How important is scalp soft tissue injury as a predictor of skull fracture. Ashis Banerjee FRCS Accident & Emergency. Department, Manor Hospital, Moat Road,.
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.
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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.
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A left carotid arteriogram performed one week after admission was pronounced to be completely normal by two experienced neuroradiologists. In particular there was no radiological evidence of extracranial vessel disease, carotid siphon arteritis or intracranial arteritis. Progressive improvement in speech function occurred over the subsequent three weeks at which time the disability was largely confined to the right hand with persistent global weakness.
Discussion The case documented in this report is typical of other cases in the literature. Hemiplegia was closely related to ophthalmic zoster and the patient was normotensive, relatively young, and had no other risk factors for cerebrovascular disease. The normal carotid arteriogram noted in this case is of particular interest. Cerebral arteriography has been performed on 21 previously reported cases with this syndrome. Abnormalities of the middle cerebral artery have been observed in 15 cases, the anterior cerebral and pericallosal each in five cases, the intra-cranial internal carotid in four, the posterior cerebral in three as well as the superior cerebellar, the operculofrontal and the callosomarginal each in one case. The typical appearance is segmental narrowing, described by MacKenzie et al.3 as smooth tapering, although beadlike narrowings have been observed as well as total occlusion. In two previous cases these angiographic findings have not been found. Doyle et al.5 reported a case where an incomplete angiogram did not demonstrate any lesions; however, this patient subsequently died after progression of the disease and at autopsy a thrombus occluding the middle cerebral artery was evident. Verghese and Sugar6 reported a case where an aneurysm
How important is scalp soft tissue injury as a predictor of skull fracture
Ashis Banerjee FRCS Accident & Emergency Department, Manor Hospital, Moat Road, Walsall WS2 9PS Keywords: scalp bruising; scalp laceration; skull X-ray; wound palpation
The assessment and management of the 'minor head injury' is fraught with pitfalls. The present guidelines for determining the need for skull X-rays are, unfortunately, somewhat ambiguous, open to wide variations in interpretation, and relatively non-specific. In a 6-month period from August 1989 to January 1990, three cases of 'minor head injury' were encountered, in whom X-rays were initially thought to be unnecessary on clinical grounds. In two ofthese patients the outcome was eventually fatal. The purpose of presenting these cases is to ascertain the relevance of scalp injury as a marker of skull fracture. Case reports Case 1 A 4-year-old boy was brought to the Accident & Emergency Department after falling off a rocking horse. He did not lose consciousness and vomited once afterwards. He was found to be alert, active, and running about. No significant scalp injury was noted and X-rays were thought to be unnecessary.
of the anterior communicating artery and a carotid bifurcation plaque were thought to be incidental findings. Our patient is therefore the first case of this syndrome where an adequate angiographic study has been completely normal. Arteriography was performed on our patient 4 days after the period of maximal neurological deficit, therefore it is unlikely that an angiographic lesion was missed. Granulomatous angiitis ofthe central nervous system has been reported in four cases following HZO6. In each case involvement of small cerebral arteries was prominent. It is probable therefore that HZO can be complicated by arteritis involving vessels of varying size. Carotid siphon arteritis and major intracerebral vessel arteritis certainly underlie some cases of contralateral hemiplegia. However, the finding of a normal carotid arteriogram in our case, along with the pathological demonstration of small vessel arteritis in other reports in the literature, suggests that major vessel involvement is not a uniform finding in this syndrome. References 1 Gilbert GJ. Herpes zoster ophthalmicus and delayed contralateral hemiparesis. JAMA 1974;229:302-4 2 Walker RJ, Gammal TE, Allen MB. Cranial arteritis associated with herpes zoster. Radiology 1973;107:109-10 3 MacKenzie RA, Forbes GS, Karnes WE. Angiographic findings in herpes zoster arteritis. Ann Neurol 1981;10:458-64 4 Pratesi R, Freemon FR, Lowry JL. Herpes zoster ophthalmicus with contralateral hemiplegia. Arch Neurol 1977;34:640-1 5 Doyle PW, Gibson G, Dolman CL. Herpes zoster ophthalmicus with contralateral hemiplegia: identification of cause. Ann Neurol 1983;14:84-5 6 Verghese A, Sugar AM. Herpes zoster ophthalmicus and granulomatous angiitis. J Am Geriatr Soc 1986;34:309-12 (Accepted 3 July 1990)
After a period of observation of 2 h, during which he did not vomit again, he was sent home in the care of his mother. In the early hours ofthe morning, about 5 hours after leaving hospital, he was found lying limp in bed and apparently lifeless. Although rushed back to hospital, he could not be resuscitated. Postmortem examination showed a linear parietal skull fracture with an associated subdural haematoma.
Case 2 A 22-year-old man was brought in by the police on a Saturday night having been assaulted with a wooden implement. He denied losing consciousness at any stage. He walked into the department. On examination, no significant scalp or other injury was found. He was detained in the Accident & Emergency Department, having nowhere to go for the night. Skull X-rays were not deemed necessary. During his stay in hospital he talked coherently although abusively at times. After 4 h he suddenly became unconscious without warning. A unilateral fixed dilated pupil was noted. X-rays showed an extensive temporo-parietal skull fracture. After evacuation of an extradural haematoma he failed to regain consciousness and was declared dead after 2 days on a ventilator. Case 3 A 45-year-old man walked into the Accident & Emergency Department after hitting his head forcibly on metal scaffolding. He did not lose consciousness and walked half a mile to hospital, for the express purpose of having a scalp wound sutured. X-rays were thought to be unnecessary. On digital palpation of the wound after local infiltration anaesthesia, a bony defect was palpable in the outer table of the skull. The wound was a 3 cm long incised wound on the vertex of the scalp. X-rays showed a stellate fracture
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