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Biomedical subjects

A E Walker

Publications and source records attributed to A E Walker.

At least 19 recordsLinked to original sources
PubMed1992

Keratitis, ichthyosis, and deafness (KID) syndrome: management with chronic oral ketoconazole therapy.

Extensive cutaneous mycoses have been described in patients with the keratitis, ichthyosis, and deafness (KID) syndrome. We present a case occurring in a 48-year-old woman where improvement in the ichthyosiform dermatosis, stabilization of her ocular disease, and apparent partial prevention of further cutaneous malignancies occurred in association with ketoconazole therapy.

Administration, Oral↗
PubMed1990

Long-term effects of severe penetrating head injury on psychosocial adjustment.

The long-term effects of severe penetrating head injury on adjustment levels were studied. Forty-one World War II veterans who suffered penetrating injury to the brain were interviewed 40 years after their initial injury using the Washington Psycho-Social Seizure Inventory (WPSI). The results support a comparable behavioral impact of right and left hemispheric lesions. Similarly, no significant relations were found between anterior and posterior locus of damage and psychosocial difficulties, although the results pertaining to the right-anterior group could be interpreted as suggestive of much greater maladjustment in all life dimensions assessed by the WPSI. Findings are discussed in terms of theoretical positions on hemispheric specialization and long-term expectancies that hold implications for planning rehabilitation programs for such patients.

Aged↗
PubMed1990

Ca2+ transients are not required as signals for long-term neurite outgrowth from cultured sympathetic neurons.

A method for clamping cytosolic free Ca2+ ([Ca2+]i) in cultures of rat sympathetic neurons at or below resting levels for several days was devised to determine whether Ca2+ signals are required for neurite outgrowth from neurons that depend on Nerve Growth Factor (NGF) for their growth and survival. To control [Ca2+]i, normal Ca2+ influx was eliminated by titration of extracellular Ca2+ with EGTA and reinstated through voltage-sensitive Ca2+ channels. The rate of neurite outgrowth and the number of neurites thus became dependent on the extent of depolarization by KCl, and withdrawal of KCl caused an immediate cessation of growth. Neurite outgrowth was completely blocked by the L type Ca2+ channel antagonists nifedipine, nitrendipine, D600, or diltiazem at sub- or micromolar concentrations. Measurement of [Ca2+]i in cell bodies using the fluorescent Ca2+ indicator fura-2 established that optimal growth, similar to that seen in normal medium, was obtained when [Ca2+]i was clamped at resting levels. These levels of [Ca2+]i were set by serum, which elevated [Ca2+]i by integral of 30 nM, whereas the addition of NGF had no effect on [Ca2+]i. The reduction of [Ca2+]o prevented neurite fasciculation but this had no effect on the rate of neurite elongation or on the number of extending neurites. These results show that neurite outgrowth from NGF-dependent neurons occurs over long periods in the complete absence of Ca2+ signals, suggesting that Ca2+ signals are not necessary for operating the basic machinery of neurite outgrowth.

Animals↗
PubMed1979

The prediction of posttraumatic epilepsy. A mathematical approach.

Simple mathematical equations can be used to estimate the probability of posttraumatic seizures. Risk factors and time since the injury are taken into consideration in the calculations. The equations are based on a constant probability model derived from published data. When these formulae are applied to data from a variety of published studies, the predicted incidence of posttraumatic epilepsy based on the mathematical model agrees well with the incidence observed in the study groups.

Brain Injuries↗
PubMed1979

Clinical evaluation of long-term epidural monitoring of intracranial pressure.

Forty-two epidural sensors for measuring intracranial pressure were implanted in 38 patients over the last four years. The sensor is a passive device consisting of an inductance and a pressure sensitive capacitance resonant at about 50 megahertz. The study involved 17 cases of hydrocephalus, nine of pseudotumor cerebri, and the remainder included cases of cranial trauma, brain tumors, and aneurysms. Four of the sensors failed in patients and were removed. Two of these had to be replaced to continue the pressure monitoring. The intracranial pressure is still being monitored in 22 patients, while 15 have been lost to follow-up for various reasons. Fourteen patients have been followed for about a year, and four for two years. The baseline drift rate in most sensors is between 1 and 2 mm H2O per day, with a few having greater rates of drift. Calibration errors were found in some of the sensors after implantation. These errors were corrected by direct measurement of the cerebral spinal fluid pressure via lumbar puncture. The sensors have proven to be a valuable adjunct in the management and diagnosis of neurosurgical patients by simplifying the intermittent and continuous recording of intracranial pressure. This was so despite the presence of calibration errors and a drift which necessitated an occasional lumbar puncture for making corrections.

Brain Diseases↗
PubMed1978

Pulsatile cerebral echo in diagnosis of brain death.

Conclusive diagnosis of brain death can be made by the demonstration of prolonged cessation of cerebral blood flow. This report describes a simple method to determine the presence or absence of the blood flow in the brain by recording the pulsatile midline echo on one channel of the electroencephalogram (EEG) or on any four-channel monitoring system in the intensive care unit. A firm transducer holder has been developed to eliminate artifacts caused by transducer motion, The pulsations of the midline echo are assumed to be the result of displacement of the midline structures by the arterial injection of each cardiac systole. Thus, the absence of these midline pulsatile echoes correlates with the absence of cerebral blood flow and, if the absence persists over 30 minutes in the presence of normal blood pressure, then the result is brain death. Twenty-eight cases of clinical brain death with electrocerebral silence of EEG and 18 obtained patients with various types of cerebral pathology were examined by the echo-pulsation technique. Twenty-six of the 28 cases showed no pulsation of the midline echo. The validity of the technique was documented in four cases by four-vessel cerebral angiogram.

Adolescent↗
PubMed1978

Pemphigus vulgaris in a 15-year-old girl.

Pemphigus vulgaris is uncommon in adolescence and only ten well documented cases in this age group were found in a recent review (5). Because the condition is often more severe in the younger age group it is important to consider it in the differential diagnosis of bullous eruptions of childhood and to perform direct and indirect immunofluorescence studies.

Adolescent↗
PubMed1977

Histological reaction to various conductive and dielectric films chronically implanted in the subdural space.

Thirty different test patches of various thin film materials were chronically implanted in the subdural space of cats to determine their suitability as components for proposed neuroprosthetic devices. In particular, materials employed by the microelectronics industry were screened, and reactions were found to be quite dependent on specific formulations or surface preparations of otherwise similar materials. A nonspecific but severe complication of pressure necrosis under thin films that spontaneously roll and curl in vivo was noted.

Animals↗
PubMed1977

Sedative drug surveys in coma: how reliable are they?

Routine blood tests of comatose patients for drugs that depress the CNS are highly desirable, but techniques of analysis are not well standardized and the results do not correlate well with clinical condition. Determining the role of sedative drugs in coma requires a high degree of suspicion and sound clinical judgment.

Adolescent↗
PubMed1976

Immunological mechanisms in the pathogenesis of vinyl chloride disease.

Vinyl chloride (VC) disease is a multisystem disorder incorporating Raynaud's phenomenon, acro-osteolysis, thrombocytopenia, portal fibrosis, and hepatic and pulmonary dysfunction. Immunological and immunochemical investigations showed the presence of circulating immune complexes in 19 out of 28 patients with the disease and in a further two out of 30 workers exposed to VC. The immunological data were reviewed in relation to the clinical picture of the disease and to the available evidence on the metabolism of VC. The results suggest that VC disease is an immune complex disorder and that the immune response is initiated by the adsorption of VC or a metabolite on to tissue or plasma protein.

Autoantibodies↗