SUMMARYCell bodies within the periaqueductal grey (PAG) of the midbrain of the propofol-anaesthetized rat were stimulated using the excitotoxin kainic acid. This resulted in a rise in arterial blood pressure and a tachycardia, together with a reduction in the sensitivity and a rightward resetting of the baroreflex. These changes mimicked the cardiovascular effect of bilateral hindlimb ischaemia in the rat. Further experiments in conscious rats indicated that electrolytic lesions in the PAG prevented the reduction in baroreflex sensitivity induced by limb ischaemia, but did not abolish the rightward resetting of the reflex or the pressor response and tachycardia when compared with sham-lesioned controls. It is postulated that the PAG, a site of importance both in the integration of the defence reaction and the processing of afferent nociceptive information, may form part of a pathway involved in the reduction of the sensitivity of the baroreflex following injury. This pathway is suggested to be separate from a second, as yet undefined, pathway mediating the baroreflex resetting and pressor responses associated with injury.

AManchester SUMMARY A patient with spontaneous periodic hypothermia who had both a lipoma and agenesis of the corpus callosum is described. Spontaneous periodic hypothermia associated with corpus callosum abnormalities is a distinct entity and although the mechanism underlying the hypothermic episodes is unexplained, the term "diencephalic autonomic epilepsy" does not seem appropriate. Profuse sweating for several days had been noted during one of them.When two years old he had sustained a fractured skull in a road traffic accident. His physical development was normal but he was mentally slow and had attended a special school. He had worked in a furniture factory for nearly 20 years, eventually being forced to retire by ill health. For at least 6 years he had major seizures treated with Phenytoin 100 mg twice daily. On examination he was thin with a normal male distribution of body hair. He was alert and orientated but below average intelligence (WAIS IQ= 75). He had mild dysarthria with exaggerated reflexes in the left arm and bilateral extensor plantar responses. After three weeks in hospital, during which he was well and ambulant with an oral temperature between 35 0°C and 36 5°C, blood pressure 120/80 mmHg and pulse rate 60 per minute, he suddenly developed profuse sweating accompanied by cutaneous vasodilatation which affected the whole body surface. He complained of feeling hot and after 2 hours continuous sweating his oral temperature was 31 0°C. Any rise in body temperature provoked further attacks of sweating lasting 30 minutes to several hours and with each attack the rectal temperature fell, often as low as 29 5°C (fig 1). Two days after the onset of sweating the patient became lethargic and withdrawn. His dysarthria increased, he had marked truncal ataxia and flapping tremor of the outstretched hands. After 4 days he was unresponsive and incontinent. Systolic blood pressure varied between 75-100 mmHg with marked bradycardia, sometimes as slow as 40 per minute. The ECG showed typical J-waves. Five days later his body temperature returned abruptly to his normal level. His physical and mental state recovered after two days. Seven days later he had a similar sudden episode of sweating and hypothermia which lasted 8 days. His hospital course was marked by alternating periods of relative normality and sweating with hypothermia. Shivering was never seen. Several major and left sided focal motor attacks occurred during

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