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Neurologic Side Effects of Psychiatric Treatments Al for Re- Classifica- 89-501 R.J

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Neurologic Side Effects of Psychiatric Treatments Al for Re- Classifica- 89-501 R.J ER 1990 SEMINARS IN NEUROLO(;Y-VOLU~IE 10,NO. 3 SEPTEMBER 1990 Psychiarr ter: John Neurologic Side Effects of Psychiatric Treatments al for re- classifica- 89-501 R.j. Dolan, M.D., M.R.e. PsyCh I for clus- ndromes. al for re- puc syn- .ytoarchi- uophren- Liule is known in psychiatry concerning fun- NEUROLEPTICS damentaldisease processes. The relative absence ry mOLOr .ophrenia Ilfdisease-specific rreatrnerus is therefore not sur- This broad group of compounds consritutes :5l5-32 prising. Most physical treaunents in psychiatry the cornerstone of pharmacologic treatment of (he n density t'l.en their therapeutic effects in a nonspecific psychoses, particularly schizophrenia. The int ro- Res 1980; fashion.Lack of disease spccificuy means that com- duction of potent antipsychotic agents into clinical al. Srruc- promises are conrinually made between beneficial practice in 1952 was associated with an almost im- hizcphre- andunwanted treatment effects. Indeed, the goal mediate recognition that these agents could result ogic dys- nfmost therapeutic developments, given lirnita- in neurologic side effects.!" Side effects may for n schizo- tionsinknowledge concerning disease processes, is convenience be thought of as acute and chronic, :4 nenhance wanted over unwanted effects. though in reality such a division is arbitrary and er: John Physical treatments in psychiatry, as in other artificial. There is little dispute that neuroleptics nical ap~ mnches of medicine, aim to ameliorate, arrest. cause acute neurologic side effects, but there is lodreverse disease processes. In practice, the ar- controversy as LO whether they arc either necessary ral biopsy la due LO restor reversal of psvchiarric disease is all idealistic or sufficient causes for the emergence of chronic (try 1986; nd rarely achieved goal. In this, psychiatry shares side effects, in particular tardive dyskinesia (TD). lDuchin common with neurology in thin symptom This question will be addressed further in consid- n in man. -granular reliefis the principal therapeutic aim. ering TD. The most commonly encountered neu- ill, J964, Despite these limitations. there are man)' ben- rologic side effects of neuroleptics are summarized rficiaalnd effective treatments ill psychiauy. The in Tablc I. mediationof these effects is generally ascribed to ;Iterationsin neuronal function £11 neurorcceptor ACUTE DYSTONIC REACTIONS lites.However, a lack of pharmacologic and disease Acute dystonic reactions were first reponed in ~iftcit}' means that psychiatric interventions are association with chlorpromazine treatment. Be- ssxiated with high rates of unwanted effects. Be- cause of their distribution, they were labeled cuseof their high prevalence. neurologic side ef- "Iacio-bucco-linguo-rnasticatory dyskinesia" and kmare the most important hazards of psychiatric the similarity with "excito-rnoior" syndromes seen seatments.The recognition of neurologic side ef~ in the wake of epidemic encephalitis was noted." feeLS is therefore of great clinical importance. These reactions may be focal or gelleralized. Their This review examines (he prevalence. clinical onset, which is abrupt, is associated with corn- presentalion, putative pathophysiology, and man- 1gementof neurologic side effects of psychiatric keatmems.It is not possible within the brief space Table 1. Neurologic Side Effects of Neuroleptics ofthisarticle to cover all treatments ill psychiatry; !herforee (he focus will be on rhe more conven- Acute dystonic reactions Akathisia ~al and widespread treatments. These include Parkinsonism ~eneuroleptics, lithium. antidepressants, electro- Tardive dyskinesia envulsivetherapy (EeT), anxiolyucs, and psycho- Tardive dystonia Neuroleptic malignant syndrome .rgery. Consultant Psvchiau-isr. Nationnl Hospnal tor Nervous Diseases. Queen Square. London, and Senior Lecturer. Rov.rl Fret: School of Medicine. Pond Street. London. United Kingdom Reprint requests: 01". Dolal1. National Hospital for Nervous Diseases. Queen Square. London. WelN :iRe; LK Copyright Cl 1990 by Thieme Medical Publishers, till .• 38t Par-k Avenue Smith. New York. NV 10016. f\tlligllts reserved 295 SF.MI:-JARSIN NEUROI.O(;Y VOLUME 10, NUMBER 3 SEPTEMBER mencemeut or increments of ueauneru. The man- thisia is not understood, but may be Tela ifestations are varied and ex! rerncly distressing tu blockade of nonst riatal clopamincrgic path aff ectcd p.uiems .: rhe phenomena most rre(~~,e'~liy Anticholinergic drugs arc often ineffectivei encountered are muscle spasms chiefly aflectlllg lieving the condition. Benzodiazepines may the head and neck, appearill}{ as involuntary Often. it is necessary to reduce the dosage 0 spasm of tongue and mouth mlls~les, sp~~sm of 1he neuroleptic or substitute another class of masseter preventing mouth opelllng. ranal. muscle pound. spasm leading to grimacing, and s.pas.11l of the or- PARKINSONISM bicularis o{ uli resulting in excess bhnklll~ Of bleph- arospaSlll. Ocular involvemcnr , ()(-ul(~g:yric .crisis, This is the most common neurologic side may lead 10 painful upward ga7c lasung uuuutes felt of ncurolcpucs, occurring in from 2010 or hours. Neck involvement, Irequcruly associated of patients treated with such agents.o Sym with ocular manifestauons. cOJ]sists of torticollis, which usually appear in the first 3 weeksof antecollis (II' rctrocollis. IIIVO!VClllcnt of trunk (op- ment, arc both dose-related and drug-related, isthotonos) or limbs, [h()u~h less Frequent. llIay piperazine phenoihiaziues and. bu~yroph~n lead to biz.ure gails or difficulties in walkillg. are the compounds most often Implicated ID Acute dystonic effects are usually seen in th~ cipitaung this syndrome, whereas the .subs· . first 72 hours of neuroleptic treatment. They <I(~ benzamides such as sulpiridc and thioxant fen lip to :"J% of all patients staned on these COIl~- are least often responsible. The condition ~ pounds." The pathophysiology of acute dystonic with increasing [requency with age and in reactions is unknown, though the clinical manifes- with underlying cerebral disease. tations suggest all excess dopaminergic activity. The clinical manifestations are identi possibly secondary to acute antagonism of dopa- those or Parkinson's disease, with tremor, ri . mine autoivccptors. Acute dystonic reactions are postural abnormalities, and bradykinesia. Dr most prevalent in young male pauenis.: They Gill is a frequent accompaniment. Bradykinesia, occur with any type or neuroleptic but arc seen earliest manifestation, is usually followedby most often ill associauou with the piperazine side ity. abnormalities of posture, and, lastly, chain pheuothiazines and the butjrophenoncs. tremor. Rigidity and tremor arc usually sym Thcv are reversible either spontaneously or with cal. An unusual variant seen following media trea~menl. An episode Gill usually be terminated lone-term neuroleptic treatment is the occurr ~ , abruptly b) injection of all anuparkinsonian drug. of a 5 to 7 Hz perioral tremor, so-called rabbit Trcauueru with neurolepucs can, however, be (011- drome." unued with only a slight risk of recurrence. The mechanism of drug-induced parki ism is blockade of striatal postsynaptic dopa AKATHISIA (D2) rcccptors, producing a functional defki or dopamine at those sites. Treatment of the This I cfers to a coudition characterized by a diuon involves either stopping or reducing subjective sense, frequently accompanied by ol~j('.c- neuroleptic or alternatively introducing an tive evidence. of restlessness. Although reported 111 cholinergic agent. However, tolerance to the postencephalitic and idiopathic parkinsonism, it is pyramidal effects of neuroleptics developsd now most frequently encountered ill patients on conuuuauon of an offending agent. This ph neuroleptic drugs. The condition usually presents cnon of tolerance may be related to pha in the first month 01 neuroleptic treatment. A netic factors, such as increased metabolism.' delavcd-onsci variant. tardive akathisia, is reponed drawal of the antipsychotic drug usually I in up 10 ~5'!(of patients with 'I'D. resolution 01" parkinsonism within a matter Patients with akarhisia complain of an inability weeks. though the condition may persistf to sit still. .vccompanving features include fidget~ months or longer.!'' One reason for this ap ing. rockirur back and forth. crossing and 1I1l(rOSS- '- '" ~ . be the persistent presence of active metabolaes the or ing leg~, constant pacing. Motor acuvuy re- lip to 3 mouths after discontinuation of t lieves the inner subjective urge to move and. not meut.!' sllrpri~ingh. the condition is frequently mistaken for agitation. The association 01"all inner ur-ge and an outward motor response hears some resem- TARDIVE DYSKINESIA blance to a tic , though, akathisia differs in that the urgc 10 1110n:' is constant and the motor component TD is a hyperkinetic involuntary move is conti n uou stereotyped, and repei iuve. disorder of diverse and widespread manifesue 296 The pathophysiology of drug-induced aka- The occurrence of the syndrome in assoca 1990 NECROLOGIC SIDE EFFECTS OF PSYCIIIATRIC TREtlTMENT~OOL,\N -d to sith neuroleptic medication was first described in described abnormal movements in chronic psy- Nays. 1957,shortly after the introducuon into clinical chotic patients thus: "Connected with these are. n re- practice of phenothiazine ncuroleptics. J:! Further further, smacking and clicking of the tongue .... help. ebservauons of a hyperkinetic syndrome occurring But besides we observe especially in the lip mus- f the inclose temporal association
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