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Biomedical subjects

K D Barron

Publications and source records attributed to K D Barron.

At least 55 records · Page 3Linked to original sources
PubMed1981

Early diagnosis of spinal epidural metastases.

Early signs of spinal cord injury on neurologic examination have been the primary indication to proceed with myelography in patients with possible spinal epidural metastases. With this approach, loss of ambulation occurs in more than one half of the patients. In an attempt to diagnose epidural metastases before the onset of myelopathy, we designed a prospective study based on the development of back pain, a precursor of spinal cord injury in nearly all cancer patients. Eighty-seven patients were studied. A high incidence of epidural metastases was found in patients with myelopathy (78 percent). In addition, patients with radiculopathy alone frequently had epidural tumor (61 percent). In 36 percent of the patients who presented with back pain but who had normal neurologic findings, there was evidence of epidural metastases on myelography; all of those patients had vertebral metastases on plain roentgenogram. Over-all, the plain roentgenogram of the spine correctly predicted the presence or absence of epidural tumor in 83 percent of the patients. Whereas 93 percent of the patients with myelopathy had more than 75 percent myelographic block, this occurred in 53 percent of those with radiculopathy and in only 33 percent of those with back pain and normal neurologic findings. In most cancer patients, spinal epidural metastases are both detectable and significantly less extensive before the onset of spinal cord injury.

Adolescent↗
PubMed1981

Adenosine-stimulated astroglial swelling in cat cerebral cortex in vivo with total inhibition by a non-diuretic acylaryloxyacid derivative.

The intact cerebral cortices of cats were exposed in vivo under normothermic conditions and superfused with isotonic artificial cerebrospinal fluid containing added 0.125 mM adenosine. This resulted in chloridecation-rich cerebrocortical swelling which was shown by electron microscopy to be associated with an expanded astroglial compartment. The addition of DCPIB, a non-diuretic acylaryloxyacid analogue of ethacrynic acid and an inhibitor of coupled chloride-cation transport in cerebral cortex in vitro, totally blocked astroglial swelling and the concomitant increases in tissue ion contents. These studies support our previous experiments on the mechanism of formation of astroglial swelling. The pathological consequences of astroglial swelling and the clinical applications of these findings are discussed.

Adenosine↗
PubMed1980

Axon reaction in dorsal motor vagal and hypoglossal neurons of the adult rat. Light microscopy and RNA-cytochemistry.

Qualitative light microscopical observations, morphometric measurements, and cytophotometric values for nucleolar and cytoplasmic RNA were compared in axotomized rat dorsal motor vagal and hypoglossal neurons. These data were correlated with consective cell counts and examination of the peripheral nerves. Vagal neurons showed an early prominent chromatolysis, later accompanied by increased cytoplasmic basophilia. Morphometric data showed a transient slight cytoplasmic enlargement but no nucleolar hypertrophy. Nucleolar RNA was unchanged, but cytoplasmic RNA was elevated 7 to 84 days postoperatively. Cell counts demonstrated a final cell loss of about 70%. Hypoglossal neurons showed a moderate chromatolysis. Nucleolar and cytoplasmic areas were enlarged for a short period. Nucleolar and cytoplasmic RNA were elevated about 3 to 14 days and about 3 to 28 days postoperatively, respectively. Cell counts demonstrated a loss of 25% at the longest postoperative survival period. The results indicate that axotomized adult mammalian extrinsic neurons--even those destined to die--accumulate RNA. This response contrasts with axon reaction in many axotomized mammalian intrinsic neurons which appear to undergo depletion of RNA.

Animals↗
PubMed1980

Olivary hypertrophy: histochemical demonstration of hydrolytic enzymes.

Of four patients with palatal myoclonus, three had infarcts resulting from atherosclerosis, and one had cerebral emboli from a left atrial myxoma. Three specimens showed lesions in the brainstem and bilateral hypertrophy of the inferior olivary nuclei; the fourth revealed unilateral olivary changes caused by an infarct in the contralateral dentate nucleus. After incubation for acetylcholinesterase, neuropilar and capillary wall staining were absent or much reduced, but there was increased denisty of reaction product in the neuronal cell bodies and in numerous tortuous dendrites. Methods for acid phosphatase showed strong activity in the dendrites and glomeruloid structures of the diseased olives. Reactions for nonspecific esterase indicated dendritic expansion and reduced staining density in nerve cell bodies, but augmented glial reactivity.

Acetylcholinesterase↗
PubMed1980

Biology of glial swelling in experimental brain edema.

Most studies of clinically relevant cerebral edema emphasize the effect of added tissue fluid in white matter on gross distortion with transtentorial and subfalcine brain herniation. Our recent studies on altered tissue fluid compartmentation in cerebral gray matter suggest that significant microdistortion of relationships of capillaries to subserved tissue follows swelling of astroglia therein. Grave consequences to solute and gas exchange in focal regions may well be expected and are emphasized. The elucidation of the mechanisms of formation and inhibition of astroglial swelling by chemical agents, including chemically useful acylaryloxyacetic acid derivatives, are discussed. Furthermore, the effect of these agents in altering mortality and morbidity in a controlled, random study of animal head injury is presented.

Animals↗
PubMed1979

Alterations in cat cerebrocortical capillary morphometrical parameters following K+-induced cerebrocortical swelling.

Histochemical, electron microscopic, and morphometrical techniques were employed in the determination of the effects attributed to K+-induced cerebrocortical swelling on cat cerebrocortical capillary diameter, length, surface area, volume, and minimal intercapillary distance. Bilaterally exposed and intact temporoparietal cerebral cortices of 4 conditioned adult cats were simultaneously superfused with isotonic, artificial CSF containing 3.5 mM K+ (control) and 54 mM K+ experimental), for 1h at 37 degrees C with monitoring of systemic vital function, hematocrit, arterial blood gases, and determination of cerebrocortical tissue water content. The mean values for cerebrocapillary diameter were 5% (P less than 0.05) greater in swollen tissues when compared with comparable mean values determined for controls. The values for minimal intercapillary distance determined from control and experimental animals plotted as relative frequency histograms represented two distinct populations (P less than 0.005). The significance of altered capillary morphometric parameters are discussed in relation to K+-induced cerebrocortical swelling.

Animals↗
PubMed1979

Cytologic observations on axotomized feline Betz cells. 1. Qualitative electron microscopic findings.

Adult cats survived left lateral funiculotomy 1 to 153 days. The pericruciate cortex was studied electron microscopically in these as well as sham-operated and unoperated animals. Ten days after surgery Betz cells of the right pericruciate cortex displayed disaggregation of cytoplasmic ribosomes; random dispersal and degranulation of the normally compact arrays of cisterns of rough ER; in some cells perinuclear and peripheral disposition of remaining Nissl bodies; retispersion of the Golgi apparatus; and, uncommonly, neurofilamentous hyperplasia. Fourteen days postoperatively cytoplasmic ribosomes were largely regrouped in rosette arrangements and Golgi membranes were evenly distributed in the cytoplasm. Further reversion of the ER toward a normal appearance occurred 28 days postoperatively but substantial perikaryal atrophy had supervened in many neurons by 49-153 days after surgery. Evidence of nerve cell death was not found. Concentric membranous arrays derived from ER and associated with autophagic bodies and mitochondria were identified in dendrites of normals and cats that had been operated upon, perhaps more frequently contralateral to the spinal operation. Electron-dense and electron-lucent degenerative changes in dendrites also occurred, especially early after operation. Degenerating myelin sheaths were detected in the pericruciate cortex of animals that had been operated upon and sometimes were captured in the process of phagocytosis by oligodendrocytes as well as astrocytes and microglia. The long-term persistence of axotomized Betz cells, albeit in an atrophic state, and the reversibility of some of the cytologic responses to axon injury suggest that these neurons may retain a capacity for axon regeneration that could be mobilized, as by pharmacologic means.

Animals↗
PubMed1979

Cytologic observations on axotomized feline Betz cells. II. Quantitative ultrastructural findings.

Quantitative electron microscopic examination was made of Betz cells of two unoperated cats as well as cats subjected to left lateral funiculotomy 5, 10, 28 and 49 days before sacrifice. The percent cytoplasmic composition of chromatolyzed, right-sided Betz cells contributed by cisternal elements of RER, Golgi apparatus and dense bodies and the percent perikaryal membrane apposed by subsurface cisterns were unchanged from the normal despite marked qualitative alterations of the cytoplasm. However, 49 days postoperatively mitochondrial numerical density of axotomized, right-sided Betz cells was significantly less than at 0, 10 and 28 days post funiculotomy. Importantly, normal-appearing Betz cells ipsilateral to corticospinal tract section showed an increase in mitochondrial numerical density 5 days postoperatively. Operation did not induce change in the % perikaryal coverage by axosomatic boutons. Retraction of axosomatic boutons, though often reported for other neuronal populations undergoing axon reaction, is not a necessary feature of the axon reaction of feline Betz cells.

Animals↗
PubMed1979

Clinical recovery from Schilder disease.

A 7-year-old girl presented with progressive dementia. 99-mTechnetium pertechnetate brain imaging and flow, cerebral angiograms, and a pneumoencephalogram revealed a large, bilateral frontal lesion that crossed the corpus callosum. At surgery, the consistency of affected brain tissue was soft. The histologic diagnosis was Schilder disease. Postoperatively, prednisone therapy was initiated because of clinical evidence of increased intracranial pressure, including funduscopic change. Within 4 months, the prednisone was discontinued, and the child completed the school year at the top of her class. Three years later she continued to function as a superior student, without demonstrable clinical neurologic abnormality.

Brain↗
PubMed1978

Abnormal ultrastructural appearances in axons of feline pericruciate cortex after lateral funiculotomy.

Following left lateral funiculotomy, axons of cat pericruciate cortex exhibited neurofilamentous hyperplasia and complex, adaxonal, oligodendrocytic invaginations into electron-lucent or (commonly) electron-dense, degenerating axoplasm. These changes were absent form sham-operated and unoperated animals. Neurofilamentous hyperplasia was exclusively right-sided and appeared in myelinated axons 5--49 days postoperatively and in nonmyelinated axons 14--153 days after surgery. Oligoglial invaginations were present 1--49 days after surgery and were predominantly right-sided. Intramyelinic, axo-dendritic synapses appeared in operated cats 5--10 days postoperatively. Intra-axonal accumulations of ribosomes were found also. These changes also occurred exclusively or predominantly contralateral to spinal surgery. Other ultrastructural abnormalities, e.g., amorphous transformation of axoplasm and accumulations of dense bodies in intra-myelinic, dark cytoplasm, had a less certain relationship to lateral funiculotomy. The axonal alterations that were limited to operated cats possibly represent a true retrograde axonal degeneration occurring at a distance from the site of axonic interruption and unaccompanied by evidence of nerve cell death.

Animals↗
PubMed1978

5'-Nucleotidase of microglial cells in the facial nucleus during axonal reaction.

Transection of the facial nerve causes proliferation of microglial cells in the facial nucleus. The miroglial cells can be seen in perineuronal and perivascular positions. A high activity of 5'-nucleotidase is demonstrated cytochemically in the plasma membranes of these cells. The increase of enzymatic sites for the production of adenosine during axonal reaction might be of functional significance for the regenerating motor neuron.

Animals↗
PubMed1978

Periodic respiration in erect posture in Shy-Drager syndrome.

Tilt-table polygraphic study in four patients with Shy-Drager syndrome demonstrated periodic apnoea in the erect posture. In one patient reduced hypercapneic ventilatory response and necropsy findings of neuronal loss and astrocytosis in the pontine tegmentum suggested dysfunctional respiratory neurones in the brainstem. One patient had Cheyne-Stokes respiration during the late stage of the illness.

Apnea↗