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Biomedical subjects

H C Powell

Publications and source records attributed to H C Powell.

At least 73 records · Page 4Linked to original sources
PubMed1988

Ultrastructural and morphometric analysis of long-term peripheral nerve regeneration through silicone tubes.

Light and electron microscopy were used to investigate long-term regeneration in peripheral nerves regenerating across a 10 mm gap through silicone tubes. Schwann cells and axons co-migrated behind an advancing front of fibroblasts, bridging the 10 mm gap between 28 and 35 days following nerve transection. Myelination of regenerated fibres started between 14 and 21 days after transection and occurred in a manner similar to that reported during development. Although these early events were successful in producing morphologically normal-appearing regenerated fibres, complete maturation of many of these fibres was never achieved. Axonal distortion by neurofilaments, axonal degeneration and secondary demyelination were seen at 56 days following nerve transection. These changes progressed in severity with time as more axons advanced through the distal stump towards their peripheral target. Since regeneration occurs in the absence of endoneurial tubes, and because constrictive forces act on the nerve during regeneration, we suggest that these extrinsic factors limit the successful advancement of axons through the distal stump to their target organ.

Animals↗
PubMed1988

Proximodistal gradient in endoneurial fluid pressure.

Endoneurial fluid pressure measurements were made in the interstitial space of rat L5 dorsal root ganglia and in the corresponding sciatic nerves. Endoneurial fluid pressure was always higher in the ganglia than in the paired distal nerve. This proximodistal gradient in endoneurial fluid pressure may be the driving force responsible for the proximodistal convection of endoneurial fluid.

Animals↗
PubMed1988

Dose-dependence of endoneurial fluid sodium and chloride accumulation in galactose intoxication.

Endoneurial edema in galactose neuropathy was studied in a colony of Sprague-Dawley rats fed diets containing 0%, 10%, 20% or 40% D-galactose for approx. 200 days. Endoneurial fluid was analyzed by X-ray microanalysis for electrolyte concentration, by microgravimetry of whole nerve segments for water content, by measurement of endoneurial fluid pressure and by morphometry in transverse sections of nerve. Galactose intoxication resulted in dose-dependent increases in endoneurial fluid sodium and chloride that were directly associated with increases in nerve water content and endoneurial fluid pressure. The presence of edema and its dose-dependence was also confirmed by morphometric analysis of sciatic nerves at the light microscopic level. The data demonstrate that electrolyte-induced osmotic imbalances in endoneurial fluid are dependent on the amount of galactose ingested and suggest that the dose-related accumulation of sodium and chloride in endoneurial fluid contributes substantially to the pathogenesis of galactose neuropathy.

Animals↗
PubMed1988

Monoclonal antibody defines determinant between Theiler's virus and lipid-like structures.

Theiler's murine encephalomyelitis virus is known to cause a chronic demyelinating disease in mice. The contributions of immunologic factors, i.e. humoral and cellular responses to virus and/or myelin components, and direct virus-cell interactions leading to demyelination are still unclear. One important factor could be antibody initiation of myelin destruction. Here we describe four monoclonal antibodies that react with Theiler's murine encephalomyelitis virus. Three of these neutralize the virus and one of these three could also bind to various lipid-like structures including galactocerebroside, a myelin component. Further, this monoclonal antibody reacted with oligodendrocyte-like cells in vitro. All four monoclonal antibodies reacted with VP-1 by Western blot analysis. Thus, an immune response generated by virus that cross-reacts with a myelin element such as galactocerebroside could play a role in directing autoimmune processes toward myelin destruction.

Animals↗
PubMed1988

Selective vulnerability of unmyelinated fiber Schwann cells in nerves exposed to local anesthetics.

When peripheral nerves of experimental rats are exposed to local anesthetics, distinctive and reproducible pathologic changes occur involving the perineurial sheath and endoneurial contents. Application of intermediate strength concentrations of the local anesthetics, 2-chloroprocaine, lidocaine, etidocaine, and intermediate or high concentrations of procaine to the surface of rat sciatic nerves resulted in the following changes. By 48 hours, the perineurial sheath exposed to the drug was disrupted and became permeable to granulocytes which infiltrated the subjacent endoneurium in conjunction with edema formation in the endoneurial interstitium. Application of 10% procaine to exposed nerve resulted in extensive demyelination. The most striking pathologic change occurring with either intermediate or high doses was accumulation of lipid droplets in Schwann cells, a phenomenon that occurred often in myelin-producing Schwann cells but much less frequently in unmyelinated fiber Schwann Cells. Lipid accumulation appears to be one of several reactive changes that affect Schwann cells of myelinated fibers and is dose-dependent. On the other hand, while reactive changes were infrequently seen in unmyelinated fiber Schwann cells, these cells appeared more susceptible to injury as shown by electron microscopy. Injury to Schwann cells by local anesthetics is temporary because these cells can replicate quickly. Autoradiographic studies of thymidine incorporation 1 week after procaine administration to the sciatic nerve showed intense proliferation of Schwann cells, but no such activity in controls. These findings support the view that their neurotoxic properties may account in some part for the function of local anesthetics, that Schwann cells of small unmyelinated fibers are more vulnerable to these agents than those of myelinated fibers, and that destruction of their supporting cells is followed by vigorous mitotic activity in the endoneurium.

Anesthetics, Local↗
PubMed1987

Giant axonal neuropathy: correlation of clinical findings with postmortem neuropathology.

We report the clinical and postmortem neuropathological findings in a case of long-standing giant axonal neuropathy. The patient, a caucasian male with kinky hair, was first seen at 4 years of age because of increasing unsteadiness of gait. Clinical examination showed nystagmus, cerebellar ataxia, distal sensory loss, and weakness. A sural nerve biopsy at 8 years of age revealed giant axonal neuropathy. The patient became increasingly demented and was incapacitated by weakness and ataxia; he died at 18 years of age. Histological examination of the brain and spinal cord showed numerous Rosenthal fibers, a distal axonopathy that most severely affected the corticospinal tracts, middle cerebellar peduncles, and posterior columns, and olivocerebellar degeneration.

Adolescent↗
PubMed1987

Relationship of adjuvants and swine influenza vaccine to experimental neuropathy in rabbits.

Experimental neuropathy, characterized by endoneurial edema and demyelination, was induced by inoculating rabbits with a combination of Freund's complete adjuvant (FCA), gangliosides, lecithin and cholesterol. A less severe demyelinating neuropathy could be induced by treatment with FCA alone but no significant change could be elicited by injection of swine influenza vaccine (SFV) alone. When FCA was combined with gangliosides, lecithins, cholesterol and SFV, neuropathy occurred, but the changes were less severe than if these agents were used without SFV. Sera were tested for myelin basic protein (MBP) and galactocerebroside (GC) antibodies in each experimental group. Neither SFV alone nor SFV combined with Freund's complete adjuvant, gangliosides, cholesterol and lecithin evoked significant antibody titers to MBP or GC. However, rabbits inoculated with FCA, gangliosides, lecithin and cholesterol had rising titers of antibody to both MBP and GC over the 3-month experimental period. One rabbit inoculated with FCA alone had significant antibody to MBP. The findings suggest that Freund's complete adjuvant alone can induce demyelination in the peripheral nerves of rabbits and that SFV may modulate the immune response acting either as an adjuvant or suppressant in the experimental demyelinating disease.

Animals↗
PubMed1987

Node of Ranvier formation along fibres regenerating through silicone tube implants: a freeze-fracture and thin-section electron microscopic study.

Thin-section and freeze-fracture electron microscopy have been used to examine the morphogenesis of the node of Ranvier in peripheral nerves regenerating through silicone tubes. A major question posed by this study is whether node formation in fibres regenerating across a gap recapitulates that occurring in normal development. Node formation occurs concurrently with myelination and follows a similar spatial gradient of progression from a proximal to distal direction along the regenerated nerve. Presumptive nodal sites appear prior to myelin formation and are identified as a prominent subaxolemmal density in thin sections and axonal particle patches in freeze-fracture. Following the appearance of presumptive nodes in regenerating fibres, dimeric particles are inserted into the axolemma adjacent to the node. These particles are in close apposition to the overlying Schwann cell terminal processes and with maturity adopt the same circumferential orientation seen in adult nodes. The nodal axolemma of regenerating fibres shows a characteristic increase in the prominence of its subaxolemmal densification and number of heterogeneously sized particles. Mature regenerated nodes demonstrate a complete annulus of nodal particles indistinguishable from control nodes. The results of the present study show that the nodal architecture of regenerating fibres is a faithful reconstruction of normal mature nodes, thus indicating that the morphological correlates associated with saltatory conduction at the node are present in regenerated nodes.

Animals↗
PubMed1987

Peripheral nerve demyelination in rabbits after inoculation with Freund's complete adjuvant alone or in combination with lipid haptens.

The pathology of demyelination in rabbits with experimental allergic neuritis (EAN) or galactocerebroside-induced neuritis was compared to that in rabbits inoculated with either an emulsion of lipid haptens (gangliosides, lecithin and cholesterol) and Freund's complete adjuvant or Freund's complete adjuvant (FCA) alone. In rabbits inoculated with bovine peripheral myelin in FCA, perivenular demyelination associated with infiltrates of lymphocytes and macrophages occurred after 30 days, while those animals inoculated with galactocerebroside (GC) in Freund's adjuvant did not develop lesions until 60-90 days. GC rabbits had demyelination and severe nerve edema without cellular infiltrates. In rabbits inoculated with FCA alone, demyelination was restricted to ganglia and proximal nerve roots. Myelin basic protein (MBP) and GC antibodies from EAN, GC and lipid hapten-inoculated rabbits were detected by ELISA in sera at all post-inoculation time points. Appreciable P0 and P2 antibody titers were detected only in EAN animals. The results indicate that Freund's complete adjuvant alone or in combination with lipid haptens is capable of producing neuropathic effects in the rabbit independent of those produced by EAN or galactocerebroside neuritis.

Animals↗
PubMed1987

Acute ascending necrotizing myelopathy caused by herpes simplex virus type 2.

A 57-year-old diabetic man died of a rapidly ascending necrotizing myelitis. Autopsy results proved that the etiologic agent was herpes simplex virus type 2 (HSV2). The clinical findings, autopsy immunohistopathology, and electron-microscopy suggest that either primary HSV2 infection or reactivation of HSV2 infection within dorsal root ganglia was followed by spread to the spinal cord. Viral infection of the CNS occurred by direct extension and led to death by involvement of the brainstem. Although there is only one previous report of HSV2 myelitis in the literature, our findings suggest that HSV2 might be a more common etiologic agent of necrotizing myelitis. Because CSF cultures are usually negative, viral inclusions are not usually seen, and morphologically identifiable virions are exquisitely rare, previous cases were probably descriptively diagnosed as acute ascending necrotizing myelitis without etiologic identification.

Brain↗
PubMed1987

Intracysternal crystalline cytoplasmic inclusions in a cardiac myxoma.

Electron microscopy of an atrial myxoma removed at surgery from a 56-year-old woman revealed unusual intracysternal inclusions in the cytoplasm of tumor cells. These structures appeared in the rough endoplasmic reticulum and consisted of multilaminar arrays of crystalline plates of regular periodicity, about 10 nm apart. Although crystalline and other intracysternal inclusions may occur in different pathologic disorders, their occurrence in an atrial myxoma is a hitherto unreported observation.

Animals↗
PubMed1986

Delayed nerve regeneration in streptozotocin diabetic rats.

Nerve regeneration across a 10-mm gap was delayed in streptozotocin diabetic rats 3 and 4 weeks after transecting the sciatic nerve. Opposite ends of each cut nerve were introduced into a silicone tube, leaving a 10-mm gap. Electron microscopy was used to evaluate the progress of regeneration in sections at 2-mm intervals across the 10-mm gap. After 3 weeks, control axons had bridged the 10-mm gap, and myelin sheaths extended for 6-8 mm. By contrast, axons and their myelin sheaths were seen no further than 2 mm from the proximal stump in diabetic animals. By 4 weeks, axons had bridged the gap in diabetics; however, they appeared immature and showed dystrophic changes. The findings suggest that although regeneration does occur in diabetic nerves, it is significantly delayed and qualitatively impaired.

Animals↗
PubMed1986

Endoneurial sodium accumulation in galactosemic rat nerves.

Microdrop samples of endoneurial fluid and serum from galactosemic rats were analyzed with energy dispersive spectrometry (EDS). The sodium concentration of endoneurial fluid from galactose-fed rats (295 meq/liter) was nearly twice that of age-matched controls (152 meq/liter) and indicates that sodium is present in an osmotically significant concentration that is capable of causing the edema and increased endoneurial fluid pressure (EFP) associated with galactose neuropathy. It is suggested that accumulation of endoneurial sodium is linked to the movement of sugar into the endoneurium.

Animals↗
PubMed1986

Guillain-Barré syndrome associated with Hashimoto's thyroiditis.

A 73-year-old patient developed tetraplegia, cranial neuropathies and autonomic instability and died of clinical complications of Guillain-Barré syndrome. He was incidentally found to have subclinical Hashimoto's thyroiditis. The literature since 1966 is reviewed for the association of Guillain-Barré syndrome with thyroiditis, other endocrine abnormalities, and some diseases thought to be caused by autoimmune mechanisms.

Aged↗
PubMed1986

Edema and increased endoneurial sodium in galactose neuropathy. Reversal with an aldose reductase inhibitor.

Galactose neuropathy was produced in rats by feeding a diet containing 30% D-galactose. After 12 weeks of galactose ingestion, all rats developed bilateral cataracts, polydypsia and polyuria. These galactose-intoxicated animals were divided into two groups that both continued with the galactose diet: animals that were treated with the aldose reductase inhibitor, ICI 128,436, for 4-6 weeks, and a control group of animals that received just excipient. At the end of the study, endoneurial fluid pressures, nerve water contents and endoneurial fluid electrolyte concentrations were determined from sciatic nerves of treated and untreated animals. The extent of neuropathy in each animal was evaluated by light microscopy. Treatment of galactose-intoxicated rats with ICI 128,436 restored to normal levels the elevated endoneurial sodium concentration, increased water content and interstitial fluid pressure characteristic of galactose neuropathy. These results, obtained with an agent that blocks the sorbitol pathway, associate elevated sodium with an osmotic force contributing to edema and increased endoneurial fluid pressure in galactose neuropathy and suggest that endoneurial sodium levels are linked to blood-sugar concentration.

Animals↗