Hepatitis B virus infection is common in institutions caring for the mentally handicapped. Hepatitis B virus and hepatitis C virus share routes of transmission but the prevalence of hepatitis C virus infection in this population is unknown. We have tested 101 patients from two institutions in South-East England caring for adults with mental handicap for the presence of hepatitis C antibody, hepatitis B core antibody, and if necessary hepatitis B surface antigen. None tested positive for hepatitis C antibody, but 43 had hepatitis B core antibody of whom 14 were chronic carriers positive for hepatitis B surface antigen. Unlike hepatitis B virus, hepatitis C virus infection appears to be uncommon in UK institutions.

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Barore¯ex failure syndrome is a rare complication of iatrogenic or traumatic damage to the (mainly carotid) arterial baroreceptors in the neck. It is characterized by sympathetic overactivity in response to environmental stress. Failure of the barore¯ex to buffer changes in blood pressure (by altering central sympathetic out¯ow) results in large¯uctuations in blood pressure, often with associated ushing, sweating, headache and anxiety 1. Hypertension may be severe and cases of encephalopathy and intracerebral haemorrhage have been reported 2,3. Orthostatic hypotension is unusual, and is more typical of syndromes with pure autonomic failure. As in this case, spot plasma catecholamine concentrations may be raised, but 24-hour urine values are normal. This, together with the prompt, or exaggerated, suppressive effect of clonidine, is characteristic and differentiates barore¯ex dysfunction from phaeochromocytoma 4. Clonidine and phenoxybenzamine have been used successfully to treat this syndrome 1 , but we would also advocate the use of labetolol, which shares their combined a and b adrenergic blocking properties. Improvement in the patient's blood pressure pro®le without an increase in maintenance therapy suggests a degree of baroreceptor recovery. Morbidity from cervicocephalic dissections is usually due to thromboembolic stroke or, rarely, complete arterial occlusion. The`migrainous' presentation described here is typical of internal carotid artery dissection. Horner's syndrome (due to disruption of branches of the superior cervical ganglion), pulsatile tinnitus and lower cranial nerve phenomena are features that often precede retinal or cerebral embolic events. Fibromuscular dysplasia accounts for around 15% of non-traumatic internal carotid artery dissections 5,6 , especially if bilateral 5,7. It is an incidental ®nding in 51% of the population 8 and tends to be diagnosed in mid-life, being more common in women than in men and in patients with connective tissue disorders such as Marfan's syndrome 5,8. The long-term outlook after arterial dissection is generally good, with over 75% of patients making a complete recovery without sequelae 6. MR angiography is the investigation of choice and prophylactic anticoagulation, though unproven in trials, remains standard practice 9 .

We report a case in which erythromycin was used in place of rifampicin after a severe reaction to the latter in the treatment of pulmonary Mycobacterium kansasii infection. Case reportAn 83 year old man presented with physical deterioration, weight loss, and selfneglect. There was no history ofcough or haemoptysis, or ofprevious tuberculosis. His weight was 42-8 kg and he had an intermittent low grade pyrexia. Examination otherwise showed nothing remarkable. Investigations revealed normochromic, normocytic anaemia (haemoglobin concentration 11 1 g/dl) and an erythrocyte sedimentation rate (ESR) of 103 mm in the first hour. Chest radiography showed ill defined soft tissue shadowing with cavitation affecting both upper zones, particularly on the left, and shadowing at the left base. Mantoux testing gave a negative result. Fibreoptic bronchoscopic washings and brushings contained moderate numbers ofacid fast bacilli subsequently identified as M kansasii. The organism was sensitive to rifampicin, ethambutol, erythromycin, and co-trimoxazole but resistant to streptomycin and isoniazid.Meanwhile anti-tuberculosis treatment had been started with rifampicin (450 mg), isoniazid (300 mg), and ethambutol (600 mg) daily. After two weeks' treatment he developed a hepatic reaction with vomiting, jaundice, and deranged liver function. Treatment was therefore curtailed. Reintroduction of rifampicin two weeks later, when liver function was normal, precipitated a cutaneous reaction. Treatment was therefore continued with isoniazid, ethambutol, and pyridoxine. Two weeks later, when the organism had been identified and the sensitivities were known, erythromycin stearate (500 mg thrice daily) was added.Treatment was continued for a further 11 months, which resulted in clinical improvement, as evidenced by weight gain (48-6 kg), resolution ofthe anaemia (haemoglobin concentration 13-3 g/dl), and a fall in the ESR to 15 mm in the first hour. The chest radiograph showed considerable hardening of the inflammatory shadowing and total clearing of the changes at the left base, leaving some residual thin walled cavities at both apices. Repeat bronchoscopy was not felt to be warranted.The patient remained well until six months after finishing