[Studies on the autoregulation of cerebrovascular circulation. I. Acute pressure-induced changes of the cerebral vascular resistance in normo- and hypercapnia].
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The conventional view is that a 'blood-brain barrier' prevents the passage into the bloodstream of noradrenaline released as a transmitter in the brain. When we tested directly for noradrenaline spillover, sampling via high right and left internal jugular venous catheters in 22 untreated patients with primary hypertension, release of noradrenaline into the cerebrovascular circulation was detected. The concentration of noradrenaline was 14.8% (mean 0.29 nmol/l) higher in right jugular venous than arterial plasma, and 29.8% (mean 0.55 nmol/l) higher in left (both P less than 0.02, Student's paired t-test). Asymmetry in the cerebral venous drainage pattern (right jugular typically largely represents cortical flow, left jugular subcortical flow) and flow rate (usually lower on the left) may underlie the higher venoarterial plasma concentration gradient on the left. Cerebral noradrenaline overflow was calculated from the cerebral plasma flow, the venoarterial noradrenaline plasma concentration gradient across the brain and transcerebral extraction of radiolabelled noradrenaline. Mean cerebral noradrenaline spillover was 220 pmol/min, accounting for 9.1% of total noradrenaline release to plasma (determined by isotope dilution). Since the ganglionic blocker arfonad reduced whole-body noradrenaline spillover (principally derived from sympathetic nerves), but not cerebral spillover, the noradrenaline overflow appears to originate from brain neurones and not cerebrovascular sympathetic nerves. Jugular venous noradrenaline measurements may provide a direct 'window' into noradrenergic brain mechanisms in primary hypertension, with bilateral sampling perhaps allowing differentiation of cortical from subcortical neurotransmitter function.
Strokes have been known since ancient times. Today, stroke is the second most frequent cause of death and the most frequent cause of invalidity. In about 80% of cases, stroke is caused by cerebral ischemia and in about 20% by intracerebral hemorrhage, subarachnoidal hemorrhage, venous thrombosis and other cerebrovascular diseases. The brain is one of the most richly perfused tissues and depends fundamentally on the supply of oxygen and glucose. In order to assure adequate cerebral blood flow, the brain is capable of autoregulation through the interaction of diverse autoregulatory mechanisms (myogenic, neurogenic and metabolic factors, blood viscosity, renin-angiotensin-system and endothelium). Reduction of cerebral blood flow below the threshold of about 25 ml/100 g x min leads to an impairment of the functional metabolism and later to impairment of the structural metabolism. Pathophysiologically, a large number of isolated pathobiochemical processes (loss of energy, lactate acidosis, excitating amino acid release, ion balance disorders, calcium overload, free radical release, etc.) start to interfere with each other. Delayed edema and inflammation lead to secondary brain damage. Apoptosis is probably induced by ischemia and can cause secondary deterioration. The basic principles in the treatment of ischemia are firstly the rapid restoration of cerebral blood flow (lysis, carotid endarterectomy) and secondly--following infarction--a limitation of brain damage (preservation of ischemic but not necrotic brain tissue, prevention of secondary complications). Stroke treatment requires profound diagnostic and therapeutic expertise and interdisciplinary cooperation of neuroradiologists, neurosurgeons, vascular surgeons and cardiologists. Stroke can best be managed in special "stroke units", which have now been established in nearly all parts of Germany. Beside acute management of stroke and neurological rehabilitative treatment, emphasis has to be laid on primary (public information, education, treatment of risk factors) and secondary prophylaxis (treatment with antiaggregants, anticoagulants, a. o.).
The effect of decreased anterior (carotid) bloodflow on the auditory brain stem response (ABR) was studied in a group of middle-aged males with angiographically confirmed decreased carotid circulation who were candidates for internal carotid end-arterectomy. Individual and mean latencies from the experimental group were compared to latencies of a control group matched for age, sex, and hearing loss. Mean absolute latency of wave V was significantly longer in the group with decreased anterior circulation when compared to the matched control group. These findings are similar to those from studies examining decreased posterior (vertebrobasilar) circulation. Both the matched control and experimental group were also compared to clinic norms and judged for abnormality. None of the control group ABRs were judged abnormal, after correction for hearing loss, while 29% of the ABRs were judged abnormal from the group with decreased anterior circulation. Postoperative testing was performed 1 week after surgery to determine any immediate effects of revascularization of the ABR. No changes in absolute or interpeak latencies were observed for either ear between pre- and postoperative testing. It is concluded that patients with confirmed decreased cerebrovascular circulation may show prolongation of absolute latency of wave V on ABR testing. Revascularization surgery in these patients appears to have no affect on their ABR within 1 week of surgery.
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Rheoencephaloplethysmography revealed the increase of impedance specific for enhancement of intracranial blood flow after occlusion of both common jugular veins only in the ocular-occipital lead in humans. The intracranial component of rheoencephalography was calculated from the data of interelectrode current distribution in extra- and intracranial tissues. The maximal value of the current through intracranial tissues reached 15 per cent for the ocular-occipital lead.
The xenon CT method enables CT measurement and imaging of regional cerebral blood flow. The decisive advantages of this method are good spatial resolution, close correlation of the blood flow image with the CT plane, relatively uncomplicated handling and rapid repeatability. The xenon CT method is an asset in the diagnosis of cerebral diseases since it provides information on functional changes in addition to the morphological findings.
Blood flow velocity of 24 patients in state of the brain death were examined by transcranial Doppler sonography. Authors expound the characteristic velocity-pulse graphs recorded in progressively increasing intracranial pressure and their chronology as well. The different forms of the oscillating flow and their successive development are described. The oscillating flow, the systolic spikes and the so called "zero Flow" are the transcranial Doppler signs of the ceased cerebral blood flow, and these signs can be used as one of the evidence of the brain death.
Transcranial Doppler Sonography. Authors publish the experiences gained by 2300 examinations with Transcranial Doppler Sonography (TDS) which is a new, noninvasive ultrasound method to examine cerebral blood flow velocity in the basal arteries. The theoretical ground and the technique of the investigation is detailed. Mean values of blood flow velocity in the middle cerebral artery of 88 healthy volunteers in different age groups are reported. Authors stress on the numerous advantages of the utilization of this technique. Different pathological alterations of blood flow velocity and characteristic types of velocity-pulse figure are accounted. At last illustrative case reports proving the importance of TDS in different pathological states are presented.
The author investigated the blood flow in the common carotid arteries by means of Doppler ultrasonography in 98 patients after stroke. An UDP 10 ultrasound flow detector was used and the results obtained in patients dying during the treatment were compared with those who were discharged improved. In the cases with lethal outcome considerable (over 30%) asymmetry of blood flow was found, usually but not always with slowing of this flow on the side of the lesion. Diastolic blood flow was in this group significantly lower on the side of the cerebral lesion and compared with the group with favourable outcome. Other differences were not characteristic. The results of these investigations showed that in patients with a high-grade asymmetry of blood flow in the common carotid arteries and impairment of brain perfusion evidenced by slowing down of the diastolic blood flow the course of the stroke is often more severe. This may be of prognostic significance.
As many as 75 patients with a history of transitory disorders of cerebral circulation, minor brain strokes and brain strokes with minimum residual symptomatology were examined. Multimodality rehabilitation treatment of these patients included oxygen baths which were administered early (starting from the 4th-5th week since the moment of disorder onset) or in the long-term period. The conclusion is made that balneotherapy can be included into a complex of treatment measures along with antiaggregation remedies as early as possible, leading to improvement in 90% of patients together with recovery of normal function of hemostasis both in persons with the latent DVC syndrome and in those with hypercoagulation. It has been established that oxygen baths do not produce any angiospastic effect or material changes in the lipid content of blood serum. The treatment with the use of oxygen baths administered in the long-term period turned out less effective since only 46% of patients improved.
Repeated CBF-measurements can be performed after inhalation or intravenous injection of 133Xe. After the development of a bicompartmental model by Obrist et al. in 1975 atraumatic CBF-measurements became widely used but there were still some difficulties concerning the sensitivity of different flow-indices towards CBF changes in normals under test conditions or ischemia in stroke patients. Due to the "slippage phenomenon" mostly noncompartmental flow-indices are used for the detection of ischemic brain areas. In this study a scintillation camera, that is usually available in every nuclear medicine department, was used for atraumatic CBF-studies. A collimator consisting of hexagonal lead tubes (septa 0.2 mm thick; FWHM 1.7 cm in 10 cm) was constructed for this purpose. The obtained counting rate varied between 2432 and 9081 cps over the whole hemisphere and 116-1094 cps in regions of approximately 2.5 X 2.5 cm. In 31 patients with CVD CBF was measured with the intracarotid (i.c.) technique and 1 hour later after i.v. 133Xe-injection. Intravenous flow values were comparable to those obtained after i.c. 133Xe injection (fB X MFr = 0.904; p less than 0.001). In 12 of the used 13 regions also significant correlation coefficients were found. In order to estimate the reproducibility of the intravenous injection method CBF-measurements were performed in both hemispheres of 10 patients on two consecutive days. Highly significant correlation coefficients were found for hemispheric blood flow (r = 0.933; p less than 0.001) and temporal, frontotemporal, temporoparietal and praecentral regions, while in the high parietal, frontal and occipital region lower reporducibility was found. Normal CBF-values were obtained from 12 healthy volunteers (MF right hemisphere: 50.7 +/- 4.6 ml/100 g/min; MF left hemisphere: 50.6 +/- 4.6 ml/100 g/min). MF did not show any hyperfrontality, while F1 and the ISI gave highest flow values in frontal regions. The clinical status of 76 patients suffering from cerebral ischemia (68 with flow disturbances in one hemisphere, 8 with vertebrobasilar insufficiency) was estimated by a semiquantitative scorescale at time of admission and after an observation period lasting from 6 to 35 months. In each case CBF was measured twice: once in the subacute stage after onset of symptoms and once after the observation period. The duration of neurologic symptoms (TIA, RIND, CS) was compared to the obtained flow values. A significant relationship was found between the duration of symptoms and impairment of CBF, thus showing the prognostic value of intravenous CBF measurements.(ABSTRACT TRUNCATED AT 400 WORDS)
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