Cerebral blood flow (CBF) is regulated by vasomotor, chemical, metabolic, and neurogenic mechanisms. Even though the innervation of cerebral arteries is quite extensively described and reviewed in the literature, its role in regulation of CBF in humans remains controversial. We believe that insufficient attention has so far been focused on the potential role of the innervation of the cerebral vasculature in cerebral autoregulation in humans. We have performed an extensive search and selection of available literature on electrical, chemical, and surgical manipulations of the sympathetic innervation of cerebral arteries, and the effects of circulation sympathetically active agents on CBF. Studies on (surgical) ganglion block show a role of sympathetic tone in preventing increases in CBF in humans, which are consistent with the view based on animal studies. Both direct innervation of the cerebral arteries from cervical ganglia and stimulation of adrenergic receptors by circulating sympathomimetics prevent sudden increases of CBF associated with hypertension and hypercapnia. We postulate that under normal physiological conditions neurogenic control has little influence on cerebral autoregulation as other methods of control (vasomotor, chemical, and metabolic) are dominant. In severely challenging circumstances, such as delayed cerebral ischaemia after subarachnoid haemorrhage, these methods might be overwhelmed, increasing the relative importance of neurogenic, sympathetic control of CBF. This insight might lead to future therapeutic possibilities.
Objectives: Glutamate mediated excitotoxicity of the hyperactive subthalamic nucleus (STN) has been reported to contribute to nigral degeneration in Parkinson's disease (PD). Deep brain stimulation of the STN (STN DBS), in its role as a highly effective treatment of severe PD motor complications, has been thought to inhibit STN hyperactivity and therefore decrease progression of PD. Methods: In a prospective two centre study, disease progression was determined by means of serial 18 Ffluorodopa (F-dopa) positron emission tomography (PET) in 30 patients with successful STN DBS over the first 16 (SD 6) months after surgery. Results: Depending on the method of PET data analysis used in the two centres, annual progression rates relative to baseline were 9.5-12.4% in the caudate and 10.7-12.9% in the putamen.Conclusions: This functional imaging study is the first to demonstrate a continuous decline of dopaminergic function in patients with advanced PD under clinically effective bilateral STN stimulation. The rates of progression in patients with STN DBS were within the range of previously reported data from longitudinal imaging studies in PD. Therefore this study could not confirm the neuroprotective properties of DBS in the STN target.
Our results demonstrate the additive effect of both anxiety and depression in impairing general health-related and tinnitus-specific quality of life and application of coping strategies, and reiterate the need for investigating both symptoms in the clinical evaluation of tinnitus patients.
Objective-To determine morbidity and mortality characteristics in patients treated with electrical neuromodulation for refractory angina pectoris. Design-A retrospective multicentre study of patients treated with spinal cord stimulation between 1987 and 1997; 21 centres were contacted and 14 responded. Setting-Specialist centres worldwide. Patients-Questionnaires were returned on 517 patients, of whom 71% were male. One was lost to follow up. Mean (SD) age was 63.9 (10.1) years. Duration of angina pectoris was 8.1 (6.3) years. Results-Before spinal cord stimulation, 66% of the patients had experienced myocardial infarction, 68% had three vessel disease, and in 24% the left ventricular ejection fraction (LVEF) was < 40%. Percutaneous transluminal coronary angioplasty and bypass surgery were performed in 17% and 58% of the subjects, respectively. During a median follow up of 23 months (range 0 to 128), 103 patients died (52 from a cardiac cause, 25 from a non-cardiac cause, and 26 from an unknown cause). Annual all cause mortality was 7-8%; annual cardiovascular fatality was 3.5-5%. Mortality was univariately related to sex, number of diseased vessels, number of revascularisation procedures, previous myocardial infarction, LVEF, insulin dependent diabetes, blocking agents, and angiotensin converting enzyme inhibitors. Multiple variate analysis showed that LVEF, sex, blockers, and age > 71 years were independent predictors of mortality. During spinal cord stimulation, New York Heart Association functional class improved from 3.5 to 2.1 (p < 0.01); 25 of the deceased patients (24%) and 32 survivors (8%) experienced myocardial infarction; hospital admissions were significantly (p < 0.001) more common in the deceased group (66% v 37%). Conclusions-The clinical outcome of patients with intractable angina is not adversely aVected by the chronic use of neurostimulation. (Heart 1999;82:82-88)
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