Biomedical subjects
Publications and source records attributed to M R Gaab.
We report a fatal tumor hemorrhage in a 1-and-a-half-year old girl after ventriculoperitoneal shunting for obstructive hydrocephalus caused by a thalamic tumor. The possible pathophysiological mechanism is briefly discussed and the literature is reviewed.
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In a prospective randomized double-blind multicenter trial, the efficacy and safety of a 51-hour ultra-high intravenous dexamethasone dosing regimen was investigated in patients with moderate and severe head injury. 300 patients between 15 and 55 years of age were randomized to receive either placebo or dexamethasone: 500 mg intravenous infusion within 3 h after trauma initially, followed by 200 mg after 3 h, thereafter 8 times 200 mg at 6 hourly intervals, resulting in a total administered dose of 2,3 g in 51 hours. Primary end points for assessment of efficacy were: Modified Glasgow Coma Scale (grading 3-16) on Day 5, modified Glasgow Outcome Scale (grading 1-6) 10-14 months after injury, and the time interval until consciousness improved above a level of modified GCS > or = 8. Secondary endpoints were CT results and neurological and laboratory data. The two groups were well matched with respect to important prognostic variables, such as age, severity of trauma, and interval between trauma and application of the drug. 269 patients (89.7%) were available for final examination after 10-14 months. Results were surprisingly favourable in both groups: Lethality in the dexamethasone and placebo group was 14.3 and 15.4%, respectively, and 61.7 and 57.4%, respectively, achieved social and professional rehabilitation after 10-14 months (outcome scale 6). No statistical difference was seen between the dexamethasone and the placebo group in any of the primary end points of efficacy and safety (incidence of upper gastrointestinal bleeding, infection, and thrombosis).(ABSTRACT TRUNCATED AT 250 WORDS)
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We examined 50 patients with an extracranial/intracranial bypass using transcranial Doppler blood flow mapping, somatosensory evoked potentials, and computer-assisted EEG analysis. The investigation was supplemented by temporary compression of the extracranial supplying vessel. Transcranial Doppler sonography revealed in addition to 4 patients with nonpatent anastomoses, a bypass-mediated retrograde flow in the ipsilateral middle cerebral artery beyond a depth of 40 mm in the majority of patients. In 9 patients, retrograde flow could be demonstrated in the whole proximal (M1) MCA segment. The precommunicating segment of the anterior cerebral artery (A1) could be reliably insonated in all but 5 patients. Bypass-compression dependent alterations in the SSEP and in EEG analysis were only observed in a small number of patients. Transcranial Doppler sonography, with the aid of the flow mapping system, appears therefore, to be a reliable and repeatedly performable noninvasive technique for the assessment of intracranial hemodynamics following bypass surgery.
108 Patients with severe brain damage were examined for the course of plasma osmolality. In addition plasma values of Na+, K+, glucose and blood urea nitrogen (BUN) were measured simultaneously by auto-analyzer. The clinical status was registered daily by using a modified Glasgow coma scale. Outcome of the injured patients was registered by using the Glasgow outcome scale. 60 patients survived, 48 died, 39 of brain damage and 9 of secondary diseases, such as infection or embolism. Sustained severe brain damage is generally followed by disturbances of metabolic regulation. Quite often the osmotic regulation is disturbed. In most cases these disturbances are of hyperosmolar nature, their extent and duration being correlated to the prognosis. Hyposmolar deregulation occurs less frequently, and occasionally lead to peracute brain oedema (e.g. SIADH-syndrome). These dysregulations are interpreted as disturbances of the central function of the diencephalon, in lethal cases even as "hypothalamic death". Blood osmolality measurements should therefore be made early in states of acute cerebral disease to help establish a prognosis, control the treatment of water imbalance and to determine contra-indications to osmotherapy.
According to the hypothesis of Jannetta, an arterial compression of the left root entry zone (REZ) of cranial nerves IX and X by looping arteries could play an important role in the pathogenesis of essential hypertension. In an initial anatomical study, the positions of the left vagus and glossopharyngeal nerves in the skull were radiographically determined in 10 cadavers. By using a pattern of REZ topography developed from this information, the angiographic findings in 107 hypertensive and 100 normotensive patients were then compared retrospectively. In 80% of the angiograms of the hypertensive patients that could be evaluated, an artery crossed the left REZ of cranial nerves IX and X. Most frequently, this was the posterior inferior cerebellar artery (35.3% of cases), followed by the vertebral artery (29.4% of cases) and the anterior inferior artery (19.1% of cases). In 9 cases (13%), both the posterior inferior cerebellar artery and the vertebral artery appeared in the REZ. Frequently, a larger diameter of the left vertebral artery was found. The angiograms of normotensive patients that could be evaluated revealed an artery in the REZ in only 34.5% of cases. Our results support the hypothesis that essential hypertension may be associated with neurovascular compression of the left REZ of cranial nerves IX and X.
Intraoperative observations and animal experiments suggest that neurovascular compression at the left ventrolateral medulla is a possible etiological factor in essential hypertension. In pursuing this hypothesis, the authors examined the neurovascular relations in the posterior cranial fossa of 24 patients with essential hypertension, of 10 with renal hypertension, and of 21 normotensive control patients. Artificial perfusion of the vessels and microsurgical investigations during autopsy identified the vascular relations at the brain stem and at the root entry zone of the caudal cranial nerves. There was no evidence of neurovascular compression at the ventrolateral medulla on the left side in any patient from the control group or among those with renal hypertension. Two normotensive patients had neurovascular compression at the right ventrolateral medulla by the posterior inferior cerebellar artery. In contrast, all patients with essential hypertension had definite neurovascular compression at the left ventrolateral medulla. Additional compression of the right side was seen in three of these patients. Based on the anatomical appearance, it was possible to define three distinct types of neurovascular compression at the ventrolateral medulla. Common to all three types is the compression of the medulla oblongata at its rostral part just caudal to the pontomedullary junction and lateral to the olive in the retro-olivary sulcus. Comparative histopathological study of the microsurgically examined brain-stem specimens revealed no differences between patients with essential hypertension, those with renal hypertension, and normal controls. There was a structural integrity at the site of neurovascular compression at the ventrolateral medulla. The microanatomical findings of this study show that neurovascular relations at the ventrolateral medulla in essential hypertension give rise to pulsatile compression on the left. This supports Jannetta's hypothesis of neurovascular compression at the left ventrolateral medulla as an etiology of essential hypertension.
Several authors have presented evidence for a strict relation between regional cerebral blood flow and EEG. Therefore the EEG can serve as an adequate physiological parameter when monitoring cerebral function in the operating room. However, to exploit the inherent information as far as possible, both multichannel EEG and somatosensory evoked potentials should be recorded simultaneously. In the present article we describe a monitoring system which is capable to handle this task under the conditions of an operating room. In the first step some numerically simple algorithms are applied to detect gross artifacts. In the subsequent processing stage an analysis procedure is performed which is robust with respect to the remaining more subtile artifacts. In addition the raw signals are continually displayed on a monitor to allow for a visual evaluation of the EEG. The results of a trend analysis procedure are presented on the same graphical display by means of a compact topographical scheme. The system has been running under routine conditions for approximately two years now.
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The pathogenesis of essential hypertension still remains unclear. Recently, it has been supposed, that an arterial compression of the left root entry zone (REZ) of the cranial nerves IX and X by looping arteries may play a pathogenetic role. In this report we verified this hypothesis retrospectively by vertebral angiographies in 99 hypertensive and 57 normotensive patients. The angiographic findings were compared with the results obtained from an anatomic study, in which the positions of 10 left vagus/glossopharyngeal nerves in the skull were radiographically determined in 10 cadavers. By using a pattern of REZ topography developed from this information we obtained the following results: In 81% of the evaluable angiographies of hypertensive patients we found an artery in the left REZ of cranial nerves IX and X. The normotensive patients showed an artery in the REZ only in 41.7% of cases. Our results support the hypothesis that essential hypertension may be combined with neurovascular compression of the left REZ of cranial nerves IX/X.
13 new and 19 explanted hydrocephalus shunt valves were tested under perfusion for two weeks, using a modified ASTM test. Some manufacturers seem to have problems with quality control. Our results show large deviations in pressure-flow-characteristics in different valves, in some cases leading to an extremely high pre-shunt pressure. Test results almost corresponding to manufacturer's specifications were found in diaphragm valves and in some ball and spring valves. Results from slit valves usually varied widely, some being good, but others bad (much too high a pressure) or dangerous with even possibly fatal characteristics. Whilst laboratory performance may not correlate with clinical results, due to different impact of cerebrospinal fluid (CSF) pressure and flow on hydrocephalus shunting systems, manufacturers should provide devices that meet their supposed specifications. We developed an apparatus allowing simulation of different CSF production rates, CSF outflow resistances, CSF pressure waves caused by arterial and venous pulsation, breathing and coughing, and hydrostatic differential pressure caused by body position changes. This model enables testing of shunt valves under almost physiological conditions, thus closing the gap between conventional bench test results and clinical performance of hydrocephalus shunt valves.
The influences of 30% stable xenon/O2 mixture on somatosensory evoked potentials were investigated in 8 patients with and without Diamox application. Changes of the amplitude of the primary cortical response occurred frequently and correlated well with the psychotropical effect of xenon. They usually normalized within 2 to 3 minutes after ending xenon inhalation. There were no significant changes of the latency of the N20.
In 12 patients with developing alcohol withdrawal syndrome after abdomino-thoracic surgical procedures who were treated with Clonidine, short latency somatosensory evoked potentials were recorded. Clonidine leads to a good sedation, anxiolysis and moderated the psychotic symptoms. However, there was no significant correlation between the Clonidine medication and the SEP results over the time of drug administration concerning the primary cortical response N20 and the following N20/P25 wave. Therefore, the short-latency SEP-recording cannot provide a reliable monitoring of the good sedative effect of Clonidine in alcoholic withdrawal. The SEP responses after Clonidine are like those of morphine and are thought to have a similar central mode of action.
The effect of THAM on brain oedema parameters was initially investigated in animals with cold brain lesions; THAM was then used in head injury patients, ICP, SAP and CPP were analyzed. In the experiments with rats after freezing lesion, THAM was compared to equivalent doses of Na-bicarbonate. The animals were artificially respirated and sacrificed 6 h after trauma. THAM did significantly reduce water (wet-dry weight technique) and sodium contents in both hemispheres, whereas bicarbonate was ineffective. The potassium contents were even preserved at almost normal levels. In 80 patients receiving alternatively THAM (18-36 g/100-200 ml/1-2h), mannitol (20%, 125-250 ml/20-40 min) or sorbitol (40%, 70-140 ml/20-40 min), the ICP rapidly decreased following THAM infusion. The maximal fall in ICP (33%) was equal to that with mannitol and sorbitol. The slope of ICP decrease was equal with THAM and Mannitol but steeper with sorbitol. With THAM, however, the effect on ICP lasts longer than with osmotherapy. The EEG improved more rapidly after THAM. As shown by blood plasma values, the action of THAM is not based on osmotic effects. The increases in pH and especially in base excess suggest an intracerebral buffering. The encouraging results with THAM require a randomized clinical trial after severe head injury which is presently prepared.
Since 1978, decompressive craniotomy was performed according to a standardized protocol. Exclusion criteria were age greater than or equal to 40 years, deleterious primary brain damage, operable space occupying lesions, larger infarctions in CT scan or irreversible brain stem incarceration/ischaemic damage as shown by bulbar syndrome, loss in BAEP or oscillating flow in TCD. Indication was given by progressive intracranial hypertension not controllable by conservative methods, if ICP decompensation was correlated with clinical (GCS, extension spasms, mydriasis) and electrophysiological (EEG, SEP, CCT) deteriorations. 18 patients were decompressed by unilateral. 19 by bilateral craniotomy with large fronto-parieto-temporal bone flap and a dura enlargement by use of temporal muscle/fascia. 37 patients at an age of 18 +/- 7 (4-34) years were operated 5 h-10 d after trauma. Recovery was surprisingly good: only 5 died, 2 due to an ARDS; 3 remained vegetative, all others achieved full social rehabilitation or remained moderately disabled. The best predictor of a favourable outcome was an initial posttraumatic GCS greater than or equal to 7. These in younger patients with delayed posttraumatic decompensation before irreversible ischaemic damage occurs.
Intraoperative sector scanning enables routine imaging of the entire anatomy of intracranial and spinal spaces. Almost all of the pathological processes are exactly localised. It is an essential preliminary condition that fully sterilizable, handy ultrasound probes of 6 to 10 MHz including an accurate instrument- and puncture guide are available. Initial orientation projections similar to CT- or MRI scans are chosen using defined anatomical "landmarks". Cavities filled with aqueous fluids like ventricles, arachnoidal cysts, cystic low-grade gliomas are shown as regions of low echo intensity. Other pathological processes are usually imaged by their hyperecho-characteristics: brain oedema has an increased reflexion compared to normal brain tissue; all brain tumors are diffusely echogenic, the image allows preliminary grading e.g. of gliomas. Vascular processes like aneurysms and angiomas are well defined by wall- and perfusion characteristics. Ultrasound guiding enables even the most minutely detailed microsurgical approach; cysts and disorders of CSF circulation can be treated by simple ultrasound-monitored catheterization. Even stereotactic biopsy can often be replaced. Complications, such as hemorrhages, are recognised immediately.
In 16 patients with possible disturbed CSF circulation longterm recording of intracranial pressure (ICP) was performed. In 9 of the 16 patients the disorder became evident after the application of an exogenous volume-pressure testing procedure. This procedure enabled a classification into a group I--disturbed CSF circulation (8 patients)--and another group II--normal CSF circulation (8 patients). During a routine Xenon-CT-CBF study all patients of both groups were given to 1 g acetazolamide (DIAMOX) intravenously. Before, during and after the administration of DIAMOX the epidural ICP was continuously measured. An increase in ICP was monitored in all patients. In group I the average initial ICP was 13.6 +/- 7.6 mmHg. The maximum ICP was reached within a time interval of 13.1 +/- 4.5 min after DIAMOX administration. At this time the mean ICP was 36.4 +/- 19.2 mmHg (p less than 0.01). The average initial ICP in group II was 6.3 +/- 4.2 mmHg. The maximum ICP was reached within a time interval of 13.6 +/- 1.1 min. At this time the mean ICP was 11.9 +/- 4.8 mmHg (p less than 0.01). In respect to the maximum ICP both groups were significantly different (p less than 0.01). Despite a considerably rising ICP up to values of about 50 to 70 mmHg in several patients of group I only 1 patient complained of being sick. Presumingly, an ICP elevation caused by vasodilatation would be better tolerated than ICP elevations due to other causes.