Biomedical subjects

J I Brown

Publications and source records attributed to J I Brown.

13 recordsLinked to original sources

PubMed1998

Monitoring severe head injury: a comparison of EEG and somatosensory evoked potentials.

We report on our experience with long-term monitoring of the EEG power spectrum and somatosensory evoked potentials (SSEPs) in 103 patients with severe closed head injury (Glasgow Coma Scale-GCS < or = 8). Patients were monitored for an average of 5 days post injury and monitoring was terminated when they died, regained consciousness or their intracranial physiologic parameters (primarily intracranial pressure-ICP) were stable for 2-3 days. Patients were treated according to a standard protocol that included mechanical ventilation, sedation, and neuromuscular blockade. At 7 of 9 twelve hour time intervals post injury, SSEPs were significantly (p < .05) different between outcome groups using the Glasgow Outcome Score collapsed to 3 categories. The percent slow (delta) activity in the EEG was not significantly different between outcome groups at any time point, post injury. The total power in the EEG power spectrum differed only at the last time epoch post injury (108 hr.). Based on the superior prognostic capabilities of the SSEP, we routinely base critical management decisions on SSEP values. We have not been able to rely on EEG parameters for these same decisions due to the lack of clear distinction between good and poor prognosis groups based on common EEG parameters.

Adolescent↗

PubMed1998

Epithelioid sarcoma: presence of vascular-endothelial cadherin and lack of epithelial cadherin.

AIMS: To evaluate the pattern of cadherin expression in epithelioid sarcoma. METHODS AND RESULTS: Seven epithelioid sarcomas were immunostained by a polyclonal antibody that detects all cadherin subtypes and by monoclonal antibodies that detect epithelial cadherin (E-cadherin) and vascular-endothelial cadherin (VE cadherin). In addition, the tumours were immunostained for a variety of epithelial (cytokeratin, EMA, AUA1) and endothelial (Factor VIII-related antigen, CD34, CD31) markers. Tumours cells of all seven epithelioid sarcomas expressed cadherins. Surprisingly, E-cadherin was not detected in any of the sarcomas. VE-cadherin was detected in five of seven cases. All seven tumours expressed cytokeratins and EMA but none expressed AUA1. CD34 was detected in six of seven cases and CD31 was detected in a single case. No case expressed Factor VIII-related antigen. CONCLUSIONS: Most epithelioid sarcomas strongly express cadherins, a feature which may contribute to their epithelioid appearance. The absence of detectable E-cadherin suggests that epithelial differentiation in these tumours is, at most, incomplete. The expression of VE-cadherin by the majority of cases, in the absence of E-cadherin, is consistent with an element of mesenchymal differentiation, possibly endothelial or perineurial. The additional presence of other markers such as CD34 and CD31 in some cases favours endothelial differentiation.

Adult↗

PubMed1998

Clinical significance of CSF glutamate concentrations following severe traumatic brain injury in humans.

Glutamate excitotoxicity is a putative mechanism of secondary damage after traumatic brain injury (TBI). No relationship between glutamate release and clinical status has been shown in humans, however. We hypothesize a dose-response relationship between CSF glutamate concentrations and severity of injury, electrophysiological deterioration as measured by somatosensory evoked potential amplitudes, and clinical outcome. From August 1991 to March 1996, intensive monitoring of 55 patients with severe TBI (GCS < or = 8 after resuscitation) included twice daily CSF glutamate levels and hourly somatosensory evoked potentials (SSEPs) for an average of 5 days. Clinical outcomes were survival/nonsurvival and Glasgow outcome score (GOS) at 3 months or more post-injury. Glutamate levels were not associated with severity of injury, electrophysiological deterioration, or clinical outcome. Neither peak nor mean glutamate levels significantly improved a simple logistic regression model which used only age and presence of bilaterally unreactive pupils to predict survival. Using this methodology CSF glutamate concentrations did not display a dose-response relationship to severity of injury, electrophysiological deterioration, or predict clinical outcomes following TBI in a group of 55 patients. An early effect of glutamate, an effect dependent on time of exposure to glutamate or other modulating effects cannot be ruled out.

Adult↗

PubMed1998

Cerebral oxidative metabolism and evoked potential deterioration after severe brain injury: new evidence of early posttraumatic ischemia.

BACKGROUND: We commonly observe progressive deterioration in somatosensory evoked potentials (SSEPs) after severe head injury. We had previously been unable to relate this deterioration to raised intracranial pressure but had noted a relationship with decreasing transcranial oxygen extraction (arteriovenous oxygen difference [AVDO2]). The purpose of this study was twofold: to prove the hypothesis that deterioration in SSEP values is associated with decreasing AVDO2 and to test the subsidiary hypotheses that deteriorating SSEPs were the result of either ischemia/reperfusion injury or failure of oxygen extraction/utilization. METHODS: Monitoring of 97 patients with severe traumatic brain injury (Glasgow Coma Scale scores of < or = 8 after resuscitation) included twice daily AVDO2 measurement and hourly SSEP recording for an average of 5 days. The last 51 patients also underwent 12-hourly measurement of cerebral blood flow (CBF), with calculation of the cerebral metabolic rate of oxygen. Cluster analysis was used to classify patients based on initial AVDO2 values and subsequent SSEP trends. The time courses of CBF, SSEPs, AVDO2, and cerebral metabolic rate of oxygen were examined in the groups defined by the cluster analysis. The clinical outcomes considered were survival or nonsurvival and the Glasgow Outcome Scale scores obtained at 3 months or more after injury. RESULTS: Cluster analysis confirmed the association between high initial AVDO2 values and subsequent SSEP deterioration. Patients in this category initially had significantly higher AVDO2, lower CBF, and higher cerebral metabolic rates of oxygen but recovered to adequate levels within 24 to 36 hours after injury. SSEP values were initially identical in the patients with normal AVDO2 values and those with elevated AVDO2 but differed significantly at 60 hours after injury and beyond. CONCLUSION: The findings of increased oxygen utilization and lowered CBF in the patients with deteriorating SSEPs strongly imply that early ischemia rather than failure of O2 extraction or utilization is responsible for the associated SSEP deterioration. This issue of defining thresholds for ischemia based on AVDO2 is confounded by the dependency of CBF and AVDO2 values on the time after injury.

Adult↗

PubMed1997

An immunocytochemical study of MHC class I expression on human Langerhans cells and melanocytes.

Classical MHC class I glycoproteins (HLA-A, B, and C) present endogenous cytosolic peptide antigen fragments to CD8-positive T-cells. CD8-positive T-cell recognition and destruction of virus-infected cells are dependent on adequate cellular MHC class I expression. Constitutive MHC class I expression is ubiquitous, but known to be deficient on specific differentiated cell types which include hepatocytes, neurones, chondrocytes and myocytes. Although enabling assessment of MHC class I expression on individual cells, limitations of immunocytochemistry were encountered with this assessment on Langerhans cells and melanocytes. These dispersed intraepidermal cells were obscured by adjacent keratinocytes in sections immunostained for MHC class I glycoproteins. Initiatives designed to resolve the issue have included immunoelectron microscopy, cell culture techniques, and animal bone marrow chimera models. Despite the elegance of these techniques, the issue of MHC class I expression on Langerhans cells and melanocytes remains unresolved. In this immunocytochemical study, an alternative strategy was based upon the recognized deficiency of epithelial MHC class I expression within pilosebaceous adnexal units. Langerhans cells and melanocytes were therefore studied within this microenvironment of deficient MHC class I expression, using monomorphic and polymorphic MHC markers. Langerhans cells and melanocytes were demonstrated within pilosebaceous units of scalp skin by immunocytochemistry. Differentiation markers OKT6 (CD1a) and TMH1 defined Langerhans cells and melanocytes, respectively. Monomorphic MHC markers W6/32 and TAL IB5 defined invariant epitopes of HLA class I and II, respectively. Polymorphic MHC class I markers defined the HLA-Bw4 and HLA-Bw6 supertypic determinants. Constitutive MHC class I expression was shown to be deficient on Langerhans cells and melanocytes.

Hair Follicle↗

PubMed1994

Papilledema secondary to metastatic prostate disease.

BACKGROUND: Prostate cancer increases in incidence with age, and is common in older men. If allowed to progress or detected late, prostate cancer readily metastasizes to bone and accounts for about 11 percent of all cancer deaths. Associated conditions with prostate metastatic disease are anemia, pathological bone fractures, and paraplegia. Occasionally, prostate cancer may metastasize to the skull or spinal cord and result in papilledema. Two cases presenting with papilledema secondary to metastatic prostate disease are discussed.

Adenocarcinoma↗

PubMed1993

Deep cerebral venous system thrombosis: case report.

A 38-year-old woman with thrombosis of the deep cerebral venous system, presumed to be secondary to the use of the oral contraceptive pill, is reported. The use of cerebral angiography and magnetic resonance imaging in establishing the diagnosis and management strategies is discussed. It is concluded that magnetic resonance imaging is an appropriate investigative modality for diagnosis and therapeutic decision making, and that, as with superficial cerebral dural sinus and venous thrombosis, anticoagulation is a safe and effective therapy.

Adult↗

PubMed1989

A new objective measurement of esophageal lumen patency.

This study was performed to develop a system to measure dysphagia in an objective fashion, test its correlation with subjective estimates of dysphagia, and encourage the use of a standardized measure of esophageal stenosis. Thirty-five patients with mechanical dysphagia underwent subjective estimates of dysphagia using a dysphagia scale graded from 0 to 5, as well as a diet scale. Lumen diameter was measured endoscopically, using the open or closed biopsy forceps as a measuring guide. Patients were then given barium capsules or tablets of increasing diameter under fluoroscopy, in the upright position. Pills were given sequentially until a pill failed to traverse the esophagus in less than 20 s. The diameter of the pill failing to traverse the esophagus within 20 s correlated strongly with the endoscopically measured diameter by Spearmans rank correlation (Rs = 0.85). The weakest correlation was between endoscopically measured diameter and the dysphagia scale (Rs = 0.48). The diameter of the pill failing to traverse the esophagus within 20 s is an excellent estimate of esophageal lumen diameter. Pill size correlates much better with esophageal lumen diameter than dysphagia or diet scales. This new dysphagia assessment system should simplify standardization of the grading of dysphagia.

Barium Sulfate↗

PubMed1988