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Biomedical subjects

A W Clark

Publications and source records attributed to A W Clark.

At least 73 records · Page 4Linked to original sources
PubMed1982

Paraplegia following intrathecal chemotherapy: neuropathologic findings and elevation of myelin basic protein.

An 11-year-old boy developed a severe myelopathy after an eight-year history of acute lymphoblastic leukemia and numerous courses of intrathecal chemotherapy. Myelin basic protein in the cerebrospinal fluid (CSF) was elevated. Neuropathologic examination disclosed extensive microvacuolar changes in the white matter of the spinal cord. The pathogenesis of myelopathy following intrathecal chemotherapy administered by lumbar puncture includes an early effect on the myelin sheath. Serial assessment of CSF myelin basic protein levels in patients receiving intrathecal chemotherapy may be useful in the early diagnosis of this disorder.

Antineoplastic Agents↗
PubMed1982

Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain.

Recent evidence indicates that the nucleus basalis of Meynert, a distinct population of basal forebrain neurons, is a major source of cholinergic innervation of the cerebral cortex. Postmortem studies have previously demonstrated profound reduction in the presynaptic markers for cholinergic neurons in the cortex of patients with Alzheimer's disease and senile dementia of the Alzheimer's type. The results of this study show that neurons of the nucleus basalis of Meynert undergo a profound (greater than 75 percent) and selective degeneration in these patients and provide a pathological substrate of the cholinergic deficiency in their brains. Demonstration of selective degeneration of such neurons represents the first documentation of a loss of a transmitter-specific neuronal population in a major disorder of higher cortical function and, as such, points to a critical subcortical lesion in Alzheimer's patients.

Acetylcholine↗
PubMed1982

Neurotoxic effects of cisplatin therapy.

Swelling of the optic disc and loss of tendon reflexes developed in a 3 1/2-year-old girl after 11 high-dose courses of cisplatin (cis-dichlorodiammine platinum [II]) therapy for recurrent sacrococcygeal teratoma. Postmortem examination demonstrated optic disc swelling; the spinal cord showed loss of myelinated fibers and gliosis of the dorsal columns. To our knowledge this case is the first in which the neuropathologic changes associated with cisplatin therapy have been demonstrated by postmortem examination.

Child, Preschool↗
PubMed1982

Unilateral Duane's retraction syndrome (Type 1).

Duane's retraction syndrome (DRS) is a congenital eye movement disorder characterized by adduction deficiency, abduction limitation, globe retraction, and palpebral fissure narrowing on attempted adduction. In a case of unilateral DRS, the right side of the brainstem, cavernous sinus, and orbit were completely normal. The left abducens nucleus contained no cell bodies from motor neurons, but in its rostral portion, it contained several small cell bodies believed to be compatible with internuclear neurons. The left abducens nerve was absent. The left lateral rectus muscle was partially innervated by branches from the inferior oculomotor nerve.

Abducens Nerve↗
PubMed1982

Improved rabbit brain tumor model amenable to diagnostic radiographic procedures.

The VX2 carcinoma was used to create a rabbit brain tumor model. VX2 tumors were chemically dissociated and suspended in liquid medium. Twenty-five microliters of the tumor suspension containing 3 X 10(3), 3 X 10(4), or 3 X 10(5) viable tumor cells were injected through cranial burr holes 6 mm into the right frontoparietal lobes of 17 rabbits. Fifteen of these developed histologically documented nodular intraparenchymal tumors. Tumors were demonstrable with cerebral computed tomographic scans and by cerebral angiography. The feasibility of surgical resection of lesions using the fluorescein staining technique was also demonstrated. This animal brain tumor model is suitable for neuro-oncology research focusing on imaging and therapeutic techniques.

Animals↗
PubMed1982

Neuropathology of the antischistosomal agent amoscanate administered in high oral doses to rats.

Amoscanate is a highly effective antischistosomal agent when administered as a 5% absorbable aqueous suspension. This preparation produces lesions in the brains of young adult rats given extremely high oral doses. Lesions are confined to areas adjacent to the lateral ventricles and are dominated by necrosis of the neuropil of the medial striatum, with relative sparing of bundles of myelinated fibers in the necrotic zone. There is a striking accumulation of calcium-containing microgranules in these areas. The ependyma survives on the ventricular wall overlying the necrotic zone, but pyknosis and increased extracellular space are apparent among ependymal and subependymal cells in the region. Occasionally, fibers of the fornix are focally damaged in immediate proximity to the lateral ventricle; the corpus callosum is rarefied, and microhemorrhages also occur. It is hypothesized that high concentration of the toxic agent in ventricular cerebrospinal fluid plays an important role in pathogenesis. The neuropil of the medial striatum is selectively vulnerable.

Aniline Compounds↗
PubMed1982

Intoxication with beta, beta' -iminodipropionitrile: a model of optic disc swelling.

Human and experimental pathologic studies have suggested that optic disc swelling is due to enlargement of axons in the optic nerve head. Beta, beta' -Iminodipropionitrile (IDPN), a toxin known to produce neurofibrillary swellings in proximal portions of motor and sensory axons, was used to induce axonal lesions in the visual system of guinea pigs and dogs. Funduscopic examination showed progressive optic disc swelling. The axonal swellings, containing maloriented skeins of neurofilaments, appeared initially in the lateral portions of the optic disc; eventually, the majority of axons in the optic disc and in the retinal nerve fiber layer were enlarged. The swellings developed proximal to the level of Bruch's membrane. In addition, myelinated axons in the optic disc and retinal nerve fiber layer developed swellings proximal to the first heminode, demarcating the junction between the unmyelinated/myelinated segments. The retinal ganglion cells remained normal, and there was little axonal degeneration in the distal optic nerve. When beta, beta' -iminodipropionitrile was discontinued, the axonal swellings gradually disappeared.

Animals↗
PubMed1981

Alzheimer disease: evidence for selective loss of cholinergic neurons in the nucleus basalis.

The nucleus basalis of Meynert provides diffuse cholinergic input to the neocortex. When compared with an age- and sex-matched control, the nucleus basalis from a patient with Alzheimer disease demonstrated substantial reduction of neurons. Loss of this neuronal population may represent an anatomical correlate of the well-documented cholinergic derangement in Alzheimer disease.

Aged↗
PubMed1980

Prospective controlled trial of injection sclerotherapy in patient with cirrhosis and recent variceal haemorrhage.

64 patients with cirrhosis and recent variceal haemorrhage were studied in a prospective randomised trial of injection sclerotherapy by means of a flexible oesophageal sheath. 12 (33%) of the 36 patients in the sclerotherapy group, suffered further bleeds from varices compared with 19 (68%) of the 28 patients receiving standard medical treatment. The risk of bleeding per patient-month of follow up decreased more than threefold with sclerotherapy and the number of patients rebleeding after 2, 6, and 12 months was significantly reduced (p < 0.05). 1-year survival without further bleeding improved significantly with sclerotherapy (46% compared with 6%, p < 0.02), although the difference in overall survival assessed by cumulative life-table analysis was not statistically significant. The main complication of the technique was the development of oesophageal ulcers in some patients.

Esophageal Diseases↗
PubMed1980

Bilateral Duane's retraction syndrome. A clinical-pathologic case report.

Duane's retraction syndrome (DRS) is a congenital eye movement disorder characterized by abduction deficiency, adduction limitation, globe retraction, and palpebral fissure narrowing on attempted adduction. Although data from surgical and autopsy studies suggest a neurogenic cause for this disorder, only one well-documented case of DRS has been studied pathologically, and that report was incomplete. We describe the intracranial and orbital pathology of a clinically documented case of bilateral DRS. Both abducens nuclei and nerves were absent from the brainstem, and the lateral rectus muscles were partially innervated by branches from the oculomotor nerves. This report presents evidence that a cranial nerve anomaly may cause DRS. The reason for this neurogenic abnormality is briefly discussed.

Abducens Nerve↗
PubMed1980

Rattlesnake shaker muscle: I. A light microscopic and histochemical study.

Rattlesnake body and shaker muscles were studied using light microscopy and histochemistry. Five myofiber types are distinguishable in the body musculature. The majority are large diameter fast twitch fibers with high alkaline-stable ATPase activity and few mitochondria. In the shaker muscle the major fiber differs from all body fibers in that myofibrils do not entirely fill the fibers. The myofibrils branch repeatedly with one another, which leaves large areas of sarcoplasm devoid of filaments and gives the fibers a characteristic mottled appearance. Mitochondria and glycogen deposits are very numerous. Shaker fibers have high alkaline stable ATPase activity and, in addition, stain intensely for NADH-TR and alpha GPD. Myofibers of the shaker muscle are unusual in that they are extremely fast contracting yet are highly fatigue resistant.

Adenosine Triphosphatases↗
PubMed1980

Rattlesnake shaker muscle: II. Fine structure.

The shaker muscle of the rattlesnake is able to sustain a rate of contraction around 50/sec for at least 3 hr. Most of the muscle is composed of a single, major fiber type which contains large numbers of small myofibrils, abundant sarcomplasmic reticulum, numerous mitochondria, and large deposits of glycogen. The neuromuscsular junction of the major fiber type is extensive with several nerve terminal expansions and junctional folds that are both numerous and deep. The structure of the major fiber type suggests that it must be responsible both for the speed of contraction as well as for the indefatigability of the shaker muscle. The ultrastructure of the much less numerous minor fibers in the shaker muscle suggest that their role may be a tonic one.

Animals↗
PubMed1980

The axonal pathology in chronic IDPN intoxication.

Neurofilamentous axonal swellings occur in a number of degenerative and toxic disorders of the nervous system. In one of these, experimental intoxication with beta, beta'-iminodiproprionitrile (IDPN), accumulation of neurofilaments has been shown to result from a defect in slow axonal transport. The consequence of this functional abnormality is a series of changes in axonal morphology: Neurofilaments accumulate in the proximal axon; the proximal axon becomes swollen; the distal axon loses volume (axonal atrophy). These studies indicate that axonal atrophy occurs secondary to an impairment of slow axonal transport and suggest that a similar abnormality may underlie the pathological changes in certain other degenerative and toxic diseases of the nervous system.

Animals↗
PubMed1978

Slow axonal transport of neurofilament proteins: impairment of beta,beta'-iminodipropionitrile administration.

beta,beta'-Iminodipropionitrile (IDPN) administration prevented normal slow axonal transport of [35S]methionine- or [3H]leucine-labeled proteins in rat sciatic motor axons. Ultrastructural and electrophoretic studies showed that the neurofilament triplet proteins in particular were retained within the initial 5 millimeters of the axons, resulting in neurofilament-filled axonal swellings. Fast anterograde and retrograde axonal transport were not affected. The IDPN thus selectively impaired slow axonal transport. The neurofibrillary pathology in this model is the result of the defective slow transport of neurofilaments.

Axonal Transport↗