Ocular signs and prognosis in subdural and subarachnoid bleeding in young children.
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D-2-Hydroxyglutaric aciduria has been observed in patients with extremely variable clinical symptoms, creating doubt about the existence of a disease entity related to the biochemical finding. An international survey of patients with D-2-hydroxyglutaric aciduria was initiated to solve this issue. The clinical history, neuroimaging, and biochemical findings of 17 patients were studied. Ten of the patients had a severe early-infantile-onset encephalopathy characterized by epilepsy, hypotonia, cerebral visual failure, and little development. Five of these patients had a cardiomyopathy. In neuroimaging, all patients had a mild ventriculomegaly, often enlarged frontal subarachnoid spaces and subdural effusions, and always signs of delayed cerebral maturation. In all patients who underwent neuroimaging before 6 months, subependymal cysts over the head or corpus of the caudate nucleus were noted. Seven patients had a much milder and variable clinical picture, most often characterized by mental retardation, hypotonia, and macrocephaly, but sometimes no related clinical problems. Neuroimaging findings in 3 patients variably showed delayed cerebral maturation, ventriculomegaly, or subependymal cysts. Biochemical findings included elevations of D-2-hydroxyglutaric acid in urine, plasma, and cerebrospinal fluid in both groups. Cerebrospinal fluid gamma-aminobutyric acid was elevated in almost all patients investigated. Urinary citric acid cycle intermediates were variably elevated. The conclusion of the study is that D-2-hydroxyglutaric aciduria is a distinct neurometabolic disorder with at least two phenotypes.
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The molecular events initiating apoptosis following traumatic spinal cord injury (SCI) remain poorly understood. Soon after injury, the spinal cord is exposed to numerous secondary insults, including elevated levels of glutamate, that contribute to cell dysfunction and death. In the present study, we attempted to mimic the actions of glutamate by subdural infusion of the selective glutamate receptor agonist, kainic acid, into the uninjured rat spinal cord. Immunohistochemical colocalization studies revealed that activated caspase-3 was present in ventral horn motor neurons at 24 hours, but not 4 hours or 96 hours, following kainic acid treatment. However, at no time point examined was there evidence of significant neuronal loss. Kainic acid resulted in caspase-3 activation in several glial cell populations at all time points examined, with the most pronounced effect occurring at 24 hours following infusion. In particular, caspase-3 activation was observed in a significant number of oligodendroglia in the dorsal and ventral funiculi, and there was a pronounced loss of oligodendroglia at 96 hours following treatment. The results of these experiments indicate a role for glutamate as a mediator of oligodendroglial apoptosis in traumatic SCI. In addition, understanding the apoptotic signaling events activated by glutamate will be important for developing therapies targeting this cell death process.
A combined indirect ELISA and immunoblotting assay was used for the detection of intrathecal synthesis of IgG antibodies to herpes simplex virus (HSV) in patients with HSV encephalitis (HSVE). By using these two assays as well as three markers for blood-brain barrier, leakage can be easily excluded. A total of 21 sera and 24 cerebrospinal fluid (CSF) samples from 11 patients with HSVE were examined. For seven patients more than one pair of serum and CSF were available. For one patient IgG antibodies began to be detectable in CSF after the sixth day from the onset of the disease. In the other 10 patients the intrathecal synthesis of HSV IgG antibodies was detected later than the sixth day and reached high optical density (OD) values after the 10th day from the onset of disease, at the earliest. In contrast, intrathecal HSV antibody synthesis was not found in specimens taken from 20 patients with acute meningitis who composed our negative control group. The use of a combined indirect ELISA and of an immunoblotting assay on a single dilution of serum and CSF for HSV IgG synthesis in the central nervous system (CNS) allowed the diagnosis of HSVE after the first week of disease.
In this paper we document retial supply of the spinal cord and describe the arterial vascular pattern of the brain in the whale family Monodontidae. Observations are based on gross dissections of four brains, two each of Monodon monoceros and Delphinapterus leucas, and one spinal cord from M. monoceros. Vessels of the spinal cord arise from extradural retia in the neural canal. Arteries originating from the retia penetrate the dura between successive spinal roots (mainly ventral) and not in association with them, unlike radicular arteries of other mammals. Also, these vessels are uniformly distributed and contribute equally to a plexus surrounding the cord. An A. radicularis magna is not present, and neither are distinct anterior or posterior spinal arteries. Circulation to the brain is effected by two pairs of arteries originating from intracranial retia. The rostral pair supplies most of the forebrain (prosencephalon), whereas the more caudal pair supplies mainly the midbrain (mesencephalon) and hindbrain (rhombencephalon). The circulatory pattern is characterized by 1) complete independence of anterior cerebral arteries (no anastomoses); 2) extensive cortical supply by the anterior choroidal arteries; 3) absence of subdural communicating vessels between rostral and caudal trunks; 4) union of caudal trunks to form a small basilar artery; and 5) absence of vertebral arteries and hence of a vertebral basilar system. There are some obvious differences between subdural arteries in the Monodontidae and those in other mammals; however, their general patterns of distribution are similar, and we suggest that most of the vessels, at least in the cranium, are homologous.
Spontaneous epileptiform discharges were recorded by whole head magnetoencephalography (MEG) and subdural electrodes simultaneously from two patients with medically intractable temporal lobe epilepsy. In one patient whose epileptiform discharges emerged from the lateral temporal lobe, simultaneously recorded MEG could estimate equivalent current dipole reliably near the tumor. The amplitude of the dipole was in proportion not only to the amplitude of epileptiform discharge but also to the number of subdural electrodes involved. In the other patient, MEG detected only a small proportion of epileptiform discharges, even when they were recorded by subdural electrodes from the mesial temporal lobe. It is concluded that the amplitude and the depth of epileptiform discharges would largely affect the sensitivity of dipole localization by MEG.
Radiographic cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) do not reflect cerebral hemodynamics and oxygenation and may occur in the absence of clinical deficit and vice-versa. This report is to describe preliminary findings in further development of a non invasive method to estimate regional cerebral oxygenation and perfusion. Measurements were performed with a technique combining near infrared spectroscopy (NIRS) and indocyaningreen (ICG) dye dilution. Successful data analysis has been performed based on the decomposition in pulsatile and non-pulsatile components of NIRS absorption data collected before and during the passage of ICG through the vascular bed under the NIRS-detector. First measurements in patients with CVS suggest that the technique could become a powerful tool in the detection and treatment of CVS. This non invasive technique can be done at the bedside, it seems to be safe, easy to perform and less time-consuming compared to conventional techniques. The influence of extracerebral bone and surface tissue on cerebral NIRS signal has not been clarified yet. Therefore a new subdural NIRS probe has been developed, which gives the opportunity to measure directly the concentration of the chromophores in the brain without the influence of extracerebral contamination. In future comparative measurements with conventional NIRS probes on the scalp will allow to quantify and eliminate extracerebral contamination from the NIRS signal.
During the years 1967-1984, 91 children were operated on because of acute compressive traumatic intracranial hematoma: 16 (17%) had traumatic acute subdural hygromas. These were unilateral in 12 cases and bilateral in 4. The causes of injury were traffic accidents in 11 children, a fall in 1, and acute deceleration injuries in 5. Nine children suffered multiple injuries to the thorax, inferior extremities, and pelvis. Clinical manifestations and evolution of clinical symptoms included changes in conscious level, palsy, high fever, nystagmus, maximum dilation of either pupil and spontaneous, irregular breathing. The diagnosis was made on the basis of the clinical picture and supplementary clinical investigations: CT, EEG, echoencephalography, isotope cisternography, and arteriography. Treatment was by simple trephination of the cranium and evacuation of hygromatous liquid. All children survived the surgical treatment; 1 child died after the operation and 2 developed hydrocephalus.
In an effort to maximize the effectiveness of subdural-peritoneal shunting for the treatment of chronic subdural hematoma in infants, the author developed a new shunt system. The characteristics of this shunt include a large-caliber catheter, a very low pressure slit valve, and a one-piece design with a large flushing device. This shunt is particularly useful for patients without increased intracranial pressure, who are usually refractory to treatment using a conventional ventriculoperitoneal shunt system.
During a 14-day period, 45 of 78 rabbits were treated intravenously with chlorpromazine (5 mg kg-1 day-1). Metrizamide or iohexol was injected subarachnoidally and the neurotoxic effects of each substance on rabbit behaviour were evaluated for 3 h in both chlorpromazine-treated and non-treated rabbits. Chlorpromazine increased both the excitative and the depressive effects of metrizamide and the depressive effects of iohexol. No signs of excitation were observed in chlorpromazine-treated and non-treated rabbits after subarachnoid injections of iohexol. In spite of a free flow of clear fluid from the needle both before and after the intended subarachnoid injection, radiography disclosed that 26 of 67 suboccipital injections inadvertently resulted in a subdural deposition of the contrast medium. Contrast medium effects following subdural injection significantly differed from those following subarachnoid injection.
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