This study was conducted to analyze the prevalence and features of chronic or recurrent headache in Systemic Lupus Erythematosus (SLE), and also the relationship of such headache with other manifestations of the disease. A total of 76 patients (69 women and 7 men) with a mean age of 40 years (r: 24-74 years) were included. An overall severity index for SLE was applied. Fifty-two patients (68%) presented headache, 27 (52%) being vascular and 25 (48%) muscle contraction type. Headache in general was more frequent after the onset of SLE (p less than .001). Prevalence of muscle contraction headache in particular was greater following manifestations of SLE. Family history of migraine was recorded in 54% of the patients with vascular headache. This antecedent was more common in patients in whom migraine started before the onset of SLE (p = .05). A greater number of neuropsychiatric symptoms was observed in the patients with vascular headache and family history (p less than .02). Patients with thrombocytopenia presented headache less frequently (p less than .05). Our results showed headache, of both vascular and muscle contraction types, to be frequent in SLE. We note that there is an increased frequency of muscle contraction headache after the onset of SLE, and that there is a migraine-like headache directly related to SLE. Migrainous patients with familial history have a greater probability to suffer neuropsychiatric manifestations. Finally, it is suggested that severity of SLE is not related to presence of headache.

We studied neurologic morbidity and its evolution during hyperglycemia induced immediately after permanent unilateral common carotid artery ligation in Mongolian gerbils. A total of 60 animals were divided into five groups: one experiencing severe hyperglycemia for 1 hour after the onset of ischemia (brief hyperglycemia group, n=13), a normoglycemic control group for the brief hyperglycemia group (n=12), a group with severe hyperglycemia for 4 hours after the onset of ischemia (prolonged hyperglycemia group, n = l l ) , a normoglycemic control group for the prolonged hyperglycemia group (n = 13), and a hyperosmolar normoglycemic control group for the prolonged hyperglycemia group ( n = l l ) . Neurologic morbidity and mortality were higher in the two hyperglycemic groups than in the three normoglycemic control groups. The neurologic deficit progressed according to the duration of severe hyperglycemia. In the three normoglycemic control groups neurologic status stabilized 120 minutes after the onset of ischemia, in the brief hyperglycemia group stabilization occurred at 210 minutes, and in the prolonged hyperglycemia group neurologic deficit progressed for approximately 360 minutes, coinciding with the death of all but one gerbil, in which the neurologic deficit remained stable until death 23 hours after ischemia. We suggest that hyperglycemia is another cause of progressing cerebral infarction. (Stroke 1990;21:1621-1624) P rogressing cerebral infarction refers to that temporal clinical category for which progression or an increase in the severity of the neurologic signs has occurred within recent minutes. Other suggested causes, well-summarized by Price et al, 3 are decreased cardiac output, systemic hypotension/postural hypotension, increased blood viscosity, hypoxia, seizures, and hemorrhage into an infarct.There are no reports on progressing cerebral infarction to date that provide an analysis of plasma glucose level during the acute phase of the illness. Hyperglycemia during either global or regional brain ischemia is widely known to be detrimental.4 -6 High brain glucose Received January 5, 1989; accepted July 25, 1990. levels are thought to mediate their detrimental effect through accentuated tissue lactacidosis during and following ischemia.7 -8 Hence, by controlling hyperglycemia during the acute phase of cerebral ischemia some progressing strokes could be arrested.We examined the influence of hyperglycemia in the setting of progressing cerebral infarction. Specifically, we assessed neurologic morbidity and its temporal profile during hyperglycemia induced immediately after unilateral common carotid artery (CCA) occlusion in Mongolian gerbils. Materials and MethodsWe performed experiments on a total of 60 adult (50-80 g body wt) Mongolian gerbils (Meriones unguiculatus) (Shamrock, Henfield-Sussets, England) of either sex equally distributed among five groups: the brief hyperglycemia group (n = 13), the prolonged hyperglycemia group (« = 11), saline-treated normoglycemic control groups for both the br...

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