In order to evaluate the nature and association of audiovestibular disturbances and systemic sclerosis (SSC), 37 unselected SSC patients were studied with a detailed audiological and vestibular examination since November, 1987. Pure-tone audiometry, speech audiometry, impedance audiometry, brainstem response audiometry and vestibular function using electronystagmographic recording were performed. We found a rather frequent audiovestibular involvement (41 %). A hearing loss was found in 14 SSC patients; hearing loss was sensorineural in 10 cases and mixed in 4 cases. The latter revealed a finding similar to tympanosclerosis. Four patients showed altered vestibular test values and only one of these had normal hearing. Sensorineural deafness was the more frequent pathological finding and in all cases the site of lesion was cochlear. SSC appears to be directly responsible for audiovestibular damage, since in 12 out of 15 patients with such involvement, no other apparent cause could be revealed. SSC may be included among the autoimmune diseases which may cause audiovestibular disturbances.

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525There was a significant relationship between plasma glucose and the volume of the intracerebral lesion volume as measured on computed tomographic scan (r=.469, P=.00\), but a stronger relationship was observed between serum cortisol and lesion volume (r=.542, / > <.001). Neither hemoglobin Al nor plasma noradrenaline levels were significantly correlated with lesion volume.Fasting plasma glucose was measured in survivors over the course of the study. There was a significant decrease in the fasting glucose levels on the order of 1 mmol/L over the first 7 days after stroke onset. This is in keeping with the results of Melamed, 3 who found that hyperglycemia after stroke returned to normal levels a mean of 3.5 days after stroke. Hyperglycemia after stroke fulfills the criteria for stress hyperglycemia, ie, it is elevated in proportion to the severity of the illness, it is related to the mediators of the stress response, and it is a temporary phenomenon.van Kooten and colleagues were not able to demonstrate this phenomenon because they measured only catecholamines. While catecholamines are related to injury, 4 they are extremely sensitive to stress. Admission to a hospital is a stressful event, and this "background noise" may have obscured the relationship between glycemia and catecholamines. Even though we attempted to standardize the stress as much as possible, other factors known to alter plasma catecholamine levels, 5 such as caffeine intake, sodium intake, cardiac output, and renal clearance of catecholamines, were not controlled in either study. The estimation of picogTam quantities of adrenaline and noradrenaline is technically difficult. The plasma half-life of these substances is quite short, and a proportion of the noradrenaline or the majority of the adrenaline response may have decayed even before the first sample in the van Kooten study was taken, as the flow phase of the stress response is established after 24 hours.'In short, we agree with the findings of van Kooten et al, but we cannot agree with their conclusion that hyperglycemia after stroke is not due to a stress response. We believe that there is evidence that there is a stress hyperglycemic response in the early stages of acute stroke. The nature of the stress response, and in particular the influences of central centers in the brain on the response, has yet to be elucidated.

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