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This study in cats investigates the action of sodium nitroprusside on the pial vessels by systemic and local administration, with an intravital microscopic window technique and a photometric technique for graphic documentation of vessel diameter changes. Intravenous infusion caused vasodilatation parallel with decreasing blood pressure. Pial arterioles dilated more than venules, smaller vessels more than larger ones. Local administration caused maximal dilatation within 5--10 seconds. With blood pressure returning to normal after i.v. therapy, pial vessels remained wider than they were before hypotension at the same pressure level. From these data it is concluded that the substance acts longer on the brain vessels than on vessels elsewhere in the body, and that cerebrovascular autoregulation to blood pressure changes is disturbed during this period.

A controlled randomized study of endoscopic evacuation versus medical treatment was performed in 100 patients with spontaneous supratentorial intracerebral (subcortical, putaminal, and thalamic) hematomas. Patients with aneurysms, arteriovenous malformations, brain tumors, or head injuries were excluded. Criteria for inclusion were as follows: patients' age between 30 and 80 years; a hematoma volume of more than 10 cu cm; the presence of neurological or consciousness impairment; the appropriateness of surgery from a medical and anesthesiological point of view; and the initiation of treatment within 48 hours after hemorrhage. The criteria of randomization were the location, size, and side of the hematoma as well as the patient's age, state of consciousness, and history of hypertension. Evaluation of outcome was performed 6 months after hemorrhage. Surgical patients with subcortical hematomas showed a significantly lower mortality rate (30%) than their medically treated counterparts (70%, p less than 0.05). Moreover, 40% of these patients had a good outcome with no or only a minimal deficit versus 25% in the medically treated group; the difference was statistically significant for operated patients with no postoperative deficit (p less than 0.01). Surgical patients with hematomas smaller than 50 cu cm made a significantly better functional recovery than did patients of the medically treated group, but had a comparable mortality rate. By contrast, patients with larger hematomas showed significantly lower mortality rates after operation but had no better functional recovery than the medically treated group. This effect from surgery was limited to patients in a preoperatively alert or somnolent state; stuporous or comatose patients had no better outcome after surgery. The outcome of surgical patients with putaminal or thalamic hemorrhage was no better than for those with medical treatment; however, there was a trend toward better quality of survival and chance of survival in the operated group.

A study was performed to detect the inhibitory effect of intravenously administered aprotinin (Trasylol) on brain and CSF protease activity in 25 patients with severe head injury. The data presented include measurements of CSF protease activity, alpha-1-antitrypsin, alpha-2-macroglobulin, haptoglobulin, polyacrylamidgel-electrophoresis pattern, total protein and hemoglobin content. The results indicate that increased protease activity is present and that this induces autolytic processes which can be inhibited by aprotinin treatment. The survival rate was higher after aprotinin treatment. Total CSF protein content was significantly higher in nonsurvivors than in survivors.

Sodium Nitroprusside (Nipride) was administered by infusion pump intravenously in 27 neurosurgical patients for intraoperative, postoperative and posttraumatic blood pressure lowering. This was accomplished with intension to reduce the risk of hemorrhage during operation on highly vascularized tumors or aneurysms and to combat hypertensive crisis after surgery and brain injury. The effect was documented by direct arterial blood pressure registration and the drug proved to be fast acting, potent and readily reversible. Dosage varied between 1 and 10 microgram/kg/min with systolic pressure decreasing about 6 to 60% of the initial value. There was ill correlation between infusion rate and blood pressure drop which demanded particular caution at the beginning and the end of infusion. A decrease in pulse pressure and a moderate tachycardia were generally observed, however no complications were seen due to a Sodium Nitroprusside administration over less than 12 hours duration in our series.

Sixty-five patients with ruptured aneurysms were operated upon within 48 to 72 hours after subarachnoid hemorrhage (SAH) and were treated with a regimen of intra- and postoperative nimodipine for the prevention of symptomatic vasospasm. The clinical grading (Hunt and Hess) was I to III in 49 patients and IV or V in 16. The SAH was mild in 15 patients, moderate in 27, and severe in 23; 12 patients harbored an intracerebral hematoma, and 6 had intraventricular bleeding. Acute hydrocephalus was observed on preoperative computed tomography (CT) in 19 patients. On CT 3 days postoperatively (i.e., Day 3-4 after SAH), 30 of 65 patients still had subarachnoid blood; however, severe symptomatic vasospasm as the deciding threatening event during the delayed postoperative period was not encountered in this series. Transient symptoms of ischemia were noted in 2 patients (3%) and were accompanied by angiographic spasm in 1. Irreversible neurological deficit occurred in 2 patients (3%); in 1 of these, it was a complication of postoperative control angiography. Of the patients preoperatively graded I or II, 96% had an excellent to fair outcome 6 months postoperatively, and 1 patient (4%) had died because of a surgical complication. Among patients preoperatively graded III or IV, 86% had an excellent to fair outcome, and the remaining 14% had a poor outcome. Shunt-dependent hydrocephalus developed in 7% of the patients. Acute surgical repair of ruptured cerebral aneurysms and preventive topical and intravenous administration of nimodipine reduce management complications and improve outcome; above all, ischemic lesions from symptomatic vasospasm are reduced to a minimum.

We present the results and experiences with a prototype cardiotocograph with US-autocorrelation processing. As this method is fundamentally different from conventional signal processing we are entering into the particular problems of this new FHR-technology. A total of 70 antepartum fetal rate recording from 53 patients and 38 intrapartum CTGs were evaluated. The antepartum results were excellent, the application time could be minimized and the quality of the recordings has been essentially improved. With the intrapartum recordings a computer comparison of long and short time irregularity of FHR derived from US-autocorrelation and direct fetal EKG was performed. The results proofed an excellent approximation to beat-to beat recording using the US-autocorrelation technique. The idea of using the new method intrapartum instead of invasive CTG could not be realised. This was due to a increasing loss of signal with progress of labor. To exclude maternal HR interferences the new monitor is supposed to record maternal heart rate simultaneously to FHR.

The effect of the laser energy to the cerebral vascular reactivity and the blood brain barrier. A Nd:YAG laser with 20 watt impacts of 0.5, 1.0, 2.5 and 5.0 seconds duration time were irradiated through the cranial window made at the parietal regions of anesthetized adult cats. The disruption of the blood brain barrier was examined by checking the degree of the extravasation of Evans blue dye administrated in the vein. The cortical vessel reactivity was observed through the cranial window and evaluated using an intravital microscope and a videoangiometer. The extravasation of Evans blue dye was seen uniformly extending from the histologically changed area into the surrounding tissue in all experiments. The extent of the extravasation of dye was 1 to 1.5 mm larger than the extent of the histologically changed area produced by laser irradiation. Pial arteries in the area with histological changes dilated markedly and some of them lost their blood stream. Pial arteries in the area of Evans blue extravasation, but outside it histological changes also dilated markedly. Furthermore, pial arteries within a distance of 200 to 400 microns from the edge of the Evans blue extravasation area also dilated moderately. A statistical estimation showed that the degree of dilatation of arteries in the area outside the histological change improved significantly in the time course of five minutes.

In a group of 15 patients with chronic unilateral cerebral ischemia, a quantitative EEG study was performed before, during and after nimodipine (Bay e 9736) infusion (1 microgram/kg/min). The EEG was recorded bipolarly from the rolandic region. After computerized EEG analysis, a multiparametric asymmetry score (MAS) was calculated; this MAS provides a sensitive indicator for discrimination between neurologically normal subjects and patients with unilateral ischemia. A positive MAS is characteristic for healthy subjects, a negative one for ischemia patients. During nimodipine treatment, the MAS became more negative (increased EEG asymmetry) in 7 and less negative (decreased EEG asymmetry) in 8 patients. A correlation was found between the direction of the EEG asymmetry changes and the localization of the infarcted area as seen in the CT scan.

It is not only for CSF-removal in conservative treatment of oedema and control of the effectiveness of osmo-onco-therapy, contricosteroids, anticholinergics and aldosterone-antagonists, that external CSF drainage in severe cerebral trauma has proved of value. It has also made it possible to assess objectively the indications for bitemporal craniotomy in raised intracrainial pressure with an acute midbrain syndrome caused by tentorial herniation. Continuous monitoring of ICP permits an intervention at the right time and prevents one from operating too late, namely at a moment, when manifest neurological signs already indicate cerebral decompensaervative steps failing, a bitemporal craniectomy is indicated: in this way we lower intracranial pressure, liberate the rostral brain stem out of its strangulation and improve cerebral perfusion and metabolism.

A fluorescence-angiographic investigation is presented of pital vessel reactions to acute drug-induced hypertension in cats. Observations and documentation were carried out by an intravital-microscopic technique. Acute hypertension, where pressure values of 220 to 260 mm Hg were reached within 10 to 20 sec, was followed by marked vasodilatation: Arterioles under 50 mu in diameter and capillaries were dilated to between 200 to 300% of the resting diameter, whilst arterioles of 50 to 100 mu showed an increase of 50 to 60%. Reddening of veins and acceleration of the blood flow occurred. Vasodilatation persisted after the blood pressure values had returned to normal. In connexion with investigations of the blood pressure immediately after a head injury, the role of acute hypertension in the development of hydrostatic brain oedema is discussed.

The lumen diameters of the main cortical surface arteries were continuously monitored through a closed cranial window in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). The arterial diameter was significantly smaller in SHR (55 +/- 1 micron) than in WKY (87 +/- 1 micron) during resting conditions as well as during hypercapnic dilatation (87 +/- 2 micron compared to 117 +/- 5 micron). The per cent increase in diameter induced by hypercapnia was larger in SHR (54%) than in WKY (36%), presumably a consequence of the altered vascular wall to lumen ratio. Alpha-adrenoreceptor blockade with yohimbine and phenoxybenzamine had no significant effect on arterial diameter during hypercapnia. The diameters of the largest pial surface veins increased to the same extent in SHR and WKY during hypercapnia (about 10%).

Report on seven cases of severe head injury, where proteolytic enzyme activity in the ventricular fluid was measured within a period of eight days. The result was positive in four cases. This finding is discussed in relation to clinical features and morphology. Earlier reports and these results are considered.

The aim of this paper is to contrast new results obtained on the activities of lysosomal proteases in the brain of traumatized animals with the previously held opinions concerning the development of post-traumatic brain oedema. Two hours after a standardized head injury in the cat, acid and neutral proteases were determined in the brain homogenate. Total as well as free activity, especially of the neutral proteases, were markedly increased after head injury, a circumstance indicating the important role of lysosomes in the development of post-traumatic brain oedema. It is postulated that not hypoxia alone, but primary or secondary disturbance of lysosomal function is the predominant factor in the development of brain oedema. Release of enzymes -- especially proteases -- causes irreversibility of initial vascular oedema by autolysis of cellular structures.

An indirect anti-IgG enzyme-linked immunosorbent assay (ELISA) using a whole cell sonicate of Mycobacterium bovis as the coating antigen, was used to detect anti-mycobacterial antibodies in cattle not infected with M. bovis. False positive M. bovis ELISA scores were produced in 6 cattle experimentally inoculated with Mycobacterium avium-intracellulare-scrofulaceum (MAIS) serovars 2, 8, 9, 14 and 18 and Mycobacterium flavescens, respectively. False positive ELISA results were also found in 39.5% of cattle from which other mycobacteria were cultured and in 56.4% of necropsied cattle with other pathological conditions. No M. bovis was cultured from these animals. Other groups of animals, with no pathological conditions, which had been tuberculin-tested negative, tuberculin-tested positive and never tuberculin tested showed positive ELISA results in 15.4%, 73.6% and 42.4% of the respective groups. The variation of these non-specific responses in uninfected cattle highlights the need for careful selection of negative controls in evaluating ELISAs for the diagnosis of bovine tuberculosis.