Dear Sir, Doctors face diagnostic dilemmas when managing elderly patients with multiple pathology. A 70-year-old man was seen in outpatients with the following history. About 1 week previously he had gone to bed feeling well but had woken his wife early in the morning with what looked like a bad dream. His eyes were rolling, the body was rigid and in spasm, shaking uncontrollably. During the next 20 minutes his wife could not evoke any response: there was froth at the comers of his mouth but he was not incontinent. His wife said that over the past 18 months he had been getting attacks in which he would ‘go off momentarily for two or three seconds, as if he was going to pass out‘, but had always recovered immediately and completely. He has a past history of pulmonary tuberculosis, and had to retire from the army. He suffers from bronchitis and uses ipratropium bromide and salbutamol inhalers. He has arthritis affecting the cervical and lumbar spine, with poor mobility. On examination his blood pressure was 130/80 mmHg, pulse 70/min and regular, there was no cardiac murmur or carotid bruit, and the chest was clear. Fundi showed grade 1 changes only. There was no neurological deficit. ECG showed basic sinus rhythm and grade 1 heart block. At times the heart rate slowed to 42/min, showing marked bradycardia. Routine investigations, including skull and chest x-rays, were reported normal. With the history and ECG findings, we thought the patient might have had a Stokes-Adams attack during the night, and admitted him for further investigation. On 24-hour ambulatory monitoring he showed a heart rate varying between 42 and 121/min. There were two recordings of asystolic events in the early hours of the morning, and grade 1 heart block. His EEG was reported normal. He was referred to the cardiologist at Hull Royal Infirmary, where he had further tests carried out and was fitted with a permanent pacemaker. However, after 6 weeks he had another nocturnal episode, witnessed by his wife. His rhythm strips showed occasional pacing as well as sensing failure. The faulty electrode was removed and a new permanent, screw-in type biotronic lead placed. A 24-hour rhythm tape showed this to be working satisfactorily. He was reviewed regularly in our clinic and in Hull. After about 2 months the patient had another nocturnal ‘fit‘. His minor episodes of passing out had not recurred. He was again admitted to cardiology 4 months after we had first seen him, where about 10 days later he had an epileptic fit lasting 6–7 minutes at 4.30am. When he returned to consciousness there was no neurological deficit. Repeat EEG was normal. CT scan of the skull showed two quite well-defined high-density lesions in the right temporal region, with some calcification. These were suggestive of a large right middle cerebral artery aneurysm (perhaps multiloculated and bleeding). He was seen by the neurosurgeon, and 4-vessel angiography showed a long, irregular aneurysm, extending from the posterior communicating origin on the right, extending laterally. There was a small aneurysm arising from the origin of one of the striate vessels on the same side. A diagnosis of bleeding aneurysm was made. The epileptic fits were thought to be related to the aneurysm but not to the cardiac problem, which was stable with the pacemaker. He was operated on in spite of his age, as the risk of leaving the bleeding aneurysm was thought to be greater than that of surgery. The posterior communicating artery aneurysm was clipped, clots were removed, and the patient made a good recovery. This case, with its interesting clinical problems, has made us aware of the danger of multiple pathology, and we have learned to maintain an open-minded approach. Thanks are due to Mrs P Gillham for her secretarial services.