Paralisis De Bell, Reporte De Caso.pdf

Q J Med 2015; 108:145–146 doi:10.1093/qjmed/hcs110 Advance Access Publication 13 June 2012

Case report Facial nerve palsy in the setting of malignant hypertension: a link not to be missed From the 1Department of Medicine, Charing Cross Hospital, 2Department of Neurology, 3 Department of Clinical Pharmacology, St Mary’s Hospital, Imperial College Healthcare NHS Trust, London, UK Address correspondence to Michal Tomek, Department of Medicine, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UK. email: [email protected]

Case history A 38-year-old truck driver presented to our department with 1-week history of blurred vision and recent worsening of frontal headaches, which had been present for 6 months. He had no significant past medical history but could not recall if his blood pressure had ever been measured. His older sister had been diagnosed with malignant hypertension 4 years ago. He smoked 20 cigarettes per day. On examination, he was alert and orientated with a blood pressure of 242/150 mmHg. Visual acuity was decreased to 6/36 bilaterally and fundoscopy revealed bilateral papilloedema with exudates and haemorrhages. Neurological and systemic examination was otherwise unremarkable. Initial tests demonstrated renal impairment (creatinine 142 mmol/l), blood and protein in the urine and electrocardiographic evidence of left ventricular hypertrophy. A computerised tomogram (CT) of the brain was normal. A diagnosis of malignant hypertension was made and the patient’s blood pressure was lowered gradually with a combination of oral modified-release nifedipine, bisoprolol and bendroflumethiazide. Two days after admission the patient developed acute-onset left-sided facial weakness. Examination revealed a lower motor neuron facial palsy and impaired taste in the anterior left tongue but no other abnormalities. Magnetic resonance imaging (MRI) demonstrated bilateral ischaemic white matter

changes in the cerebral hemispheres and diffuse small vessel disease, without a brainstem lesion that would explain the facial palsy. Although it was felt that the facial weakness was most likely related to the severe hypertension, he was treated empirically with a short course of prednisolone and aciclovir for possible Bell’s palsy. Further investigations excluded the presence of a vasculitic or primary renal disorder or other secondary causes of hypertension such as hyperaldosteronism, renal artery stenosis or phaeochromocytoma. He was discharged home once his blood pressure was under control. At follow up, mild renal impairment had persisted but his blood pressure remained well controlled. His facial weakness resolved completely over several months.

Discussion The commonest cause of acute unilateral facial weakness is Bell’s palsy (accounting for 60–75% of cases),1 which has traditionally been regarded as idiopathic. Although a viral aetiology has been suggested, a recent meta-analysis found little benefit of antiviral therapy in Bell’s palsy.2 An association with hypertension has also been observed, suggesting a possible vascular mechanism.3 Interestingly, the majority of previously reported cases of this association have occurred in children.4–8 Here we present a case of facial nerve palsy developing in an adult

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M. TOMEK1, A. NANDOSKAR2, N. CHAPMAN3 and C. GABRIEL2

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M. Tomek et al. recent literature, there was a delay in identification of the underlying severe hypertension.7,8 Given that facial nerve palsy can be the initial (and only) presenting feature of malignant hypertension,13 we urge clinicians to maintain a high index of suspicion, if only so that patients presenting with ‘idiopathic Bell’s palsy’ have their blood pressure recorded and so avoid the potentially disastrous consequences of a delayed diagnosis of malignant hypertension. Conflict of interest: None declared.

References 1. Gilden DH. Bell’s palsy. N Engl J Med 2004; 351:1323–31. 2. Lockhart P, Daly F, Pitkethly M, Comerford N, Sullivan F. Antiviral treatment for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2009; 4:CD001869. 3. Savadi-Oskouei D, Abedi A, Sadeghi-Bazargani H. Independent role of hypertension in Bell’s palsy: a casecontrol study. Eur Neurol 2008; 60:253–7. 4. Still JL, Cottom D. Severe hypertension in childhood. Arch Dis Child 1967; 42:34–9. 5. Lloyd AVC, Jewitt DE, Still JDL. Facial paralysis in children with hypertension. Arch Dis Child 1966; 41:292–4. 6. Trompeter RS, Smith RL, Hoare RD, Neville BG, Chantler C. Neurological complications of arterial hypertension. Arch Dis Child 1982; 57:913–7. 7. Siegler RL, Brewer ED, Corneli HM, Thompson JA. Hypertension first seen as facial paralysis: case reports and review of the literature. Pediatrics 1991; 87:387–389. 8. Harms MM, Rotteveel JJ, Kar NC, Gabree¨ls FJ. Recurrent alternating facial paralysis and malignant hypertension. Neuropediatrics 2000; 31:318–20. 9. Moxon M. Apoplexy into canal of Fallopius in a case of Bright’s disease causing facial paralysis. Trans Path Soc London 1869; 20:420–2. 10. Clarke E, Murphy EA. Neurological manifestations of malignant hypertension. Brit Med J 1956; 2:1319–26. 11. Ellis SL, Carter BL, Leehey MA, Conry CM. Bell’s palsy in an older patient with uncontrolled hypertension due to medication nonadherence. Ann Pharmacother 1999; 33:1269–73. 12. Shmorgun D, Chan WS, Ray JG. Association between Bell’s palsy in pregnancy and pre-eclampsia. QJM 2002; 95:359–62. 13. Tirodker UH, Dabbagh S. Facial paralysis in childhood hypertension. J Paediatr Child Health 2001; 37:193–4.

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patient in the setting of malignant hypertension. The onset of the paralysis appeared to coincide with the rise in blood pressure, with gradual resolution following blood pressure control. The link between hypertension and facial nerve palsy was first suggested in 1869 by Moxon, who described a patient with facial weakness in the setting of renal disease (and presumed hypertension, although this predated indirect measurement of blood pressure and so can only be inferred).9 Since then, a number of reports of the association have been published; however, only a handful of these occurred in adults,9–11 and only one such case has been reported since the early 1980’s.11 A case series from 1967 reported the presence of facial palsy in 6 of 55 (11%) children with severe hypertension;4 an earlier report from the same institution had suggested an incidence as high as 20%.5 In another series of 45 children with severe hypertension, all had developed some neurological manifestation (principally seizures) but only 2 (4%) had facial palsy.6 In contrast, a study of 190 adult patients reported presence of isolated facial nerve palsy in 5 (2.6%) subjects, while overall neurological manifestations were present in 79 (42%) patients.10 Although the pathogenic mechanisms underlying hypertension-induced facial paralysis remain unclear, the cause has been hypothesized to lie in the widespread arteriolar injury characteristic of malignant hypertension. Specifically, the facial nerve is thought to be particularly vulnerable to hypertension-induced injury (due to haemorrhage, oedema or focal ischaemia) in the enclosed space of the facial canal.6 This is supported by autopsy findings of facial canal haematoma in two previously published cases,5,9 suggesting nerve compression due to haemorrhage and thrombus formation. Similar pressure effects may also occur due to thickened vessel walls or the formation of peri-neural oedema, such as has been postulated to occur in pre-eclampsia-induced Bell’s palsy.12 In conclusion, we report a case of an adult patient with facial paralysis associated with malignant hypertension. While knowledge of this link has existed for over a century, it is no longer well recognized, particularly in the adult population. As a result, in two cases reported in the more