Movement Disorders in Psychiatric Patients

Open access Review BMJ Neurol Open: first published as 10.1136/bmjno-2020-000057 on 1 December 2020. Downloaded from Movement disorders in psychiatric patients Laura Perju- Dumbrava,1 Peter Kempster1,2 To cite: Perju- Dumbrava ABSTRACT movements such as mannerisms, stereo- L, Kempster P. Movement The observability of movement gives it advantages when typies and tics were well documented in disorders in psychiatric trying to draw connections between brain and mind. the preneuroleptic era, and the postural patients. BMJ Neurology Open Disturbed motor function pervades schizophrenia, though 2020;2:e000057. doi:10.1136/ and behavioural disturbances of chronic it is difficult now to subtract the effects of antipsychotic bmjno-2020-000057 catatonic states were then quite common treatment. There is evidence from patients never exposed in psychiatric institutions (figure 1). to these drugs that dyskinesia and even parkinsonism are Received 15 March 2020 Kraepelin, who delineated schizophrenia Revised 29 June 2020 to some degree innate to schizophrenia. Tardive dyskinesia Accepted 04 July 2020 and drug- induced parkinsonism are the most common in his nosological writings (he called it movement disorders encountered in psychiatric practice. dementia praecox), recorded a variety of 2 While D2 dopamine receptor blockade is a causative hyperdynamic movements in his patients. factor, both conditions defy straightforward neurochemical It is possible to observe motor features of explanation. Balanced against the need to manage preneuroleptic schizophrenia in histor- schizophrenic symptoms, neither prevention nor treatment ical documentary footage. The 1938 silent is easy. Of all disorders classified as psychiatric, catatonia film production Symptoms in Schizophrenia sits closest to organic neurology on the neuropsychiatric depicts stereotypy, catalepsy, echopraxia, spectrum. Not only does it occur in the setting of but also orofacial movements that resemble unequivocally organic cerebral disease, but the alterations tardive dyskinesia.3 4 of consciousness it produces have ‘organic’ qualities copyright. even when the cause is psychiatric. No longer considered More recent research supports a funda- a subtype of schizophrenia, catatonia is defined by mental link between schizophrenia and move- syndromic features based on motor phenomenology. Both ment disorder. In a cohort of never- treated severe depression and obsessive-compulsive disorder Indian schizophrenic patients, McCreadie et may be associated with ‘soft’ extrapyramidal signs al found more than half exhibiting sponta- that resemble parkinsonian bradykinesia. As functional neous dyskinesia.5 They suggested that tardive neuroimaging studies suggest, movement and psychiatric and spontaneous dyskinesias, although aeti- disorders involve the same network connections between ologically different, are phenomenologi- http://neurologyopen.bmj.com/ the basal ganglia and the cerebral cortex. cally similar. A review of 13 studies looking at antipsychotic-naïve patients with a first INTRODUCTION episode of psychosis concluded that the Movement, David Marsden once wrote, is one median rate of spontaneous dyskinesia is 6 of the robust bridges between neurology and 9%. Adolescents with prodromal psychotic psychiatry.1 Its observability gives it special symptoms showed subtle hyperkinetic move- advantages when trying to draw connections ment abnormalities, particularly of the facial between brain and mind. Movement disor- region, in a carefully controlled observational 7 ders are encountered widely in psychiatric study. Patients with schizophrenia who have on October 2, 2021 by guest. Protected © Author(s) (or their practice, often as side effects of psychotropic employer(s)) 2020. Re- use medication. This brief overview will high- never had antipsychotic drugs score signifi- permitted under CC BY-NC. No light ways in which psychiatric diseases show cantly higher for parkinsonism than aged- 6 8 commercial re- use. See rights convergence with the motor system. matched controls. The observant Kraepelin and permissions. Published by had already remarked this tendency in his BMJ. 1 patients—‘the face vacant, immobile, like a Neurosciences, Monash MOVEMENT DISORDERS OF SCHIZOPHRENIA mask…’; ‘simple movements are stiff, slow, Medical Centre Clayton, Clayton, 2 Victoria, Australia Disturbed movement pervades schizo- forced…’. Subtle parkinsonism is seen both 2School of Clinical Sciences of phrenia, though it is difficult now to in newly diagnosed and in chronic but never- Medicine, Monash University, subtract the effects of antipsychotic treat- medicated schizophrenia.3 Of the mild extra- Clayton, Victoria, Australia ment. There is evidence from patients pyramidal signs documented in these studies, Correspondence to never exposed to these drugs that dyski- rigidity and poverty of movement were Dr Laura Perju- Dumbrava; nesia and even parkinsonism are to some most apparent. Meta-analysis also showed lauraperju@ gmail. com degree innate to schizophrenia. Anomalous a smaller but significant excess of mild Perju- Dumbrava L, Kempster P. BMJ Neurol Open 2020;2:e000057. doi:10.1136/bmjno-2020-000057 1 Open access BMJ Neurol Open: first published as 10.1136/bmjno-2020-000057 on 1 December 2020. Downloaded from considers dopamine dysregulation as a final common pathway, allowing for upstream contributions from other neurotransmitters—glutamate, gamma amino- butyric acid, serotonin—through which schizophrenia’s predisposing genetic and environmental factors might be acting.11 SCHIZOPHRENIA AND FUNCTIONAL MOVEMENTS Functional (psychogenic) movement disorders are incon- gruous with the motor abnormalities of neurological diseases and show attention dependency, with distracti- bility, during clinical examination. Psychological models of functional neurological disorders have, in recent years, given way to more biologically orientated ones that empha- sise disturbed higher level sensorimotor processing. In Figure 1 A group of schizophrenic men in manneristic fact, surveys show that psychopathology in these patients 12 poses, from Kraepelin’s textbook.2 The text states: ‘They is not greatly over- represented. Although uncommon, were put without difficulty in the peculiar positions, and kept functional movements do occur in schizophrenia.13 This them, some with a sly laugh, others with rigid seriousness’. is of interest in relation to another characteristic of functional motor syndromes—the lack of sense of agency parkinsonism in healthy first- degree relatives of patients (control over one’s actions) that attends them.14 Passivity with schizophrenia.8 phenomena of psychosis result in perceptions of external Reserpine, first isolated from the Indian snakeroot control of movement.15 It is possible that the under- plant (Rauwolfia serpentina), and chlorpromazine, mining of agency in functional movement disorders and a spin- off of antihistamine research by the pharma- schizophrenic passivity have a common pathophysiolog- ceutical company Rhône- Poulenc, revolutionised the ical basis. treatment of schizophrenia when both were intro- copyright. duced in the early 1950s. Though reserpine’s action as an irreversible inhibitor of the vesicular mono- TARDIVE MOVEMENT DISORDERS amine transporter was not then known, the motor Once dopamine receptor blocking agents (DRBAs) behavioural effects of the drug were a key to Arvid were in wide usage, tardive movement disorders Carlsson’s discovery of the role of dopamine as a appeared as a ‘new’ problem in psychiatric practice.16 neurotransmitter, for which he won the Nobel Prize, The definition of tardive dyskinesia in the Diag- and then to understanding the chemical defect of nostic and Statistical Manual of Mental Disorders, http://neurologyopen.bmj.com/ Parkinson’s disease (PD). Carlsson showed in 1963 5th edition (DSM-5) recognises that long exposure that chlorpromazine blocked dopamine receptors, to neuroleptics is not always required: ‘involuntary and this realisation led to the development of a dopa- athetoid or choreiform movements lasting at least a mine hypothesis of schizophrenia.9 few weeks, developing in association with the use of a The original supposition that hyperactive dopa- neuroleptic medication for at least a few months, and mine neurotransmission equates with psychotic symp- persisting beyond 4–8 weeks’.17 Older age, acquired toms was later refined with knowledge about regional brain damage, first generation antipsychotics, cumu- dopaminergic pathways and receptor subtypes. Thus, lative antipsychotic dosage, and duration of schizo- hallucinations and delusions were linked to subcor- phrenia are all risk factors.18 Case- controlled research tical release of dopamine, increased D2 receptor acti- has identified a number of possible genetic predispo- on October 2, 2021 by guest. Protected vation and disturbed cortical transmission through sitions. Polymorphisms in the dopamine D2 and D3 the nucleus accumbens. Negative symptoms of schizo- receptors are examples. Some of these associations, phrenia (apathy, anhedonia, social withdrawal) could, though, have not been as strong after further study on the other hand, be explained by reduced D1 or meta- analysis.19 Typical tardive dyskinesia has an receptor activation in the prefrontal cortex, decreased orobuccolingual topography, producing repetitive activity of the caudate nucleus and possible addi- licking, lip smacking and chewing movements. Varia- tional D3 receptor changes.10 Despite shortcomings, tions include

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