Inadvertent intrathecal use of ionic contrast agents: treatment with immediate ventriculolumbar lavage.
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Biomedical subjects
Publications and source records attributed to M Spranger.
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BACKGROUND AND PURPOSE: A permanent elevation of ICP after severe brain injury for instance in subarachnoid or intracerebral hemorrhage or neurotrauma is associated with a poor clinical outcome. Although increasingly being used in the intensive care of patients with elevated ICP, continuous epidural ICP monitoring in ischemic stroke has not been firmly established yet. PATIENTS AND METHODS: We prospectively evaluated the clinical course and outcome of patients with raised ICP due to space occupying ischemic middle cerebral artery (MCA) infarction as seen in CT, who underwent continuous ICP monitoring. Epidural ICPprobes were inserted ipsilaterally (all patients) and contralaterally (additional in 7 patients) to the side of infarctation. Glasgow Coma and Scandinavian Stroke Scales (GCS and SSS) were obtained initially and in the further clinical course. All patients were subjected to a standardized treatment protocol for raised ICP. ICP values were correlated with clinical presentation at the time point of deterioration, with outcome and CT findings. Effectiveness of different treatment modalities to lower ICP were analyzed and discussed. RESULTS: 9 of 48 patients survived the MCA infarct (19%), with the cause of death being transtentorial herniation with subsequent brain death in all 39 patients. Mean SSS at admission was 20.6 (survivors 21.5 +/- 5.6, nonsurvivers 19.8 +/- 6.5). All patients showed clinical signs of herniation before the increase of ICP. All 39 patients who died developed ICP values higher than 35 mmHg and no patient with ICP values of more than 35 mmHg survived. CCT changes dit not necessarily reflect the absolute measured ICP values. All treatment modalities for raised ICP including osmotherapy, controlled hyperventilation, tromethamol and barbiturates were initially effective, but only in a minority of patients ICP control could be sustained. CONCLUSIONS: We conclude that ICP monitoring in large hemispheric infarction may predict clinical outcome. ICP monitoring was not helpful in guiding long term treatment of ICP. It remains doubtful, whether ICP monitoring has a positive influence on clinical outcome of acute severe ischemic stroke.
We investigated possible neurotoxic components in the cerebrospinal fluid (CSF) of patients with bacterial meningitis. On murine cerebellar neuronal cell cultures, CSF exerted a dose-dependent toxic effect, which was attenuated by the NMDA receptor antagonist MK-801. Glutamate concentrations in the CSF of patients with bacterial meningitis were measured by an enzymatic assay and found to be significantly elevated (p < 0.001) as compared to viral meningitis and non-inflammatory neurological diseases. The concentration of glutamate in the CSF of patients with bacterial meningitis varied considerably and correlated with the severity of the disease as scored by the Glasgow Coma Scale. Cells in the CSF, mainly comprising polymorphonuclear granulocytes, did not release any glutamate into the culture medium, whereas blood monocytes produced remarkable amounts. These findings implicate an important role of monocytic inflammatory cells in bacterial meningitis by the release of glutamate, which may contribute to neuronal cell death.
A father and his two sons presented with slowly progressive muscular weakness, contractures of the spine, elbows and ankles, and cardiac conduction disturbances in the father. Clinical and histological findings are discussed in relation to the hitherto reported cases of autosomal dominant variant of the Emery-Dreifuss syndrome and the distinction from the rigid spine syndrome.
BACKGROUND AND PURPOSE: Persistently elevated intracranial pressure (ICP) has been associated with poor clinical outcome after severe brain injury, such as neurotrauma, intracerebral hemorrhage, and subarachnoidal hemorrhage. Although ICP monitoring is increasingly being used in intensive care treatment of patients with ischemic stroke, its value has not been established. PATIENTS AND METHODS: The clinical course of 48 patients with the clinical signs of increased ICP due to large hemispheric or middle cerebral artery territory infarction defined by CT and subjected to ICP monitoring was prospectively evaluated. Epidural ICP probes were inserted ipsilaterally to the site of primary brain injury in all and also contralaterally in seven patients. Initial clinical presentation was assessed by the Scandinavian Stroke Scale (SSS) and the Glasgow Coma Score (GCS). All patients were treated according to a standardized treatment protocol for elevated ICP. ICP values were correlated with the clinical presentation at the time point of deterioration, with outcome, and with CT findings. Different treatment strategies to lower ICP were analyzed as to their effectiveness. RESULTS: Only nine of the 48 patients survived the infarct (19%). The cause of death was transtentorial herniation with subsequent brain death in all 39 patients. The patients' mean SSS on admission was 20.6 (survivors 21.5 +/- 5.6, nonsurvivors 19.8 +/- 6.5). In all patients clinical signs of herniation preceded the increase in ICP. Patients with ICP values > 35 mm Hg did not survive. CT changes did not always correspond with the measured ICP values. All medical strategies to lower ICP, including osmotherapy, hyperventilation, THAM-buffer, and barbiturates, were initially effective, but only in a minority of patients was ICP control sustained. CONCLUSIONS: ICP monitoring of large hemispheric infarction can predict clinical outcome. Pharmacologic intervention had no sustained effect. ICP monitoring was not helpful in guiding long-term treatment of increased ICP. It remains doubtful that ICP monitoring in acute ischemic stroke has a positive influence on clinical outcome.
We report on 2 sisters with an autosomal-recessive multiple pterygium syndrome, type Escobar, consisting of multiple pterygia with severe contractures, short stature, and minor facial and external genital anomalies. The striking finding was severe muscular atrophy. We speculate that a neuromuscular disorder is the underlying pathogenesis of Escobar syndrome.
Subacute necrotizing encephalomyelopathy (Leigh's syndrome) is a rare neurodegenerative disease in the adult. The precise metabolic defect is unknown, but abnormalities of a mitochondrial enzyme system related to cytochrome-c oxidase or pyruvate dehydrogenase are described. The clinical picture usually consists of an altered breathing pattern, oculomotor paralysis, other signs of cranial nerve dysfunction, ataxia, myoclonic jerks, nystagmus, generalized seizures, optic atrophy and demyelinating peripheral neuropathy. Hypopnea leads to CO2-retention with consecutive loss of consciousness demanding mechanical ventilation. Respiratory failure is the most frequent cause of death. Here we describe two patients with adult onset Leigh's syndrome and we discuss the longterm treatment strategies including vitamin B1 and CPAP mask.
In animal models of cerebral ischemia hypothermia has been shown to have a beneficial effect. Reduction of infarct size, fewer potentially neurotoxic metabolites, and a better neurological outcome were observed compared to sham-operated animals. In clinical practice hypothermia has been widely used in cardiovascular surgery and occasionally in neurosurgery. The first trials with hypothermia in patients with severe head injury have also shown beneficial results. However, studies on therapeutic hypothermia in the clinical management of acute stroke are not yet available.
The co-localization of activated macrophages and damaged neurons observed in brain injury and degenerative brain diseases may hint to macrophage-induced neuronal cytotoxicity. Recently, macrophages have been found to secrete neurotoxic molecules such as radical oxygen intermediates and glutamate, the latter interacting with N-methyl-D-aspartate (NMDA) receptors. As shown in the present study, brain macrophages termed microglial cells co-cultured with differentiated cerebellar neurons excert potent neurotoxic effects. Neurotoxicity is unlikely to be due to cytokines since tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6 and interferon (IFN)-alpha/IFN-beta/IFN-gamma had no such effects. In contrast, when treating neurons with H2O2 or oxygen radical-generating systems cytotoxicity was induced. Furthermore, microglia were found to produce O2- and H2O2 when triggered with phorbol 12-myristate 13-acetate. However, in co-cultures of neurons and microglia, oxygen-radical scavengers catalase and superoxide dismutase, failed to protect neurons from microglia-induced killing. Moreover, when using undifferentiated neurons which are susceptible to H2O2 but not to NMDA receptor-dependent killing, microglia did not destroy the neurons. Thus, the amount of reactive oxygen intermediates produced by microglia in co-culture do not reach the critical concentrations required for neurotoxicity. As dibenzocyclohepteneimide, an antagonist to NMDA receptors neutralized neurotoxicity in microglia-neuronal co-cultures, excitatory amino acids released by microglia are suggested to compose the major determinant of neurotoxicity.
FOS and JUN proteins are transcription factors thought to be involved in coupling neuronal excitation to target gene expression. Cortical infarction of consistent size and location was produced by irradiating the rat brain with Xenon light through the intact skull for 20 min following systemic injection of the photo-sensitizing dye, rose bengal. To investigate the time course and distribution pattern of five cellular immediate early gene (IEG)-encoded proteins after focal ischemia, the expression of c-FOS, FOS B, c-JUN, JUN B and JUN D was studied immunocytochemically in sham-operated control animals and at different postischemic time intervals up to 24 h. A separate group of animals was pretreated with the non-competitive N-methyl-D-aspartate (NMDA) antagonist MK-801. Photochemically induced focal ischemia caused a rapid induction of FOS and JUN proteins in the entire ipsilateral cortex apart from the ischemic focus. Immunoreactivity in the ipsilateral subcortical gray and white matter and in the entire contralateral hemisphere was indistinguishable from control animals. Individual IEG-encoded proteins were sequentially induced with increased levels of immunoreactivity persisting for different time periods up to 24 h. c-FOS, FOS B, c-JUN and JUN B exhibited a characteristic distribution pattern as reflected by different staining intensities in individual cortical layers. The rapid IEG induction in the entire ipsilateral sensorimotor and limbic structure-associated cortices after photochemically induced infarction most likely reflects spreading depression caused by ischemia and mediated by NMDA receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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We have found a regional distribution of IL 1 beta mRNA and IL 1 activity in the normal adult rat brain, which reveals at least partially a colocalization with nerve growth factor (NGF). The predominantly neuronal signal patterns were found over the granule cells of the dentate gyrus, the pyramidal cells of the hippocampus, the granule cells of the cerebellum, the granule and periglomerular cells of the olfactory bulb, and over dispersed cells of the ventromedial hypothalamus and of the frontal cortex. In these areas also the highest levels of IL 1 activity were observed. In the striatum and septum much lower levels of IL 1 beta mRNA and IL 1 activity (shown for the striatum), most likely synthesized by glial cells, could be determined. IL 1 beta-expressing cells were mainly found in brain regions that also synthesize NGF mRNA as shown by in situ hybridization. NGF mRNA could be demonstrated over pyramidal cells of the hippocampus, granule cells of the dentate gyrus, periglomerular cells of the olfactory bulb and over prefrontal cortex neurons. These data indicate that IL 1 beta, among other factors, might also play a regulatory role in the synthesis of NGF in the CNS, as has been demonstrated in the peripheral nervous system (Lindholm, D., R. Heumann, M. Meyer, and H. Thoenen. 1987. Nature (Lond.). 330:658-659).
A number of clinical trials suggest that the antithrombotic effect of aspirin is limited to men. To test the possibility that this is due to a sex difference in the inhibitory effect of aspirin on platelet behavior, we studied whole-blood platelet aggregation in men and women and in male patients with carcinoma of the prostate receiving hormone therapy. The in vitro inhibitory effect of aspirin on so-called spontaneous platelet aggregation induced by stirring whole blood and monitored by the decrease in the number of singleton platelets was greater in men (mean +/- SD inhibitory ratio 1.54 +/- 0.30 in men, 1.23 +/- 0.22 in women; p less than 0.001). The inhibitory effect of aspirin was reduced in orchiectomized male patients and was restored by the addition of testosterone to blood samples. Estradiol had no detectable influence on the inhibitory effect of aspirin. Testosterone thus seems to influence platelet aggregation and its inhibition by aspirin as assessed by whole-blood in vitro aggregometry. Possible mechanisms for this effect of testosterone and its relevance to the choice of antithrombotic therapy are discussed.
A South African family with autosomal dominant split hand, split foot (SHSF) malformation has been studied. The pedigree was unusual in that three unaffected siblings with normal parents had each produced affected offspring. New mutation, germinal mosaicism and autosomal recessive inheritance are unlikely. Possible explanations of this contentious situation may be an unstable premutation or non-penetrance due to an inhibiting factor associated with the gene responsible for SHSF. Pregnancy monitoring by ultrasound of unaffected close relatives of a person with SHSF is recommended.
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The diagnostic accuracy of CT in cases of lumbar disk prolapse was investigated on the basis of a group of 158 of our own patients who were divided into three separate groups. CT findings were compared on the one hand with myelograms and on the other with results of surgery. Simultaneously performed myelographic and CT examinations produced different diagnostic findings in 7 out of 80 lumbar disks (approx. 9%). These deviating findings ranged from gradual differences (in 3 cases) to completely contradictory findings (in 4 cases). In 31 patients who underwent surgery, approximately the same amount of false-positive and false-negative findings were obtained in preoperative diagnosis using CT as with myelography. The overall accuracy calculated for non-invasive computerized tomography was 93.7%, while for myelography it was 90.7%. Out of a further 91 patients in whom myelography was not performed and whose condition was checked surgically, the diagnosis had been established correctly by CT in 88. This represents a degree of accuracy of 96%. The vertical and lateral location of the disk prolapses as determined by CT corresponded with findings at surgery in every case. It is concluded from the results of these investigations that CT should be given absolute priority over myelography in the diagnosis of lumbar disk prolapse and that if there is a correlation between clinical history, neurological deficiency symptoms, and CT findings, myelography is unnecessary, even for surgery. Only if there are discrepancies between the findings myelography is indicated as a supplementary examination. CT and myelography are examination methods which complement, rather than complete with one another.
Apart from infection and loosening of the implants, spontaneous fracture of the femoral neck is a specific early complication of the hip joint surface replacement according to Wagner. Based on our case material we demonstrate the problems involved, investigating not only the deficient operation technique but also the reasons for its deficiency which, in our opinion, are to be found in the method itself.