Somatosensory evoked potentials (SEPs) to median nerve stimulation and auditory brainstem evoked potentials (BAEPs) were recorded in 16 comatose patients who had suffered transtentorial herniation (TH) due to intracranial haematoma, hydrocephalus or tumour. An attempt was made to correlate the changes in the N14-P15 component of the central conduction time (CCT) and the I-V interpeak latencies (IPLs) of the BAEP with the clinical severity of TH. The N14-P15 component was not affected in seven patients at the diencephalic or early third-nerve stage, and six of these seven showed normal I-V IPLs. All six patients at the late third-nerve/midbrain stage or worse, however, showed abnormalities in the N14-P15 components. Interestingly, five patients showed dissociation of SEP and BAEP abnormalities suggesting a differential sensitivity of the medial and lateral lemnisci in the brainstem to ischaemia and/or compression. All five patients in whom the P15 potential was absent on either side had a poor outcome and there was a correlation between the electrical failure in the N14-P15 component and the degree of brainstem damage caused by TH as assessed clinically. Reversible loss of the P15 potential by brainstem retraction has been shown in intraoperative SEP monitoring during aneurysm surgery. Prolonged compression of the upper brainstem seems to cause irreversible loss of the P15 which should be regarded as being due to irrecoverable brainstem dysfunction.
The box method of freezing the brain in situ was assessed in baboons. The cooling rate of the tissue was monitored in several regions located at various depths from the skull surface. These measurements allowed us to examine the time required for the tissue to reach 0 degree C, in relation to its depth measured from the top of the skull. To define brain regions with proven ischaemia, frozen tissue sections were surveyed for areas of decreased pH. In addition, concentrations of ATP, phosphocreatine, and lactate were determined in gray matter located at various depths from the top of the brain surface. Normal tissue pH and low lactate concentration, without any significant decrease in high-energy phosphate levels, were found in regions at a depth less than approximately 10 mm from the brain surface. Deep structures including the inferiomedial aspect of the temporal lobe, the lateral geniculate body, and the limbic system (hippocampus) consistently showed mild tissue acidosis, indicating that these regions were subjected to some degree of ischaemia before they were reached by the freezing front. In some cases, acidosis was also detectable in the thalamus, basal ganglia, and in the deeper part of some sulci. We conclude that, with baboons, in situ freezing using the box method is valid for metabolic studies of the cerebral cortex and structures located at a depth less than approximately 10 mm from the top of the brain surface.
The present experiment was designed to examine the effect of vasogenic brain edema produced by exposure to air on the electrical activity of the thalamocortical pathway and local cerebral blood flow (1CBF) measured by the hydrogen clearance method. A large area of unilateral cerebral hemisphere of anaesthetized cats was exposed to air for 12 hours, and vasogenic brain edema was produced in the cortical and subcortical structure.Water content of the primary sensorimotor cortex, white matter, and thalamus, which was measured by the specific gravity method, significantly increased by 1.9,4.1,and 0.7% g water/g tissue, respectively, after 12 hours of exposure to air. After six hours of exposure, the blood flow in the cortex, white matter, and thalamus significantly decreased from control levels of 56.8±12.7, 21.7±5,2, 44,1±13.4ml/100g/min to 46.5±13.2, 16.3±5.0, and 31.3±11.9ml/100g/min, respectively. These decreases were accompanied by diminution in the amplitude of the direct cortical responses (DCRs) and prolongation of N1 latencies of the somatosensory evoked responses (SERs) recorded at the primary sensorimotor cortex. Both electrical activities were progressively suppressed in proportion to the reduction of ICBF after six hours of exposure. These results suggest that thalamocortical ischemia is probably responsible for the neural electrical suppression observed in this experimental edema.There was a significant correlation between the amount of edema and the degree of ischemia in the white matter. Accumulation of the edema fluid may induce ischemia affecting sensory conduction through the white matter as suggested by prolongation of the N1 latency of SER.
Recently interest has increased in cerebrovascular moyamoya disease (Suzuki and Takaku, 1979; Krayenbühl, 1975), spontaneous occlusion of the circle of Willis (Kudo, 1975) or cerebral basal rete mirable (Nishimoto and Takeuchi, 1968). Kodama and Suzuki (1978) have reported five aneurysms in 35 adults with this condition, suggesting a high incidence and a specific location of the aneurysm in moyamoya disease. A case of basilar artery aneurysm associated with this disease and a review of 13 aneurysm-associated cases reported up to now in Japan constitute this report. A 54-year-old woman was admitted soon after an episode of subarachnoid haemorrhage on May 2, 1977. Physical examination disclosed no neurological deficit but there was meningeal irritation and lumbar puncture showed bloody CSF.
Central conduction time (CCT) has been monitored in 37 patients undergoing temporary arterial occlusion in aneurysm surgery. 17 patients had internal carotid, 17 had middle cerebral, and 4 had basilar artery occlusion. Internal carotid or middle cerebral artery occlusion lasting less than 12 minutes has not been associated with postoperative morbidity, in any case without appreciable change in CCT after occlusion. Prompt prolongation of CCT was warned the surgeon, but CCT prolongation up to 10 ms could occur without permanent neurological deficit, except in one Grade 4 patient. 10 of 18 patients who lost the N 20 cortical potential showed postoperative neurological deficit, which was promptly recoverable in 7 patients. The speed of loss or recovery of N 20 enabled a patient's prognosis to be predicted. Irrecoverable postoperative deficit is unlikely if the N 20 takes longer than 4 minutes to disappear, to reappears within 20 minutes after recirculation.
A 20-year-old female presented with dysphasia and slight hemiparesis following a head trauma, who had a non-treated growing skull fracture which had remained asymptomatic for about 18 years, despite an encephalocele in the left parietal region. Neuroimaging demonstrated secondary brain damage and herniated brain resulting in gliosis. Electroencephalography revealed epileptic discharge in the affected region. Dural repair and cranioplasty resolved her neurological deficits. Early corrective surgery should be performed for growing skull fracture to prevent secondary brain damage.
Two patients underwent an antero-lateral partial vertebrectomy (ALPV) as decompression for their progressively deteriorating thoracic myelopathy. The first patient suffered from ossification of the posterior longitudinal ligament (OPLL), located between T1 and T2. Meanwhile, the second patient suffered from a herniated disc at T1-2. In both patients, a linear skin incision, approximately 5 cm long, was made along the medial border of the sternocleidomastoid muscle, on the patients’ right side. The longus colli muscles were dissected at the levels between T1 and T2. The ALPVs were done using a high-speed drill under the operating microscope and the OPLL extending partially to and through the dura. Once the OPLLs were excised, a pulsating movement of the dura was observed. ALPVs done between T1 and T2 allowed partial discectomy and an 18-mm excision of the posterior longitudinal ligament. No fusion technique was used in either patient. This study highlights that anterior compression of the upper thoracic spine can be excised at the level between T1 and T2 using an ALPV.
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