Measurements of intracranial pressure by ventricular catheter were performed in 47 patients with severe head injuries. Thirty-three patients with decompressive operations such as osteoclastic craniotomy and dilatation by means of duraplastic have been compared with 14 patients with closed heads with regard to volume pressure response (intracranial elasticity). This was determined either by intraventricular injection of 2ml saline or by drainage of cerebrospinal fluid. The examination clearly shows that patients with closed heads have a much higher intracranial elasticity than patients who have decompressive operations, so that in the first group minor differences of the intracranial volume cause extreme deviations of the intracranial pressure. Therefore, the decompressive operation has been advised in severe head injuries with increased intracranial pressure as a measure additional to high dose dexamethasone therapy and hyperventilation.
After giving a brief summary describing the development of different methods for stabilisation of traumatic spine fractures the authors discuss their own results on 125 patients, who were treated between January 1st 1983 and September 15th 1988. The different surgical procedures (Harrington-instrumentation, transpedicular osteosynthetic stabilisation, fixateur interne) are compared. In the neurological physical examination 25% of the patients improved at least one degree in the Frankel-scale. In four patients there was worsening of the neurological findings. The radiological postoperative studies analyzed the angles of kyphosis and scoliosis within the traumatized spine segments. In overall-comparison of surgical procedures the fixateur interne showed best results (repositional loss of kyphosis angle 6.8 degrees, no fracture instability). Worse results were found for Harrington-stabilisation (repositional loss 9.1 degrees, fracture instability in three cases) and for transpedicular osteosynthetic stabilisation (repositional loss 12.4 degrees, fracture instability in two cases). In conclusion the authors describe the possible different complications for the three methods of judging from the clinical aspect and propose the following standard way of procedure: Fusion of the vertebral bodies with a stable implant and the possibility for intraoperative repositioning, postero-lateral spongiosa-grafting, fusion of the vertebral arc joints, transpedicular spongiosal filling of the traumatized vertebral body, resection of traumatized tissue from intervertebral discs and intercorporal blocking.
Intravenous Nimodipine was administered to 109 patients (65 female and 44 male) with either pre- or post-operative progressive neurological deterioration from cerebral vasospasm following subarachnoid hemorrhage from a ruptured aneurysm. In 91 of the patients the efficacy of Nimodipine in relieving ischemic symptoms was assessed and in all of the 109 patients the tolerance was evaluated. The aneurysms were related to following arteries: anterior communicating artery (41%), middle cerebral artery (24%), internal carotid artery (10%), vertebro-basilar arteries (4%) and others (5.5%); 11% of the patients had multiple aneurysms. On 16 of the 91 patients no surgery was performed. On 16% of the remaining 75 patients surgery was performed within 72 hours after the hemorrhage, 57% were operated between day 4 and day 15 and 29% after day 16. The ischemic neurological deficits occurred preoperatively in 67% of the patients and post-operatively in 23%. At the beginning of treatment 84% of the patients were graded III-V according to the Hunt and Hess grading system. Most of the patients received doses of 24-48 mg Nimodipine daily as constant i.v. infusion for 7-10 days. The grade of neurological deficit at the end of the treatment was evaluated according to the Glasgow Outcome Scale. 59 (65%) of the patients showed complete recovery or marked improvement of the ischemic symptoms while 22% remained unchanged and 11% died due to severe vasospasm. Administration of Nimodipine seemed to be more efficient in cases where treatment was started within 24 hours. In the patient group which was treated pre-operatively, recurrent hemorrhage was recorded in 8% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)
The present studies were performed in order to determine whether "filtration edema" will develop as a consequence of cerebral vasoparalysis, vasoparalysis in combination with arterial hypertension or arterial hypertension alone. A series of dogs, anaesthetised with i.v. Chloralose-Urethane were exposed 1) to cerebral vasoparalysis, produced by hypercapnia (PaCO2 about 150 mm Hg) and hypoxaemia (PaO2 40-60 mm Hg); 2) to arterial hypertension and 3) to a combination of cerebral vasoparalysis and arterial hypertension. Following cerebral vasoparalysis and arterial hypertension, a significant decrease of total cerebrovascular resistance and moderate increase of venous resistance was observed. Regional cerebral blood flow (133Xe), intracranial pressure, as well as the pressure in postcapillary venous outflow (sinus sagittalis wedge pressure and confluence sinuum pressure) were increased. Neither normotonic vasoparalysis nor vasoparalysis in combination with slight arterial hypertension (MABP more than 90 min above 180 mm Hg) resulted in cerebral edema. In contrast, cerebral vasoparalysis in combination with severe arterial hypertension (MABP more than 90 min above 220 mm Hg) resulted in a statistically significant increase in the water content in the white matter without evidence of protein extravasation. Multiple small foci of Evans blue extravasates, however, were found in the cortex following arterial hypertension in combination with vasodilation, indicating a damage of the blood brain barrier. In these blue stained cortical areas the water content was significantly in creased. The following conclusions were drawn from the results. Vasoparalysis during normotension does not produce brain edema despite the slightly elevated hydrostatic pressure gradient between intravasal and extracellular space. Only considerable increase of this hydrostatic pressure gradient caused by a combination of vasoparalysis with severe arterial hypertension is able to produce brain edema in the white matter. In addition, acute hypertension may cause minor multifocal damage of the blood brain barrier in the cerebral cortex. It is concluded that so-called brain swelling, which has been described by several authors in states of cerebral vasoparalysis, is not predominantly caused by brain edema but by vascular congestion. The clinical aspects of the result are discussed.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.