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Biomedical subjects

K Norcross

Publications and source records attributed to K Norcross.

18 recordsLinked to original sources
PubMed1989

Neurobehavioral and magnetic resonance imaging findings in two cases of decompression sickness.

Two divers underwent neurobehavioral examinations and magnetic resonance imaging (MRI) while hospitalized during the first 2 weeks after sustaining decompression sickness (DCS). Their neurologic findings included a Brown-Séquard Syndrome consistent with spinal cord lesion, and focal deficits consistent with cerebral lesion(s). MRI revealed subcortical white matter lesions in the brains of both divers, whereas no lesion of the spinal cord was demonstrated. The patients exhibited neurobehavioral sequelae including disturbances of memory, divergent thinking, and visuospatial and motor functioning. Focal neurologic deficits resolved in both patients, and their cognitive and memory problems improved slowly. Findings in these two divers raise the possibility that cerebral insult more frequently accompanies spinal cord injury in DCS than previously thought.

Adult↗
PubMed1986

A cobalamin metabolic defect with homocystinuria, methylmalonic aciduria and macrocytic anemia.

We have identified a patient with methylmalonic aciduria and homocystinuria due to a defect in cobalamin metabolism of the cb1C type mutant. At the time of admission at eight months of age the patient was malnourished, hypotonic and had macrocytic anemia. Neonatal screening for hypermethioninemia associated with homocystinuria had been normal. Serum vitamin B12 was markedly increased and folate concentration was above normal, as were urinary homocystine and methylmalonic acid. The patient had abnormal brain stem auditory and visual evoked potentials. Fibroblast activity of N5-methyltetrahydrofolate: homocysteine methyltransferase was reduced to approximately 10% of concurrent controls. A course of therapy with hydroxocobalamin resulted in a 90% reduction in excretion of methylmalonic acid and normalization of the evoked potentials. These studies support the efficacy of hydroxocobalamin therapy in this disease, suggest that methylmalonic acid may be the most appropriate metabolite to monitor for therapeutic response, and in importance of electrophysiologic studies in character in objectively monitoring the response to treatment metabolic disease.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1986

Burnout.

Explore the source record for details and available documents.

Burnout, Professional↗
PubMed1985

Vascular malformations of the thalamus with normal angiograms.

We describe two patients with fatal vascular malformations of the thalamus whom we thought had gliomas. They had progressive neurological impairment with subacute onset as adults. Computed tomography showed lesions of increased density with slight post-contrast enhancement; cerebral angiography was normal. Without biopsy, they received radiation therapy without benefit. Two other patients with similar radiological studies have done well with conservative treatment. We believe that these lesions have a distinctive appearance on CT, that vascular malformations can be diagnosed, even with normal cerebral angiograms, and distinguished with reasonable certainty from gliomas.

Adult↗
PubMed1985

Minneapolis hip prosthesis in severe destructive lesions of the femur.

The use of the Minneapolis prosthesis was abandoned about 1955 by its originators, who had used it without acrylic for uncomplicated fractures of the femoral neck. This is the first report of its use with 'cement' fixation. It has been found to be very useful and reliable for arthroplasty of the hip in 57 patients with carcinomatous or other severe destructive lesions in the trochanteric region of the femur, being more convenient and easier to use than alternative prostheses and especially valuable in metastatic disease. Technical points relating to operative techniques are described, and postoperative Hamilton-Russell traction is recommended.

Adult↗
PubMed1978

Selective blockade by scopolamine of synaptic responses in cat's caudate nucleus and its modification by lesions of the substantia nigra.

Because it is commonly believed that acetylcholine is a synaptic transmitter in the caudate nucleus and that the reduction of striatal biogenic amines in Parkinson's disease leads to acetylcholine supersensitivity in the caudate nucleus, we investigated the effects of the muscarinic blocking agent scopolamine on synaptic responses of neurons in the intact feline caudate nucleus and in the caudate nucleus depleted of dopamine by long-standing nigrostriatal lesions. In the intact caudate nucleus, micro-iontophoretic application of scopolamine selectively blocked the neuronal responses to stimulation of the caudate nucleus near the recording site without affecting the responses to stimulation of the sensorimotor cortex or the substantia nigra in the same fashion. This suggests that acetylcholine is a synaptic transmitter of caudate interneurons. Responses to thalamic stimuli were also blocked by scopolamine, suggesting that acetylcholine may be a transmitter of thalamic afferents although the course of these afferents is unclear. In the dopamine-depleted caudate nucleus scopolamine was more effective than in the intact caudate nucleus blocking the neuronal responses to stimulation of the caudate nucleus. This greater blocking effect by scopolamine suggests an increased effect of endogenous acetylcholine in this response and supports previous observations of an increased excitatory effect of iontophoretic acetylcholine in the dopamine-depleted caudate nucleus. These results suggest that the acetylcholine supersensitivity which follows nigrostriatal degeneration may be due to increased effectiveness of synaptic transmission by cholinergic interneurons in the caudate nucleus.

Acetylcholine↗
PubMedDate not supplied

Evoked potential abnormalities in children with chronic cholestasis.

To assess the effect of chronic cholestasis and vitamin E deficiency on nervous system function, we did multimodality evoked potential testing of 17 children (mean age = 47 months) who had chronic liver disease. Evoked potential testing was repeated periodically in 11 patients 1 to 33 months after the initial study. Eight children had abnormal delays of the P100 peak of the visual evoked potential, and these children each had significantly higher total serum bile acid levels than did children who had normal visual evoked potentials (p = 0.002). Bilateral brainstem auditory evoked potential abnormalities consistent with conductive hearing losses were initially present in six patients. However, persistent conductive losses were found in four patients, all of whom had arteriohepatic dysplasia. Four children had mildly abnormal somatosensory evoked potentials that were due solely to a mild peripheral neuropathy. Biochemical measures of vitamin E status were not consistently associated with either normal or abnormal visual, brainstem auditory or somatosensory evoked potentials or a combination of evoked potential abnormalities, and an abnormality of one evoked potential type was not associated with an abnormality of any other. A similar lack of relationship between evoked potential results and plasma vitamin A measurement was noted. Following marked improvement in or resolution of cholestasis in four patients, the visual evoked potential became normal, but other evoked potentials did not change. Visual evoked potential improvement was greatest in two patients who underwent orthotopic liver transplantation. This is the first report that demonstrates frequent, potentially reversible visual system abnormalities that are associated with cholestasis and cannot be attributed solely to vitamin E and/or A deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Abetalipoproteinemia↗