for Network, Adelaide, South leading to dysfunction of basal ganglia Australia, Australia circuitry responsible for motor control. an average 8.5 years until death demon- 4School of Medicine, Discipline However, parkinsonism due to a wide range strated that the majority (94.1%) had at of Psychiatry, The University of possible causes also occurs in up to one- least one pathology on autopsy, the average of Adelaide, Adelaide, South third of patients taking antipsychotic medi- individual had three pathologies and 25% Australia, Australia 2 8 5Brain Injury Rehabilitation cations. This syndrome may significantly had PD pathology. The other pathologies Unit, Hampstead Rehabilitation impair function and quality of life. detected included Alzheimer’s pathology, Centre, Adelaide, South cerebral amyloid angiopathy, cerebrovas- Australia, Australia Pathophysiology of parkinsonism cular disease, hippocampal sclerosis and TAR 8 Correspondence to In PD, it is proposed that there is an imbalance DNA- binding protein 43. A majority (53.9%) Dr Alice Powell; of activation of excitatory and inhibitory path- of this cohort had developed parkinsonism alice. powell@ sydney. edu. au ways involving the basal ganglia (a collection by their last visit.8 Interestingly, this study also Powell A, et al. BMJ Neurol Open 2020;2:e000034. doi:10.1136/bmjno-2019-000034 1 Open access BMJ Neurol Open: first published as 10.1136/bmjno-2019-000034 on 27 January 2020. Downloaded from copyright. Figure 1 Schematic diagram of excitatory and inhibitory basal ganglia pathways implicated in parkinsonism. Dopaminergic projections from the SNc have an excitatory influence on direct pathway striatopallidal fibres via D1 receptors leading to disinhibition of thalamic nuclei and enhanced thalamocortical drive facilitating cortically initiated movements. Dopamine also has an inhibitory effect on indirect pathway striatopallidal fibres via D2 receptors, which impedes voluntary movement through thalamic inhibition. The direct pathway is also activated by glutamatergic projections from the sensorimotor cortex and the http://neurologyopen.bmj.com/ indirect pathway via gamma- aminobutyric acid (GABA) from the putamen. GPe, globus pallidus externa; GPi, globus pallidus interna; SNc, substantia nigra pars compacta; STN, subthalamic nucleus. highlighted that a proportion of patients with both PD Similarly, contemporary understanding of neurotrans- and other pathologies did not demonstrate any clinical mitter systems involved in psychosis has evolved beyond 8 parkinsonism. dopamine dysregulation with multiple other neurotrans- mitters associated with the syndrome. There is evidence Beyond dopamine: the role of other neurotransmitters in parkinsonism and psychosis that a relative hypocholinergic state favours the emer- 11 Other neurotransmitter systems are also implicated in PD gence of psychotic symptoms in PD. PD psychosis has on September 29, 2021 by guest. Protected motor symptoms and drug-induced parkinsonism (DIP) also been conceptualised to reflect an imbalance between and may help explain why DIP may occur with medica- dopamine and serotonin neurotransmission.12 Atypical tions that do not have direct effects on dopamine levels antipsychotics, such as quetiapine and clozapine, demon- or receptors. For example, due to the interrelationship strate significant serotonin receptor antagonism.13 This between dopaminergic and cholinergic pathways, parkin- serotonin receptor activity differentiates typical from sonism has been conceptualised as resulting from relative 9 atypical antipsychotics and was touted as resulting in dopamine deficiency and relative acetylcholine excess. lower extrapyramidal side effects (EPSE) such as parkin- This hypothesis is supported by observations that parkin- sonism both due to the downstream effect on dopamine sonism is aggravated by centrally acting cholinergic medi- cations and improved by anticholinergic medications.10 release and the need for a lower D2 receptor occupancy Gait impairment in PD is pathophysiologically complex for antipsychotic efficacy. With the ongoing use of atyp- and freezing of gait, specifically, may be associated ical antipsychotics, it has been demonstrated that there is with dysfunction in the noradrenergic and cholinergic still a risk of causing EPSE, and the ‘atypical’ nature may systems.4 be lost with dose increases. 2 Powell A, et al. BMJ Neurol Open 2020;2:e000034. doi:10.1136/bmjno-2019-000034 Open access BMJ Neurol Open: first published as 10.1136/bmjno-2019-000034 on 27 January 2020. Downloaded from Drug-induced parkinsonism gait is infrequent in DIP compared with other causes of DIP is defined as the presence of parkinsonism without a parkinsonism.26 Non- motor symptoms, such as late- onset history of parkinsonism before the use of the offending rapid eye movement sleep behaviour disorder, reflect the drug and onset of parkinsonian symptoms during use of involvement of other neurotransmitter systems and are the drug.5 DIP is relevant to patients to a broad range less likely to be a feature of DIP.20 Hyposmia, now part of of patients since antipsychotic agents are prescribed for the supportive diagnostic criteria for PD due to degen- a range of psychiatric indications including adjunctive eration of the olfactory system,1 can be non- specific, therapy for depression, anxiety disorders, personality particularly in older patients but is
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