OBJECTIVES:To relate the 30-day perioperative rate of stroke or death in carotid endarterectomy (CEA) to preoperative qualifying symptoms and to the presence of cerebral infarction (CI) demonstrated on computed tomography (CT).DESIGN:Retrospective clinical study.MATERIAL AND METHODS:Two hundred and seventy-two consecutive CEAs for symptomatic stenosis in 262 patients were analysed.RESULTS:The total complication rate was 5.9%. Patients with retinal symptoms (n = 81) had no complications, TIA patients (n = 76) had 6.6% (p < 0.001). Patients qualifying with minor stroke (n = 113) had complications in 9.7% (N.S. compared to TIA patients). Patients qualifying with cortical symptoms had a significantly higher complication rate compared to those with retinal (8.4% vs. 0%, p = 0.004). The presence of a preoperative CT-verified infarction resulted in a higher risk for stroke or death (9.8% vs 2.8%, p = 0.008). Within the subgroup presenting with minor stroke, the presence of CI resulted in stroke or death in 13.9%. In patients without CI the corresponding figure was 2.4% (p = 0.017).CONCLUSION:The qualifying symptoms and the presence of CI visualized by CT influence the complication rate in CEA. When evaluating risk and comparing outcome, these parameters should be included in reporting standards.

Background During physical exercise, cardiac output may increase several-fold to comply with the metabolic requirements from the musculature and to maintain adequate cerebral circulation. in patients with chronic heart failure the cardiac reserve is limited. Objectives The purpose of this study was to evaluate cerebral perfusion during dynamic exercise in patients with chronic heart failure compared with healthy controls. Methods By using transcranial Doppler ultrasonography we examined the effects of one- and two-legged knee extensor exercise on the middle cerebral artery blood flow velocity (V-MCA) in six male patients with chronic heart failure (aged 46-69 years, mean age 59 years, ejection fraction 23 +/- 13%) compared with five healthy male controls (aged 51-60 years, mean age 55 years), V-MCA was examined at rest and at maximum knee extensor exercise with one and two legs. Results At rest and during one-legged exercise no significant differences in V-MCA were present between patients and controls, However, when two legs were used, V-MCA decreased below baseline in all patients (-9%), which markedly different (P < 0.02) from controls (+18%). Conclusions The results suggest that cerebral perfusion may be compromised in chronic heart failure patients during peak dynamic exercise involving a large muscle mass.

Factors controlling cerebral blood flow (CBF) during exercise are complex and incompletely known. Different techniques have shown partly contradictory results of changes in regional and global cerebral perfusion during dynamic exercise in healthy subjects. To elucidate the global CBF response to supine stepwise increasing physical exercise, we measured blood flow in the left common carotid artery (QCCA) and the left internal carotid artery (QICA) simultaneously with the blood flow velocity in the ipsilateral middle cerebral artery (VMCA) using duplex ultrasonography and transcranial Doppler ultrasonography. During moderate exercise intensity (60-67% of maximal capacity), the VMCA increased 14% (P < 0.001), the QICA 17% (P < 0.01), and the QCCA 33% (P < 0.001) compared with baseline values. High physical exercise intensity (80-90% of maximal capacity) tended to reduce VMCA and QICA compared with moderate exercise, in contrast to a continued increase in QCCA. The results indicate an increased global CBF during exercise. This increase was reduced during hard exercise due to a decrease of the arterial PCO2 secondary to hyperventilation.

The effect on the middle cerebral artery blood flow velocity (V(MCA)) of moderate and hard physical exercise on an ergometer cycle was examined in 10 healthy volunteers using transcranial Doppler sonography (TCD). During exercise, the heart rate increased by 136% and the systolic blood pressure by 37% (mean values). During initial moderate exercise, V(MCA) increased by 51%; in a following period of maximal physical work, V(MCA) decreased again by 20% in 9 of 10 volunteers although the heart rate continued to increase by 10% and the systolic blood pressure by 5% (mean values).Constriction of the MCA may explain the initial increase of V(MCA), suggesting a role for large cerebral arteries in autoregulation. Our data indicate that the subsequent decrease of V(MCA) is caused by arteriolar constriction, a likely cause of which was hyperventilation during the excessive work period.

intracranial hypertension 22 Bias 107 Binswanger's disease 82.87 Blepharospasm 308 -. anatomical basis 308 Blood flow velocity 359 -pressure 359 Brainstem 256.320 -infarction 3

The effect of electric stimulation of the sympathetic cord in the upper thoracic level on the middle cerebral artery blood flow veloCitY (V(MCA)) in humans was examined using transcranial Doppler sonography monitoring during surgery for palmar hyperhidrosis. Sympathetic stimulation resulted in marked and rapid increases Of V(MCA). The responses were preceded by prompt increases of mean arterial blood pressure (MABP) and heart rate (HR). Division of the sympathetic cord cranially or caudally to the stimulation site partially reduced the V(MCA), MABP and HR responses. Both these operations reduced sympathetic pathways to the heart as reflected by a decrease in HR and MABP. The integrity of the sympathetic pathway from the stimulation site through the superior cervical ganglion and the carotid plexus was not a prerequisite for a V(MCA) response. Our data suggest that the V(MCA) increase mainly results from stimulation of the heart and the cardiovascular system, resulting in marked increases of blood pressure and heart rate.

Nitroglycerin (NG) induces in cluster headache patients and controls an increase in systemic diastolic blood pressure and/or heart rate and a decrease in blood flow velocity in the middle cerebral artery (VMCA). Termination of NG induced cluster headache-like attack was correlated to an increase of VMCA compared to the VMCA before NG administration ( p < 0.01). This increase was not found in patients without attack or in controls. The NG induced “dynamite headache” in the controls subsided when blood pressure and heart rate were normalized, but the decrease of VMCA still prevailed. Orbital phlebograms have shown pathologic changes in cluster headache and in Tolosa-Hunt syndrome but not in controls. Ocular sympathetic nerves are involved in cluster headache but seldom in Tolosa-Hunt syndrome. It is suggested that the start of a cluster headache attack is due to an increase and the termination of the attack to a decrease of blood flow to the sympathoplegic phlebopathic cavernous sinus.

Studies of the urinary excretion of radioactive iodine and stable iodine, of the concentration of protein-bound iodine in serum, and calculation of the daily production of thyroid hormones, together with clinical investigation showed that: 1) with regard to the incidence of nodularity (86 per cent), the endemic goiter on the Åland Islands is comparable with that on the Finnish mainland; 2) in normal subjects, the average 48-hour excretion of radioactive iodine was 49.3 per cent of the administered dose; 3) the daily urinary excretion of stable iodine (corrected for methodologic error) was about 49.5 μg.; 4) with increasing size of the thyroid gland there was a statistically significant decrease in the excretion of radioactive iodine; in the group with the largest goiters this excretion was only 32.2 per cent; 5) in normal subjects the calculated daily roduction of thyroid hormones was the equivalent of about 62.5 μg. of iodine per day when corrected for methodologic error; it rose with increasing thyroid volume to a level of about 124.5 μg. per day for the group with the largest goiters, a value which differed significantly from that for the control group. A relatively or absolutely diminished availability of iodine to the thyroid, avidently resulting from deficient intake of iodine, plays a significant part in the development of goiter on the Åland Islands. The increased daily production of thyroid hormones in the goiter group can be explained by an increased reutilization of the iodine liberated. The pattern of iodine metabolism in this endemia is compared with pattern in other endemic regions. The relationship with the tendency towards thyrotoxicosis, regarded as a characteristic feature of the Finnish endemia, is discussed.