500
Journal of the Royal Society of Medicine Volume 84 August 1991 7 Chan YF, Yuen MYP, Tung Ma L, Li MK. Recurrent dedifferentiated liposarcoma of the spermatic cord simulating malignant fibrous histiocytoma. Pathology 1987;19:99-102 8 Rieu JP, Catala F, Boyer JL, Carton M. Liposarcoma of the spermatic cord. Ann Urol (Paris) 1988;22:137-8 9 D'Abrera VS, Burfitt-Williams W. A giant scrotal liposarcoma. Med J Aust 1973;2:854-6 10 Garcia AE, Martin GG, Torrenti H, Monserrat JM. Liposarcoma of the spermatic cord. Rev Argent Urol 1968;37:44-8
3 Vorstman B, Block NL, Politano VA. The management of spermatic cord liposarcomas. J Urol 1984;131:66-9 4 Ishida A, Takeuchi H, Tomoyoshi T. Giant liposarcoma of the spermatic cord: report of a case. Acta Urol Japan 1985;31: 1059-64 5 Hoshino T, Yajima M, Iwasaki A, Hirokawa M, Matsushita K. Liposarcoma of the spermatic cord: a case report. Acta Urol Japan 1987;33:1296-9 6 Mhiri MN, Sellami F, Sellami M, Ben Hamed Y, Smida ML. Malignant paratesticular tumours apropos of three unusual cases. Ann Urol (Paris) 1989;23:23-26
(Accepted 7 March 1991)
Neuroleptic malignant syndrome: a diagnostic dilemma
management only. The event was accompanied by a rise in the CPK to a peak of 1417 IU/l (normal range: 25-175).
S M Sagar BSc MRCP Department of Medicine, Greenwich District Hospital, Vanbrugh Hill, London SElO 9HE Keywords: neuroleptic; catatonia; rigidity; pyrexia; hypersensitivity
The neuroleptic malignant syndrome (NMS) is an idiosyncratic reaction following treatment with neuroleptic drugs such as haloperidol or fluphenazinel2. It is characterized by an extrapyramidal motor disorder resulting in muscular rigidity; altered thermoregulation resulting in pyrexia; and autonomic dysfunction causing sweating, tachycardia and labile blood pressure. There is often a rise in serum skeletal muscle creatinine phosphokinase (CPK)3. It has a mortality of 20%4 which is a consequence of late diagnosis since its features may be confused with signs of other organic and pyschiatric disorders5'6. Three cases of NMS diagnosed during one year at this district general hospital are reported.
Case reports Case 1 A 36-year-old man presented with sudden onset ofheadache. Examination revealed meningism and cerebral angiography demonstrated a subarachnoid haemorrhage. The patient became confused and aggressive and following a diagnosis of acute psychosis, 20 mg haloperidol 4 times daily for one week followed by 50 mg of fluphenazine intramuscularly with procyclidine were administered. After one week, he became catatonic and developed rigidity, pyrexia, diaphoresis, dehydration and a labile blood pressure. Serum urea and aspartate transaminase became elevated. No evidence of sepsis was found and a diagnosis of drug-induced extrapyramidal disorder was made. Despite intensive supportive therapy, the patient died.
Case 2 A 39-year-old man with Henoch-Schonlein purpura was treated with steroids and developed a paranoid psychosis. Twenty-five milligrams of fluphenazine was administered intramuscularly and repeated after 2 weeks. Two days afterwards, he became confused, pyrexial and developed a tachycardia, neck stiffness and catatonia. A lumbar puncture was normal. He recovered after one week with supportive
Correspondence to S M Sagar, Newfoundland Cancer Clinic, Health Sciences Centre, Prince Phillip Drive, St John's Newfoundland, AlB 3V6, Canada
Case 3 A 46-year-old schizophrenic man became acutely agitated. Remission had previously been maintained with intramuscular fluphenazine. This acute episode was treated with chlorpromazine and intravenous haloperidol with procyclidine. Five days later, he became drowsy, pyrexial and developed increasing muscle tone and coma. A pyrexia of 39.5°C, hypotension of 85/60 mmHg and a tachycardia of 130 beats per minute were recorded. He became dehydrated, unresponsive to painful stimuli and developed a generalized lead-pipe rigidity with a pill-rolling tremor. Further investigations included: serum urea 43.9 mmol/l, creatinine 464 mmol/l, haemoglobin 19.9 g/dl, white cell count 7.9x 10l/l. Blood cultures grew no organisms and a lumbar puncture was normal. Serum CPK rose to a peak of 1030 IU/1 and aspartate transaminase rose to 332 IU/1 (normal range: 10-40). A diagnosis of NMS was made and managed with intensive supportive care. After 10 days, the pyrexia remitted and renal function normalized, but catatonia persisted and the CPK remained elevated. Treatment with bromocriptine and dantrolene was commenced. After 5 weeks, the CPK had returned to normal, autonomic instability had resolved, but the patient remained rigid, mute and withdrawn. He was reviewed by a consultant psychiatrist who diagnosed a psychotic catatonic stupor and prescribed electroconvulsive therapy (ECT). After a single treatment, the rigidity diminished and the patient developed spontaneous movements and recovered his speech. After five ECT treatments, rigidity completely resolved and the patient became less withdrawn and could deliver a rational conversation.
Discussion NMS contains features of catatonia, but paradoxically is precipitated by a neuroleptic drug which would otherwise resolve a catatonic state secondary to a mental psychosis. In its extreme form, catatonia is a life-threatening condition which can be precipitated by psychiatric or organic disorders through an effect on limbic and striatal dopamine neuronal pathways7. Hypothalamic malfunction results in labile temperature and blood pressure control, and sustained muscle rigidity results in an elevated CPK and myoglobinaemia. An accurate psychiatric diagnosis is essential before commencing treatment with potent neuroleptics. However, the author has not seen NMS develop after administration of neuroleptic drugs as antiemetics in cancer patients treated with opiates or cytotoxic agents, although a case has recently been reported8. The development of signs which indicate NMS should be critically assessed by the physician. In particular, deterioration in conscious state and development of neck stiffness require the exclusion of meningitis or a subarachnoid haemorrhage. Pyrexia and hypotension resulting from autonomic instability must be differentiated from
0141-0768/91/ 080500-02/$02.00/0 © 1991
The Royal Society of Medicine
Journal of the Royal Society of Medicine Volume 84 August 1991 a septicaemia. The relatively benign Parkinsonian extrapyramidal side-effects of neuroleptics should be differentiated from NMS, since the former respond well to an anticholinergic drug such as procyclidine. NMS is managed by stopping the causative drug and administering intensive supportive care, although there is some evidence that early treatment with bromocriptine9, dantrolenel° or amantadine"l may produce quicker resolution and thereby a lower mortality12. The third case illustrates the difficulty in separating NMS from a catatonic psychosisls14. The differentiation of psychotic catatonia from NMS may be-suggested by a prior psychiatric history, but does not exclude neuroleptic-induced hyperpyrexia and muscle rigidity in a patient with a catatonic psychosis. The diagnosis is then made after the astute observation that the patient's clinical state has deteriorated after neuroleptic treatment. This diagnostic dilemma was experienced by Abbott and Loizou'5. Interestingly, having commenced treatment with chlorpromazine for a functional psychosis, their patient developed catatonia which was initially considered to be psychiatric in origin. They treated the patient with ECT and observed rapid improvement, but the patient relapsed after reintroduction of phenothiazines. ECT may be considered as a primary treatment for NMS if the patient is rapidly deteriorating despite supportive therapy and other organic disorders have been carefully excluded'6.
Acknowledgments: I thank Dr David Robson, Consultant Physician and Dr Jonathan Webb, Consultant Physician for their guidance and allowing me to report their patients.
References 1 Kellam AMP. The neuroleptic malignant syndrome, so-called. A survey ofthe world literature. Br JPsychiatry 1987;150:752-9 2 Adityanjee Singh S, Singh G, Ong S. Spectrum concept of neuroleptic malignant syndrome. Br J Psychiatry 1988;153: 107-11
Contralateral hemiplegia complicating herpes zoster ophthalmicus
J D McNeil MB BS FRACP M Horowitz MB BS FRACP
Department of Medicine, Royal Adelaide Hospital, Adelaide, South Australia
Keywords: herpes zoster ophthalmicus; hemiplegia; intracranial vasculitis; post viral stroke
Contralateral hemiplegia complicating herpes zoster ophthalmicus (HZO) was first recognized by Dumary in 1896 and subsequent reports have confirmed this association. Although the clinical syndrome is well defined, the pathogenesis is less clear. Angiographic studies in this syndrome have revealed carotid siphon abnormalities in some cases and segmental constriction of major intracerebral vessels in others"3. Indeed at one point it was suggested that large vessel arteritis was so well established as the pathological process in this unusual syndrome that arteriography was an unnecessary investigation.' In this paper we report the case of a patient with HZO complicated by contralateral hemiplegia in whom carotid angiography was normal. It is probable that small vessel arteritis underlies a number of cases of contralateral hemiplegia seen in association with HZO.
501
3 Szabadi E. Neuroleptic malignant syndrome. BMJ 1984; 228:1399-400 4 Caroff SN. The neuroleptic malignant syndrome. J Clin Psychiatry 1980;41:79-83 5 Velamoor VR, Fernando MLD, Williamson P. Incipient neuroleptic malignant syndrome? Br J Psychiatry 1990;156:581-4 6 Shalev A., Hermesh H, Munitz H. Mortality from neuroleptic malignant syndrome. J Clin Psychiatry 1989;50:18-22 7 Stoudemire A, Luther JS. Neuroleptic malignant syndrome and neuroleptic-induced catatonia: differential diagnosis and treatment. Int J Psychiatry Med 1984;14:57-63 8 O'Neill WM. The neuroleptic malignant syndrome. Clin Oncol
1990;2:241-2 9 Mueller PS, Vester JW, Fermaglich J. Neuroleptic malignant syndrome: successful treatment with bromocriptine. JAMA
1983;249:386-8 10 Coons DT, Hillman FJ, Marshall RW. Treatment of the neuroleptic malignant syndrome with dantrolene sodium: a case report. Am J Psychiatry 1982;139:944-6 11 Gelenberg AJ, Mandel MR. Catatonic reactions to high potency neuroleptic drugs. Arch Gen Psychiatry 1977;34t947-50 12 Rosenberg MR, Green M. Neuroleptic malignant syndrome. Review of response to therapy. Arch Intern Med 1989;149: 1927-31 13 Castillo E, Rubin RT, Holsboer-Trachsler E. Clinical differentiation between lethal catatonia and neuroleptic malignant syndrome. Am J Psychiatry 1989;146:324-8 14 Fleischhacker WW, Unterweger B, Kane JM, Hinterhuber H. The neuroleptic malignant syndrome and its differentiation from lethal catatonia. Acta Psychiatr Scand 1990;81:3-5 15 Abbott RJ, Loizou LA. Neuroleptic malignant syndrome. Br J Psychiatry 1986;148:47-51 16 Harland CC, O'Leary MM, Winters R, Owens J, Hayes B, Melikian V. Neuroleptic malignant syndrome: a case for electroconvulsive therapy. Postgrad Med J 1990;66:49-51
(Accepted 31 December 1990)
Case report
A 51-year-old Caucasian male presented with an acute onset ofright hemiparesis and dysphasia. A history was obtained, of onset of pain in the left opthalmic division of the trigeminal nerve 23 days earlier, followed 2 days later by a rash characteristic of herpes zoster. Five days after this, the patient experienced blurred vision in the left eye and an ophthalmologist noted evidence of keratitis. The patient was a non smoker and had no pre-existing illness. Examination of the nervous system revealed a moderate global dysphasia, right upper motor neuron facial weakness and a mild right hemiparesis. Cranial pulses were of normal amplitude and no bruits were audible. Blood pressure was 140/90 mmHg and a resolving herpes zoster rash was present in the left ophthalmic nerve distribution with an associated herpetic keratitis. Over the 3 days following admission, right hand motor function deteriorated steadily to a point where no useful function remained. Investigations revealed a normal e sedimentation rate, haemoglobin, white cell count, plasma electrolytes, electrocardiogram and chest X-ray. Computerized axial tomography of the skull, with and without contrast, was within normal limits both on admission and when repeated 10 days later. A slow wave abnormality in the left temporo-parietal area was seen on electroencephalography. Examination of the CSF revealed clear fluid under normal pressre, the protein and glucose concentrations were within normal limits and there were 65 lymphocytes and 65 erythrocytes per mm3. there was no growth on subsequent viral and bacterial cultures of the CSF.
0141-0768/91/
080501-02$02.00/0 © 1991 The Royal Society of Medicine
Journal of the Royal Society of Medicine Volume 84 August 1991 7 Chan YF, Yuen MYP, Tung Ma L, Li MK. Recurrent dedifferentiated liposarcoma of the spermatic cord simulating malignant fibrous histiocytoma. Pathology 1987;19:99-102 8 Rieu JP, Catala F, Boyer JL, Carton M. Liposarcoma of the spermatic cord. Ann Urol (Paris) 1988;22:137-8 9 D'Abrera VS, Burfitt-Williams W. A giant scrotal liposarcoma. Med J Aust 1973;2:854-6 10 Garcia AE, Martin GG, Torrenti H, Monserrat JM. Liposarcoma of the spermatic cord. Rev Argent Urol 1968;37:44-8
3 Vorstman B, Block NL, Politano VA. The management of spermatic cord liposarcomas. J Urol 1984;131:66-9 4 Ishida A, Takeuchi H, Tomoyoshi T. Giant liposarcoma of the spermatic cord: report of a case. Acta Urol Japan 1985;31: 1059-64 5 Hoshino T, Yajima M, Iwasaki A, Hirokawa M, Matsushita K. Liposarcoma of the spermatic cord: a case report. Acta Urol Japan 1987;33:1296-9 6 Mhiri MN, Sellami F, Sellami M, Ben Hamed Y, Smida ML. Malignant paratesticular tumours apropos of three unusual cases. Ann Urol (Paris) 1989;23:23-26
(Accepted 7 March 1991)
Neuroleptic malignant syndrome: a diagnostic dilemma
management only. The event was accompanied by a rise in the CPK to a peak of 1417 IU/l (normal range: 25-175).
S M Sagar BSc MRCP Department of Medicine, Greenwich District Hospital, Vanbrugh Hill, London SElO 9HE Keywords: neuroleptic; catatonia; rigidity; pyrexia; hypersensitivity
The neuroleptic malignant syndrome (NMS) is an idiosyncratic reaction following treatment with neuroleptic drugs such as haloperidol or fluphenazinel2. It is characterized by an extrapyramidal motor disorder resulting in muscular rigidity; altered thermoregulation resulting in pyrexia; and autonomic dysfunction causing sweating, tachycardia and labile blood pressure. There is often a rise in serum skeletal muscle creatinine phosphokinase (CPK)3. It has a mortality of 20%4 which is a consequence of late diagnosis since its features may be confused with signs of other organic and pyschiatric disorders5'6. Three cases of NMS diagnosed during one year at this district general hospital are reported.
Case reports Case 1 A 36-year-old man presented with sudden onset ofheadache. Examination revealed meningism and cerebral angiography demonstrated a subarachnoid haemorrhage. The patient became confused and aggressive and following a diagnosis of acute psychosis, 20 mg haloperidol 4 times daily for one week followed by 50 mg of fluphenazine intramuscularly with procyclidine were administered. After one week, he became catatonic and developed rigidity, pyrexia, diaphoresis, dehydration and a labile blood pressure. Serum urea and aspartate transaminase became elevated. No evidence of sepsis was found and a diagnosis of drug-induced extrapyramidal disorder was made. Despite intensive supportive therapy, the patient died.
Case 2 A 39-year-old man with Henoch-Schonlein purpura was treated with steroids and developed a paranoid psychosis. Twenty-five milligrams of fluphenazine was administered intramuscularly and repeated after 2 weeks. Two days afterwards, he became confused, pyrexial and developed a tachycardia, neck stiffness and catatonia. A lumbar puncture was normal. He recovered after one week with supportive
Correspondence to S M Sagar, Newfoundland Cancer Clinic, Health Sciences Centre, Prince Phillip Drive, St John's Newfoundland, AlB 3V6, Canada
Case 3 A 46-year-old schizophrenic man became acutely agitated. Remission had previously been maintained with intramuscular fluphenazine. This acute episode was treated with chlorpromazine and intravenous haloperidol with procyclidine. Five days later, he became drowsy, pyrexial and developed increasing muscle tone and coma. A pyrexia of 39.5°C, hypotension of 85/60 mmHg and a tachycardia of 130 beats per minute were recorded. He became dehydrated, unresponsive to painful stimuli and developed a generalized lead-pipe rigidity with a pill-rolling tremor. Further investigations included: serum urea 43.9 mmol/l, creatinine 464 mmol/l, haemoglobin 19.9 g/dl, white cell count 7.9x 10l/l. Blood cultures grew no organisms and a lumbar puncture was normal. Serum CPK rose to a peak of 1030 IU/1 and aspartate transaminase rose to 332 IU/1 (normal range: 10-40). A diagnosis of NMS was made and managed with intensive supportive care. After 10 days, the pyrexia remitted and renal function normalized, but catatonia persisted and the CPK remained elevated. Treatment with bromocriptine and dantrolene was commenced. After 5 weeks, the CPK had returned to normal, autonomic instability had resolved, but the patient remained rigid, mute and withdrawn. He was reviewed by a consultant psychiatrist who diagnosed a psychotic catatonic stupor and prescribed electroconvulsive therapy (ECT). After a single treatment, the rigidity diminished and the patient developed spontaneous movements and recovered his speech. After five ECT treatments, rigidity completely resolved and the patient became less withdrawn and could deliver a rational conversation.
Discussion NMS contains features of catatonia, but paradoxically is precipitated by a neuroleptic drug which would otherwise resolve a catatonic state secondary to a mental psychosis. In its extreme form, catatonia is a life-threatening condition which can be precipitated by psychiatric or organic disorders through an effect on limbic and striatal dopamine neuronal pathways7. Hypothalamic malfunction results in labile temperature and blood pressure control, and sustained muscle rigidity results in an elevated CPK and myoglobinaemia. An accurate psychiatric diagnosis is essential before commencing treatment with potent neuroleptics. However, the author has not seen NMS develop after administration of neuroleptic drugs as antiemetics in cancer patients treated with opiates or cytotoxic agents, although a case has recently been reported8. The development of signs which indicate NMS should be critically assessed by the physician. In particular, deterioration in conscious state and development of neck stiffness require the exclusion of meningitis or a subarachnoid haemorrhage. Pyrexia and hypotension resulting from autonomic instability must be differentiated from
0141-0768/91/ 080500-02/$02.00/0 © 1991
The Royal Society of Medicine
Journal of the Royal Society of Medicine Volume 84 August 1991 a septicaemia. The relatively benign Parkinsonian extrapyramidal side-effects of neuroleptics should be differentiated from NMS, since the former respond well to an anticholinergic drug such as procyclidine. NMS is managed by stopping the causative drug and administering intensive supportive care, although there is some evidence that early treatment with bromocriptine9, dantrolenel° or amantadine"l may produce quicker resolution and thereby a lower mortality12. The third case illustrates the difficulty in separating NMS from a catatonic psychosisls14. The differentiation of psychotic catatonia from NMS may be-suggested by a prior psychiatric history, but does not exclude neuroleptic-induced hyperpyrexia and muscle rigidity in a patient with a catatonic psychosis. The diagnosis is then made after the astute observation that the patient's clinical state has deteriorated after neuroleptic treatment. This diagnostic dilemma was experienced by Abbott and Loizou'5. Interestingly, having commenced treatment with chlorpromazine for a functional psychosis, their patient developed catatonia which was initially considered to be psychiatric in origin. They treated the patient with ECT and observed rapid improvement, but the patient relapsed after reintroduction of phenothiazines. ECT may be considered as a primary treatment for NMS if the patient is rapidly deteriorating despite supportive therapy and other organic disorders have been carefully excluded'6.
Acknowledgments: I thank Dr David Robson, Consultant Physician and Dr Jonathan Webb, Consultant Physician for their guidance and allowing me to report their patients.
References 1 Kellam AMP. The neuroleptic malignant syndrome, so-called. A survey ofthe world literature. Br JPsychiatry 1987;150:752-9 2 Adityanjee Singh S, Singh G, Ong S. Spectrum concept of neuroleptic malignant syndrome. Br J Psychiatry 1988;153: 107-11
Contralateral hemiplegia complicating herpes zoster ophthalmicus
J D McNeil MB BS FRACP M Horowitz MB BS FRACP
Department of Medicine, Royal Adelaide Hospital, Adelaide, South Australia
Keywords: herpes zoster ophthalmicus; hemiplegia; intracranial vasculitis; post viral stroke
Contralateral hemiplegia complicating herpes zoster ophthalmicus (HZO) was first recognized by Dumary in 1896 and subsequent reports have confirmed this association. Although the clinical syndrome is well defined, the pathogenesis is less clear. Angiographic studies in this syndrome have revealed carotid siphon abnormalities in some cases and segmental constriction of major intracerebral vessels in others"3. Indeed at one point it was suggested that large vessel arteritis was so well established as the pathological process in this unusual syndrome that arteriography was an unnecessary investigation.' In this paper we report the case of a patient with HZO complicated by contralateral hemiplegia in whom carotid angiography was normal. It is probable that small vessel arteritis underlies a number of cases of contralateral hemiplegia seen in association with HZO.
501
3 Szabadi E. Neuroleptic malignant syndrome. BMJ 1984; 228:1399-400 4 Caroff SN. The neuroleptic malignant syndrome. J Clin Psychiatry 1980;41:79-83 5 Velamoor VR, Fernando MLD, Williamson P. Incipient neuroleptic malignant syndrome? Br J Psychiatry 1990;156:581-4 6 Shalev A., Hermesh H, Munitz H. Mortality from neuroleptic malignant syndrome. J Clin Psychiatry 1989;50:18-22 7 Stoudemire A, Luther JS. Neuroleptic malignant syndrome and neuroleptic-induced catatonia: differential diagnosis and treatment. Int J Psychiatry Med 1984;14:57-63 8 O'Neill WM. The neuroleptic malignant syndrome. Clin Oncol
1990;2:241-2 9 Mueller PS, Vester JW, Fermaglich J. Neuroleptic malignant syndrome: successful treatment with bromocriptine. JAMA
1983;249:386-8 10 Coons DT, Hillman FJ, Marshall RW. Treatment of the neuroleptic malignant syndrome with dantrolene sodium: a case report. Am J Psychiatry 1982;139:944-6 11 Gelenberg AJ, Mandel MR. Catatonic reactions to high potency neuroleptic drugs. Arch Gen Psychiatry 1977;34t947-50 12 Rosenberg MR, Green M. Neuroleptic malignant syndrome. Review of response to therapy. Arch Intern Med 1989;149: 1927-31 13 Castillo E, Rubin RT, Holsboer-Trachsler E. Clinical differentiation between lethal catatonia and neuroleptic malignant syndrome. Am J Psychiatry 1989;146:324-8 14 Fleischhacker WW, Unterweger B, Kane JM, Hinterhuber H. The neuroleptic malignant syndrome and its differentiation from lethal catatonia. Acta Psychiatr Scand 1990;81:3-5 15 Abbott RJ, Loizou LA. Neuroleptic malignant syndrome. Br J Psychiatry 1986;148:47-51 16 Harland CC, O'Leary MM, Winters R, Owens J, Hayes B, Melikian V. Neuroleptic malignant syndrome: a case for electroconvulsive therapy. Postgrad Med J 1990;66:49-51
(Accepted 31 December 1990)
Case report
A 51-year-old Caucasian male presented with an acute onset ofright hemiparesis and dysphasia. A history was obtained, of onset of pain in the left opthalmic division of the trigeminal nerve 23 days earlier, followed 2 days later by a rash characteristic of herpes zoster. Five days after this, the patient experienced blurred vision in the left eye and an ophthalmologist noted evidence of keratitis. The patient was a non smoker and had no pre-existing illness. Examination of the nervous system revealed a moderate global dysphasia, right upper motor neuron facial weakness and a mild right hemiparesis. Cranial pulses were of normal amplitude and no bruits were audible. Blood pressure was 140/90 mmHg and a resolving herpes zoster rash was present in the left ophthalmic nerve distribution with an associated herpetic keratitis. Over the 3 days following admission, right hand motor function deteriorated steadily to a point where no useful function remained. Investigations revealed a normal e sedimentation rate, haemoglobin, white cell count, plasma electrolytes, electrocardiogram and chest X-ray. Computerized axial tomography of the skull, with and without contrast, was within normal limits both on admission and when repeated 10 days later. A slow wave abnormality in the left temporo-parietal area was seen on electroencephalography. Examination of the CSF revealed clear fluid under normal pressre, the protein and glucose concentrations were within normal limits and there were 65 lymphocytes and 65 erythrocytes per mm3. there was no growth on subsequent viral and bacterial cultures of the CSF.
0141-0768/91/
080501-02$02.00/0 © 1991 The Royal Society of Medicine
![[Case report: Neuroleptic malignant syndrome and diagnostic difficulties].](/assets/img/hold.png)
