[The clinical application of Ginkgo biloba in dementia syndromes (restoration of brain performance in vascular or degenerative CNS disease)].
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Biomedical subjects
Publications and source records attributed to H Herrschaft.
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The causes, clinical indications and diagnosis and differential diagnosis of cardiac disorders which may lead to cerebral symptoms are illustrated on the basis of a review of the present day level of scientific research. Principally involved are cerebral ischaemias arising from cerebral embolisms or from reduction of cardiac output in cardiovalvular and myocardial disorders. The incidence of all embolisms of cardiac origin makes up 10% of all ischaemic cerebral infarcts, with auricular fibrillation, irrespective of its origin, mitral stenosis, myocardial infarct, mitral insufficiency and combined mitral valve defects, and, in younger patients, mitral valve prolapse, being, in this order of frequency, of primary clinical significance. The other cardiovalvular and myocardial disorders have, in comparison, a relatively low incidence of cerebral embolisms. Haemodynamically induced cerebral ischaemias frequently occur in the form of complications following acute cardiac arrest, in myocarditis and in case of primary cardiomyopathies resulting from cardiac insufficiency or complicating bradyarrhythmia. They are clinically apparent in the form of syncope, and other impairments of consciousness of various levels of seriousness with and without indications of cerebral origin, extending up to coma. In view of the high incidence of 25% of acute cerebral ischaemias in cases of cardiac disease, not only neurological but also detailed cardiological investigation is vital in all cases for a correct diagnosis and for the selection of a suitable course of treatment. Cerebral complications in bradyarrhythmia and endocarditis are discussed in the context of a review of the relevant literature together with consideration of their epidemiology, aetiology, pathophysiology and clinical profile. Pathological sinus-bradycardia, bradyarrhythmia absoluta, sinu-atrial and atrio-ventricular blockages, carotid-sinus and sick-sinus node syndrome, paroxysmal atrial tachycardia, AV-node tachycardias, and auricular fibrillation and flutter, taken as a whole, lead to cerebral complications affected patients in 5 to 10% of afflictions of the central nervous system occur in 50% of patients suffering from complete AV blockage and, at a not precisely definable frequency, in patients suffering from other bradyarrhythmias. In addition to transitory, uncharacteristic symptoms such as dizziness, vertigo, impairment of vision and balance, presyncope, syncope and Adams-Stokes syndrome dominate the clinical profile. Endocarditis, with an incidence of 0.01 to 0.05% in the overall population, results in central nervous system complications in 12 to 25% of cases on average.(ABSTRACT TRUNCATED AT 400 WORDS)
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On reviewing the literature, the meaning of risk factors causing stroke as well as their therapy or elimination as an effective prevention of cerebro-vascular disease is pointed out. Hypertension increases the risk of apoplexy by the fourfold, with regard to the diastolic values of blood pressure by the fivefold up to the tenfold. Consistent therapy of hypertension decreases significantly the incidence of cerebral apoplectic attacks. Manifested diabetes mellitus and even reduced glucose tolerance raise the risk of stroke by the threefold, even though factors frequently associated with diabetes (hypertension, overweight, hyperlipoidaemia) are taken into consideration. Hyperlipidaemia, hypercholesteraemia, and hypertriglyceridaemia stipulate an increase of the incidence of stroke by the twofold to the threefold. Morbidity rate rises if these abnormalities coincide with further risk factors (hypertension, reduced glucose tolerance, smoking cigarettes, hypertrophy of left heart-ECG), up to the sixfold. Nicotine consumption alone increases the risk of cerebral apoplectic attacks in relation to age, by the threefold up to the fivefold. In combination with the use of hormonal contraceptive drugs, the risk of morbidity rate in women rises to the sevenfold. Overweight of more than 30% aggravates twice the risk of stroke. Heart diseases of different kind increase the risk of apoplectic attacks by the twofold; in combination with hypertension by the fivefold. The intake of oral contraceptive drugs causes an increase of cerebral thrombo-embolic attacks by the threefold up to the fivefold, where by a relation to the content of oestrogen and to the disturbances of haemorheology is proven.(ABSTRACT TRUNCATED AT 250 WORDS)
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The change in global and regional cerebral circulation after intravenous administration of pyritinol was investigated in 14 patients with acute or subchronic cerebral ischemia. The measurement of the cerebral circulation was performed by intraarterial isotope clearance with 133xenon using a multidetector apparatus. With a single administration of pyritinol (400 mg) there was a statistically significant increase in the cerebral circulation in the gray matter by 6.7 ml/100 g/min corresponding to 9.7% (p less than 0.01) 10 minutes after the end of the drug injection. In the areas of all portions of the brain with defective circulation there was a significant increase in blood flow by 8.9, 0.8 and 3.2 ml/100 g/min (gray matter, white matter, total substance), corresponding to 12.3%, 4.4% and 8.1%. In areas with a normal initial status, the increase in blood flow attained statistical significance in the gray matter only (p less than 0.05).
Regional cerebral blood flow (rCBF) was investigated in 18 patients with acute cerebral ischemia by the intraarterial 133Xenon clearance method using a 10-detector-equipment. Intravenous administration of 6-10 g Piracetam caused an overall increase of the fast component of rCBF after 30 minutes corresponding to blood flow in the grey matter, of 10.0 ml/100 g/min (18.9%). The slow component of rCBF corresponding to the cerebral blood flow in the white matter remained unchanged. The regional CBF was influenced to a varying degree, the areas marked by an insufficient blood supply showing a mean increase by 17.5% and the areas marked by normal basic values showing a mean increase by 6.3%. This difference in alteration is statistically significant (p is less than 0.005) comparing the differences as %. The increase of cerebral blood flow in grey matter is interpreted as a secondary effect after activation of central nervous system metabolism by Piracetam.
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Quantitative measurements of global and regional cerebral blood flow were performed in 18 patients 1 to 3 days after the onset of symptoms of acute cerebral ischemia due to partial occlusion of the middle cerebral artery and were repeated 21 days thereafter. The first rCBF measurement revealed either an extensive ischemic focus or an ischemic focus with simultaneous reduction of the global blood flow within the corresponding hemisphere in all patients. The later measurements indicated no change in blood flow in the ischemic focus in any case, but there was a slight increase of global cerebral blood flow in 1/3 of the cases. The measurements of cerebral blood flow were correlated with the neurological, psychopathological and EEG findings and in spite of an unaltered cerebral blood circulation, all patients showed a distinct clinical imrovement. Various hypotheses for the return of neurological functions in patients with persistent cerebral ischemia are discussed.
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The alterations in global and regional cerebral blood flow (CBF) following i.v. application of 14,15-dihydro-14beta-hydroxy-[13alpha,16alpha]-eburnamenine-14-carbonic acid methylester (vincamine) were studied in 18 patients suffering from acute or subchronic cerebral ischemia. CBF measurements were made after intra-arterial injection of 133Xe using a multi-detector measuring instrument. 30 sec after a single i.v. application of 30 mg/20 min vincamine a statistically significant increase of CBF by 1.5 ml/100 g/min was found, corresponding to 6.1% (p less than 0.01). The regional CBF was influenced to a varying degree, the areas marked by an insufficient blood supply showing a mean increase by 13.4% and the areas marked by normal basic values showing a mean increase by 5.3%. This difference in alteration is statistically significant (p less than 0.02) comparing the differences as percent. The duration of the action of vincamine on the CBF, after a single dose of 30 mg/20 min i.v., was determined for a maximum of 15 min. The CBF values measured within 15 min after the completed i.v. application of vincamine showed a mean decline in blood flow values by --2.5 ml +/- 7.4%, which is statistically insignificant.
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