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Biomedical subjects

W T Longstreth

Publications and source records attributed to W T Longstreth.

At least 181 records · Page 10Linked to original sources
PubMed1987

The neurologic sequelae of cardiac arrest.

This discussion was selected from the weekly Grand Rounds in the Department of Medicine, University of Washington School of Medicine, Seattle. Taken from a transcription, it has been edited by Drs Paul G. Ramsey, Associate Professor of Medicine, and Philip J. Fialkow, Professor and Chair of the Department of Medicine.

Animals↗
PubMed1986

Mitochondrial and MB isoenzymes of creatine kinase in cerebrospinal fluid from patients with hypoxic-ischemic brain damage.

Measurements of cerebrospinal fluid (CSF) creatine kinase (CK, EC 2.7.3.2) isoenzyme activity have been used to predict outcome in patients with acute brain injury following cardiac arrest. We identified two CK isoenzymes previously unreported in CSF from 16 patients with hypoxic-ischemic brain damage. Prior to analysis, the CK in the CSF samples was reactivated with dithiothreitol. CK isoenzymes were identified using electrophoretic and immunologic methods. Total CK activity ranged from 23 to 924 U/L (mean 452). CSF-CK-BB was the predominant isoenzyme present in all cases. In addition to CSF-CK-BB, the authors identified CSF-CK-MM in 6 cases, CSF-CK-MB in 8 cases, and CSF-mitochondrial-CK in 14 cases. The presence of CSF-CK-MM was significantly related to blood contaminating the CSF (P less than 0.02). It is proposed that CSF-CK-MB results from recombination of CK-MM and CK-BB in CSF and that mitochondrial CK is released with CK-BB into the CSF from the damaged brain tissue.

Brain↗
PubMed1986

Neurologic outcome and blood glucose levels during out-of-hospital cardiopulmonary resuscitation.

We examined the interrelations of outcome, time elapsed during cardiopulmonary resuscitation (CPR), and blood glucose levels drawn from 83 patients with out-of-hospital cardiac arrest. Levels rose significantly during CPR. Although slope and intercept of regression lines differed for those dying in the field and those admitted, regression lines were similar for those who awoke and never awoke after admission. These results suggest that the previously reported association between poor neurologic recovery and high blood glucose level on admission after cardiac arrest is best explained by prolonged CPR, leading to both higher rise of blood glucose and worse neurologic outcome.

Aged↗
PubMed1985

Fleck retina in Kjellin's syndrome.

We examined members of two families with Kjellin's syndrome, an autosomal recessive disorder characterized by spastic paraparesis, dementia, and macular changes. Although the retinal lesions resemble the flecks of fundus flavimaculatus by ophthalmoscopy, they appear distinct from previously reported retinal flecks by fluorescein angiography.

Adult↗
PubMed1985

Potroom palsy? Neurologic disorder in three aluminum smelter workers.

We studied three patients with a progressive neurologic disorder, all of whom had worked for over 12 years in the same potroom of an aluminum smelting plant. All had incoordination and an intention tremor. Two of the three patients had cognitive deficits, and the most severely affected patient also had spastic paraparesis. None had involvement of the peripheral nervous system. Despite extensive evaluations, the cause of these patients' problems remains obscure. It is tempting to implicate one of the numerous substances to which the patients were exposed in the potroom, but none is known to cause the neurologic problems seen in these patients. Neurotoxic effects of aluminum in animals are directed at the central nervous system, and theoretically long-term low-level exposure to aluminum in the potroom could explain the findings in our patients.

Adult↗
PubMed1984

High blood glucose level on hospital admission and poor neurological recovery after cardiac arrest.

To evaluate the relationship between blood glucose and neurological recovery after cardiac arrest, we retrospectively reviewed our experience with 430 consecutive patients resuscitated after out-of-hospital cardiac arrest. All these patients had received variable amounts of intravenous 5% glucose solutions before admission. Awakening patients, those following commands or having comprehensible speech, were classified as to whether they suffered persistent neurological deficits. The mean blood glucose level on hospital admission was higher in 154 patients who never awakened than in 276 who did awaken (mean, 341 versus 262 mg per 100 milliliters; p less than 0.0005). Among the 276 who awakened, 90 patients with persistent neurological deficits had higher mean glucose levels on admission than did 186 without deficits (286 versus 251 mg per 100 milliliters; p less than 0.02). These significant differences persisted after excluding all patients whose glucose levels were higher than 500 mg per 100 milliliters and after controlling for potentially confounding variables using multiple regression analysis.

Blood Glucose↗
PubMed1984

Cerebrospinal fluid creatine kinase activity and neurologic recovery after cardiac arrest.

We evaluated prospectively the relation between cerebrospinal fluid creatine kinase activity (CSF CK) and neurologic recovery after out-of-hospital cardiac arrest. Without knowledge of the enzyme results, we determined whether patients awoke, followed commands, or had comprehensible speech. CSF CK was significantly higher in never-awakening than in awakening patients. After cardiac arrest, elevation of CSF CK predicts poor neurologic recovery.

Brain↗
PubMed1984

Creatine kinase isoenzymes in human cerebrospinal fluid and brain.

Extracts of normal brains obtained at autopsy and cerebrospinal fluid (CSF) from patients with global brain ischemia were analyzed for creatine kinase (CK; EC 2.7.3.2) isoenzymes. We used both qualitative and quantitative assays (electrophoresis and immunoinhibition). Brain extracts contained CK-BB isoenzyme and mitochondrial CK. In 54 CSF samples free of blood contamination and with total activities ranging from 7 to 2010 U/L (mean 202 U/L), virtually all of the CK activity was due to CK-BB, and none to CK-MM or CK-MB. We conclude that brain contains CK-BB and mitochondrial CK, but lacks CK-MM and CK-MB. After cardiac arrest, CK-BB is released into the CSF. Any CK-MM in the CSF is probably from blood contamination, in which case immunoinhibition with anti-CK-M antibodies accurately quantifies CK-BB.

Acetates↗
PubMed1983

Prediction of awakening after out-of-hospital cardiac arrest.

To develop a model that would forecast neurologic recovery after out-of-hospital cardiac arrest, we reviewed charts on 389 consecutive patients who were not awake on admission to the hospital after resuscitation from asystole or ventricular fibrillation. The outcome variable was "awakening," which was defined as having comprehensible speech or the ability to follow commands. Predictor variables that we considered included both preadmission and admission data. Using discriminant analysis, we derived models from a 60 per cent random sample of cases and tested the models on the remaining 40 per cent. We judged that the best model contained four variables from the admission examination: motor response, pupillary light response, spontaneous eye movements, and blood glucose (levels below 300 mg per deciliter predicted awakening). Overall correct classification was 80 per cent in the derivation sample and 77 per cent in the test sample. In a simplified form, the model's predictions of awakening had a sensitivity of 0.92, a specificity of 0.65, a positive predictive value of 0.80, and a negative predictive value of 0.84. This rule should be clinically useful in estimating the neurologic prognosis of patients resuscitated after out-of-hospital cardiac arrest.

Blood Glucose↗
PubMed1983

Neurologic recovery after out-of-hospital cardiac arrest.

A retrospective cohort study of the neurologic sequelae of out-of-hospital cardiac arrest was done using 459 consecutive patients resuscitated and admitted to a teaching hospital over 10 years. Awakening was defined as having comprehensible speech or following commands. One hundred and eighty patients (39%) never awakened and 279 (61%) awakened, 188 without and 91 with persistent neurologic deficits. Fifty-nine patients had cognitive deficits and 32 patients had motor and cognitive deficits. Patients who did not awaken died, with a median survival of 3.5 days. The longer a patient survived without awakening, the smaller the probability of ever awakening and awakening without deficits. Fourteen patients awakening after 4 days had some deficits, and after 14 days six had severe deficits. Neurologic sequelae of cardiac arrest are common and related to awakening. The probability of future awakening and neurologic sequelae for patients not awake at specific times after cardiac arrest can be estimated.

Adolescent↗
PubMed1982

Adult dystonic lipidosis: clinical, histologic, and biochemical findings of a neurovisceral storage disease.

A 43-year-old man presented with splenomegaly and a 20-year history of a neurologic disorder that included vertical supranuclear ophthalmoplegia, mild dementia, and a movement disorder. Adult dystonic lipidosis was diagnosed from the clinical picture and demonstration of foamy and sea-blue histiocytes in bone marrow. Ultrastructural patterns in cytolysosomes suggested accumulation of neutral fat and phospholipids. Liver content of bis-(monoacylglycerol) phosphate was increased, probably because the number of lysosomes had increased. Sphingomyelinase activity was normal in cultured skin fibroblasts. Juvenile and adult dystonic lipidosis form a clinically, histologically, and biochemically distinct neurovisceral storage disease that differs from Niemann-Pick disease.

Adult↗