This historical cohort study has provided incidence data for thyroid disease over a twenty-year period for a representative cross-sectional sample of the population, and has allowed the determination of the importance of prognostic risk factors for thyroid disease identified twenty years earlier.

Background and Purpose-Hyperglycemia following acute stroke is strongly associated with subsequent mortality and impaired neurological recovery, but it is unknown whether maintenance of euglycemia in the acute phase improves prognosis. Furthermore, the safety of such intervention is not established. Methods-In an explanatory, randomized, controlled trial to test safety, 53 acute (within 24 hours of ictus) stroke patients with mild to moderate hyperglycemia (plasma glucose between 7.0 and 17.0 mmol/L) were randomized to receive either a 24-hour infusion of 0.9% (154 mmol/L) saline or a glucose potassium insulin (GKI) infusion at 100 mL/h. The GKI consisted of 16 U human soluble insulin and 20 mmol potassium chloride in 500 mL 10% glucose. Blood glucose was measured every 2 hours with Boehringer Mannheim Glycaemie test strips, pulse and blood pressure were measured every 4 hours, and plasma glucose samples were taken every 8 hours. Insulin concentration in the GKI was altered according to BM glucose values. Results-There were no statistically significant differences between the 2 groups at baseline. Twenty-five patients received GKI, 1 of whom required intravenous glucose for symptomatic hypoglycemia. Plasma glucose levels were nonsignificantly lower in the GKI group throughout the infusion period. Four-week mortality in the GKI group was 7 (28%), compared with 8 (32%) in the control group. Conclusions-GKI infusions can be safely administered to acute stroke patients with mild to moderate hyperglycemia producing a physiological but attenuated glucose response to acute stroke, the effectiveness of which remains to be elucidated. (Stroke. 1999;30:793-799.)

As part of a prospective study of the neurologic and neuropsychological complications of coronary artery bypass graft surgery, 312 patients were compared with a control group of 50 patients undergoing major surgery for peripheral vascular disease. The purpose of comparing the 2 groups was to determine to what extent neurologic complications after heart surgery can be attributed to cardiopulmonary bypass. The 2 groups were similar with respect to age, preoperative neurologic and intellectual status, anesthetic methods, duration of operation, perioperative complications, and time spent in the intensive therapy unit. Certain potential risk factors for cerebrovascular disease were more common in the control than the coronary bypass patients. The important difference between the 2 groups was that only the latter group underwent cardiopulmonary bypass. In this group 191 of 312 (61%) and 235 of 298 (79%), respectively, developed early neurologic and neuropsychological complications. By the time of hospital discharge 17% had neurologic disability and 38% had significant neuropsychological symptoms. In the control group 9 of 50 (18%) developed neurologic complications resulting largely from trauma to lower limb sensory nerves. Two patients developed primitive reflexes. Fifteen of 48 (31%) showed neuropsychological impairment on 1 or 2 subtest scores. Moderate or severe intellectual dysfunction was not seen in the control patients in contrast to the 24% thus affected in the coronary bypass group. The difference in frequency and severity of central nervous system complications between the 2 groups is likely to reflect cerebral injury resulting from cardiopulmonary bypass. (Stroke 1987;18:700-707)

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In a prospective study of 157 patients (median age 73 years) admitted to hospital within 72 hours of acute cerebral hemisphere stroke, there was clinical evidence of homonymous hemianopia (HH) as assessed by confrontation in 99 (63%). Patients were followed with serial neurological examinations for 28 days. Complete recovery of visual fields occurred in 14 (17%) of the 81 patients with a complete HH on admission and in 13 (72%) of the 18 patients with a partial HH on admission. Cumulative fatality at 28 days was greater in patients with a complete HH (49%), compared with patients with a partial HH (11%). These two patterns of recovery and outcome probably reflect the differing extent of cerebral damage in the two groups.

one-third of all acute stroke patients may have diabetes mellitus. For patients presenting with post-stroke hyperglycaemia, impaired glucose tolerance or diabetes mellitus is present in two-thirds of survivors at 12 weeks. Admission plasma glucose > or = 6.1 mmol/l combined with glycosylated haemoglobin > or = 6.2% are good predictors of the presence of diabetes mellitus following stroke.

Buckton KE, O'Riordan ML, Ratcliffe SG, et al. A G-banded study of chromosomes in liveborn infants. Ann Hum Genet 1980;43 :227-39. 5 Gosden CM, Wright MO, Paterson WG, Grant KA. Clinical details, cytogenetic studies and cellular physiology of a 69,XXX fetus with comments on the biological effect of triploidy in man. J Med Genet 1976; 13:371-80. 6 Gosden CM, Brock DJH. Morphology of rapidly adhering amniotic fluid cells as an aid to the diagnosis of neural tube defects. Lancet 1977;i: 919-22. 7 Gosden CM, Brock DJH. Combined use of alphafetoprotein and amniotic fluid cell morphology in early prenatal diagnosis of fetal abnormalities.

A longitudinal study was performed on 118 first-ever stroke patients to evaluate neurophysiological measurements of central motor conduction time (CMCT) in the period immediately following stroke as predictors of functional outcome and mortality at 12 months. Measurements of CMCT were made as described in the accompanying article (Heald et al., 1993, Brain, 116, 1355-1370), in which the following three groups of patients were recognized within 12-72 h after the onset of symptoms: normal response group, delayed response group and no response group. Neurophysiological and clinical investigations were commenced 12-72 h (designated as day 1) after the onset of symptoms and repeated at set time intervals up to 12 months. The subjects were examined neurologically and assessed using the Motricity Index for muscle strength, the Nine-hole Peg Test to measure manual dexterity, the Barthel Score for activities of daily living and the modified Rankin Scale for functional outcome. The duration of stay in hospital and the occurrence of stroke-related death were noted. During the first week following stroke, absence of responses correlated closely with the patient's symptoms and neurological observations of abnormal muscle tone and tendon reflexes. Correlations were made in the three groups of patients of functional scores at day 1 and at 12 months. Patients with normal CMCT had consistently higher scores throughout the 12 month period and achieved significantly better functional recovery. Patients with no responses showed poor performance in neurological and functional tests throughout the 12 month period. Patients with delayed CMCT had neurological and functional scores intermediate between those of the other two groups, but outcome at 12 months was similar to those in the normal response group. Where the threshold to cortical stimulation was abnormally high, functional outcome was generally poor. Mortality was highest in the group with absent responses and the survivors spent the longest period in hospital. In conclusion, the observation of normal or delayed CMCT at day 1 identifies a group of patients with a high probability of survival and functional recovery. The absence of responses to cortical stimulation at day 1 identifies a group of patients who are at high risk of poor functional recovery at 12 months and greater probability of stroke-related death during this period.