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At least 19 recordsLinked to original sources
PubMed1989

Light-induced retinal degeneration in rdgB (retinal degeneration B) mutant of Drosophila: electrophysiological and morphological manifestations of degeneration.

Quantitative light and electron microscopy was used to monitor the extent of retinal degeneration as a function of age and temperature in the white-eyed rdgBKS222 mutant of Drosophila melanogaster. Parallel measurements of the electroretinogram (ERG) of the degenerating retina reveal a new phenomenon--the appearance of spike potentials following illumination with bright light. These spikes, which do not appear in the normal fly retina, have a relatively long duration (20-50 ms), regenerative properties, and a rate of occurrence which increases with increasing light intensity. The spikes differed from the light response in being more susceptible to CO2 and to cuts in the eye. The spikes completely disappeared at low extracellular Ca2+ levels which did not reduce the amplitude of the light response. The spike potentials become triphasic when the recording electrode is advanced to the level of the basement membrane. This suggests that the spike potentials originate from the photoreceptor axons as a result of synchronous opening of voltage-dependent channels in a large number of photoreceptor cells. The occurrence of spike potentials during the process of degeneration was studied. Two pahses can be distinguished: (1) Spike potentials appear in retinae of 2-3-day-old flies which display few morphological signs of degeneration. The frequency of appearance of spike potentials decreases in retinae of 14-16-day-old flies which show extensive degeneration of the R1-6 photoreceptor cells but no degeneration of the central R7,8 cells. (2) Spike potentials appear more frequently again in flies of 22-24 d of age. This is probably a consequence of degeneration of the remaining R7,8 photoreceptor cells. Temperature and the light-dark cycle had a critical effect on degeneration. Eight-day-old mutants raised at 19 degrees C in a normal light-dark cycle showed only little degeneration. Eight-day-old mutants raised at 24 degrees C showed only a slight degeneration when raised in the dark. However, the degree of degeneration was greatly enhanced in the mutants raised at 24 degrees C under a light-dark cycle regime. The combined electrophysiological and morphological study of the degeneration, as a function of age and temperature, revealed that (1) the degeneration process takes place even in darkness, but at a slow rate, while light greatly accelerates the degeneration. (2) The degeneration is negligible at 19 degrees C, even during light, in the first week after eclosion.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2000

Antioxidant vitamin and mineral supplements for age-related macular degeneration.

BACKGROUND: It has been proposed that antioxidants may prevent cellular damage in the retina by reacting with free radicals produced in the process of light absorption. OBJECTIVES: The objective of this review is to assess the effects of antioxidant vitamin and/or mineral supplementation on the progression of age-related macular degeneration. SEARCH STRATEGY: The Cochrane Eyes and Vision Group specialised registered, the Cochrane Controlled Trials Register - Central, MEDLINE, the Science Citation Index, and the reference lists of relevant articles were searched. Investigators of included studies were contacted. The most recent searches were performed in December 1999. SELECTION CRITERIA: All randomised trials comparing an antioxidant vitamin and/or mineral supplement (alone or in combination) to control in people with age-related macular degeneration were included. DATA COLLECTION AND ANALYSIS: The reviewer extracted data and assessed trial quality. Due to the small number of trials identified, and variable methods of collecting and presenting outcome data, no statistical summary measure was calculated. MAIN RESULTS: Four published, two unpublished and two ongoing trials were identified. Published trials to date have been small and results inconsistent. Adverse effects and quality of life for people with age-related macular degeneration have not been addressed. REVIEWER'S CONCLUSIONS: The question as to whether people with age-related macular degeneration should take antioxidant vitamin or mineral supplements to prevent progression of the disease has not been answered by research to date. The results of ongoing trials are awaited.

Antioxidants↗
PubMed2000

Photodynamic therapy for neovascular age-related macular degeneration.

BACKGROUND: In neovascular age-related macular degeneration, new vessels grow under the retina, distorting vision and leading to scarring. This is further exacerbated if the blood vessels leak. Photodynamic therapy, originally used in cancer treatment, has been investigated as a way to treat the neovascular membranes without affecting the retina. OBJECTIVES: The aim of this review is to examine the evidence for the safety and effectiveness of photodynamic therapy in the treatment of neovascular age-related macular degeneration. SEARCH STRATEGY: We searched for trials in the Cochrane Eyes and Vision Group trials register (available in the Cochrane Controlled Trials Register), the Cochrane Controlled Trials Register, Medline and Embase. We used the Science Citation Index to search for reports that cited identified relevant study reports. We contacted experts in the field for further trials information, and we searched the reference lists of identified relevant studies for further trial reports. Searches were conducted in December 1999. SELECTION CRITERIA: We included randomised trials of photodynamic therapy in people with choroidal neovascularisation due to age-related macular degeneration. DATA COLLECTION AND ANALYSIS: Two reviewers extracted the data independently. Meta analysis was not performed. MAIN RESULTS: One published trial was identified. Outcome data were available at 12 months after the first treatment. Patients received an average of 3.7 treatments. The relative risk of losing three or more lines of visual acuity at 12 months comparing the intervention with the control group was 0.72 (95% confidence interval 0.61 to 0.86). The relative risk of losing six or more lines of visual acuity at 12 months comparing the intervention with the control group was 0.62 (95% confidence interval 0.44 to 0.87). Subgroup analyses suggest that the benefits may be confined to people with no occult choroidal neovascularisation. REVIEWER'S CONCLUSIONS: Photodynamic therapy in people with classic choroidal neovascularisation due to age-related macular degeneration is effective in preventing visual loss. This evidence is drawn from a subgroup analysis of 143 participants in one trial. Outcomes and potential adverse effects of this treatment should be monitored closely. There is no evidence that photodynamic therapy is beneficial for people with evidence of occult choroidal neovascularisation. These people should be offered treatment in the context of a randomised trial.

Humans↗
PubMed1977

Time dependence of terminal degeneration in spino-cerebellar mossy fiber rosettes in the chicken and the application of terminal degeneration in successive degeneration experiments.

Mossy fiber rosettes in the granular layer of the cerebellar cortex were studied after sections of the lateral funiculus of the spinal cord of the chicken and silver impregnation with the Fink-Heimer ('67) method I. After a survival time of two or three days two types of degenerated rosettes were found. The first type is characterized by digitiform protrusions, the second type of rosette is spherical. Both types are covered by small argyrophilic particles which disappear when the degeneration proceeds. With longer survival times the rosettes become swollen and finally disintegrate and lose their argyrophilia. After a survival time of 30 days only debris of rosettes can be found. These observations were used to determine the cerebellar cortical projection mossy fibers originating from segments of the spinal cord isolated in "successive degeneration" experiments consisting of a chronic cordotomy followed by an acute cordotomy rostral to the first one.

Animals↗
PubMed1989

Chemically induced retinal degeneration in the rdgB (retinal degeneration B) mutant of Drosophila.

Chemicals which affect different steps of the phototransduction cascade were used to identify the site of action of the rdgB gene product of Drosophila. In the rdgB mutant, the photoreceptor cells degenerate after several days of exposure to light, whereas raising the flies in the dark largely prevents the degeneration. In the rdgBKS222 mutant, which was used in the present studies, the light-induced degeneration is characterized by (1) selective degeneration of the peripheral but not the central photoreceptor cells; (2) random distribution of degenerated cells among ommatidia; and (3) the degeneration is specific to the rdgB but not the wild-type photoreceptor cells. In the present study, we show that application of specific chemical agents to the eyes of rdgBKS222 flies in the dark mimics the effects of light and causes retinal degeneration indistinguishable from light. The agents used in these studies are the metabolically stable GTP analogs GTP gamma S and Gpp(NH)p as well as fluoride ions, which are known to activate the transducing guanine nucleotide binding protein (G-protein of fly photoreceptors). It is unlikely that the chemically induced retinal degeneration is mediated by effects on energy metabolism, since application of the metabolic inhibitors CN- and 2-deoxy-D-glucose did not increase the extent of retinal degeneration over that observed in control flies treated with Ringer solution. The GDP analog GDP beta S, which inhibits G-protein activity, greatly reduced the extent of retinal degeneration in the dark, over that observed in control flies treated with Ringer solution. These results suggest that activation of the G-protein precedes the step in the transduction cascade that leads to retinal degeneration and provides a powerful tool to investigate the molecular mechanism of light-induced degeneration in the rdgB mutant.

Animals↗
PubMed1989

Degeneration of neurons in the thalamic reticular nucleus following transient ischemia due to raised intracranial pressure: excitotoxic degeneration mediated via non-NMDA receptors?

Transient global ischemia was produced in rats by cisternal fluid infusion, producing a negative cerebral perfusion pressure by elevating the intracranial pressure (ICP) 25-50 mm Hg above mean arterial pressure (MAP). Animals were allowed to survive for 2-7 days following a transient ischemic episode of 5-30 min. The brains were examined for signs of ischemic degeneration in Nissl-stained sections and adjacent sections reacted with antisera against glial fibrillary acidic protein (GFAP) or aspartate aminotransferase (AAT). Neurons in the thalamic reticular nucleus (RT), a pure population of gamma-aminobutyric acid (GABA)ergic neurons which project their axons to thalamic relay nuclei, were found to have the lowest threshold for degeneration in this model, consistently undergoing degeneration under conditions which completely spared the hippocampal CA1 from degeneration. Whereas it took up to 30 min of complete ischemia to produce degeneration of CA1 neurons when ICP was raised using room temperature infusion fluids, 15 min of ischemia under these conditions was sufficient to produce extensive degeneration of neurons in the entire ventral 3/4 of the RT. Prolonged (greater than 25 min) episodes of partial ischemia (ICP less than or equal to MAP) were also sufficient to produce massive degeneration of RT neurons. The lesion in the RT was most clearly evident in sections reacted with antisera to GFAP, labeling intensely reactive protoplasmic astrocytes within the regions of the RT where neuronal degeneration had occurred. Neuronal loss and accompanying proliferation of microglial cells were evident in Nissl-stained sections but the extent of the neuronal loss was most clearly obvious in sections reacted with an antisera to AAT, an enzyme present in detectable quantities in GABAergic neurons. Pretreatment with the non-competitive NMDA antagonist MK-801 at doses sufficient to completely prevent massive degeneration of the hippocampal CA1 failed to prevent the degeneration of RT neurons, suggesting that if RT degeneration involves an excitotoxic process it acts through non-NMDA receptors.

Animals↗
PubMed2000

Evidence that Wallerian degeneration and localized axon degeneration induced by local neurotrophin deprivation do not involve caspases.

The selective degeneration of an axon, without the death of the parent neuron, can occur in response to injury, in a variety of metabolic, toxic, and inflammatory disorders, and during normal development. Recent evidence suggests that some forms of axon degeneration involve an active and regulated program of self-destruction rather than a passive "wasting away" and in this respect and others resemble apoptosis. Here we investigate whether selective axon degeneration depends on some of the molecular machinery that mediates apoptosis, namely, the caspase family of cysteine proteases. We focus on two models of selective axon degeneration: Wallerian degeneration of transected axons and localized axon degeneration induced by local deprivation of neurotrophin. We show that caspase-3 is not activated in the axon during either form of degeneration, although it is activated in the dying cell body of the same neurons. Moreover, caspase inhibitors do not inhibit or retard either form of axon degeneration, although they inhibit apoptosis of the same neurons. Finally, we cannot detect cleaved substrates of caspase-3 and its close relatives immunocytochemically or caspase activity biochemically in axons undergoing Wallerian degeneration. Our results suggest that a neuron contains at least two molecularly distinct self-destruction programs, one for caspase-dependent apoptosis and another for selective axon degeneration.

Animals↗
PubMed1985

Degeneration of thalamic neurons in "Purkinje cell degeneration" mutant mice. I. Distribution of neuron loss.

The Purkinje cell degeneration (pcd) mutation of the mouse is an autosomal recessive allele which previous studies have shown to be the cause of rapid degeneration of nearly all cerebellar Purkinje cells between 18 and 30 postnatal days of age (P18-P30), and slowly developing, progressive losses of retinal photoreceptor cells and mitral cells of the olfactory bulb. Through examination of serial frozen sections alternately stained for Nissl substance and for degenerating neuronal processes, we have found that discrete populations of thalamic neurons degenerate rapidly between P50 and P60. Severely affected nuclei, in which a majority of neurons degenerate, include the central division of the mediodorsal nucleus, the ventral medial geniculate, posterior, posterior ventromedial, and submedial nuclei, and those portions of the ventrolateral and posteromedial nuclei which immediately surround the medial division of the ventrobasal complex. More subtle cell losses occur during the same time period in restricted portions of the lateral ventrobasal, dorsal lateral geniculate, and lateral posterior nuclei, but even at P180 these nuclei are not markedly atrophic. No common denominator among target cell populations has been established. The pcd allele affects a diverse assortment of specific relay nuclei; degeneration has not been recognized in thalamic nuclei characterized primarily or exclusively by subcortical projections or by cortical projections directed relatively selectively to superficial or deep cortical laminae. The neuronal degenerations in the thalamus are not precipitated by prior or concurrent degeneration of cortical targets or afferent sources, though striking transneuronal changes, including cell death, do develop following thalamic neuronal degeneration in this mutant. No previously described murine mutant phenotype includes the rapid degeneration of highly restricted neuronal populations beginning at these relatively advanced ages.

Aging↗
PubMed1977

[Vitelline macular degeneration and Best's macular degeneration are the same disease (author's transl)].

In 1905 F. Best had discovered infantile macular degeneration with dominant transmission, later named after him. From Best's pedigree 19 members could be examined by us. Besides the usual examination-methods, EOG, ERG, Fluorescein-Angiography and Chromato-Ophthalmoscopy were applied. In this way the characteristic findings of vitelline macular degeneration could be demonstrated. 7 family-members were typically affected according to their ages. 2 of them were found to be carriers with normal macula; they had however a pathological EOG. The question, if the diagnosis of Best's macular degeneration should be used further in the system of the hereditary macular degenerations or whether it is indeed the same disease as vitelline macular degeneration, is discussed. Best's macular degeneration and vitelline macular degeneration are synonymous. We recommend, that the term vitelline macular degeneration ought to be used intead of Best's macular degeneration. It remains F. Best's merit, that this disease has been recognised and des

Adolescent↗
PubMed1995

Müller cell changes precede photoreceptor cell degeneration in the age-related retinal degeneration of the Fischer 344 rat.

Previously, we have used descriptive pathology and histomorphometry, as well as functional testing to characterize the age-related retinal degeneration in the Fischer 344 rat. These studies suggested an association between Müller cells and photoreceptor cells in this process. The purpose of the present study was to further investigate the respective roles of these cell types in the development and progression of the retinal degeneration. Retinas from male Fischer 344 rats aged 3-24 months were first studied by light and electron microscopy. Since Müller cells abundantly express GFAP during pathological states, GFAP content was studied by immunocytochemistry and by immunoblotting following one- and two-dimensional gel electrophoresis. Microscopically, at 12 months, Müller cells showed a gradient of immunoreactivity for GFAP that was minimal in the central retina, positive for their radial processes in the equator, and abundantly expressed in the periphery. At this age, the photoreceptor cells were just beginning to degenerate in the far periphery, while they appeared healthy in the equatorial and central regions. By 24 months, Müller cell hypertrophy was seen in the peripheral regions where photoreceptor cell degeneration was most severe, while the immunoreactivity of the Müller cell processes spread further toward the central regions, ahead of the degeneration of the photoreceptor cells. Thus, Müller cell changes actually preceded photoreceptor degeneration in time and location. This phenomenon was confirmed by measurement of GFAP after one- and two-dimensional PAGE. These findings show that Müller cell changes precede chronic photoreceptor cell degeneration in the aging Fischer 344 rat and are consistent with the hypothesis that Müller cell alteration may be the primary mechanism of this age-related retinal degeneration.

Aging↗
PubMed2000

Pathogenesis of axonal degeneration: parallels between Wallerian degeneration and vincristine neuropathy.

Peripheral neuropathies and Wallerian degeneration share a number of pathological features; the most prominent of which is axonal degeneration. We asked whether common pathophysiologic mechanisms are involved in these 2 disorders by directly comparing in vitro models of axonal degeneration after axotomy or exposure to the neurotoxin vincristine. Embryonic rat dorsal root ganglia (DRG) were allowed to extend neurites for 5 days in culture, and then were either axotomized or exposed to 0.01 microM vincristine. Neurites universally degenerated by 3 days after axotomy or after 6 days of vincristine exposure. The neuroprotective effects of a low calcium environment or pharmacologic inhibition of the cysteine protease calpain were compared in these 2 models of axonal degeneration. Addition of EGTA or growth in zero-calcium media provided significant protection against axonal degeneration after either axotomy or vincristine exposure. Treatment with the experimental calpain inhibitor AK295 was equally protective in both models. Chronic exposure to AK295 was not toxic to the cultures. These data suggest that common mechanisms involving calcium and calpains are involved in both axotomy-induced and vincristine-induced axonal degeneration. In addition, calpain inhibition may provide a strategy for preventing axonal degeneration and preserving neurologic function in a variety of PNS and CNS disorders.

Animals↗
PubMed1994

Retinal degeneration in motor neuron degeneration: a mouse model of ceroid lipofuscinosis.

PURPOSE: To evaluate the retinal degeneration of the motor neuron degeneration (mnd) mouse, and to confirm its inheritance pattern and gene location. METHODS: In screening the mnd/mnd mouse for ocular disease, a retinal degeneration was found that was evaluated by serial electroretinography, histology, electron microscopy, indirect ophthalmoscopy, and genetic and linkage analysis. RESULTS: In homozygous mnd mice, photoreceptor and outer nuclear layers show cell loss by 5 weeks after birth. By 2 months, the peripheral retina is preferentially thinner than central retina, and by 6 months the entire retina is reduced in thickness. The electroretinogram was extinguished by 6 months. Transmission electron microscopy at 3 and 6 months showed distinct cytoplasmic inclusions characteristic of the curvilinear profiles seen in human ceroid lipofuscinosis. Genetic analyses show that the retinal degeneration in mnd mice is inherited as a single autosomal gene with recessive expression, and a three-point cross placed the retinal degeneration at the mnd locus on the proximal end of mouse chromosome 8. Crosses with other known strains with retinal degeneration were normal. CONCLUSIONS. The mnd mouse model is similar to the juvenile onset Spielmeyer-Vogt form of ceroid lipofuscinosis (Batten disease), and provides a good model for the retinal degeneration found in these patients.

Alleles↗
PubMed1995

Domoic acid-induced neuronal degeneration in the primate forebrain revealed by degeneration specific histochemistry.

Domoic acid is a potent excitotoxin produced by diatoms which is subsequently passed along the marine food chain. Its chemical structure and toxicological properties are similar to kainic acid. Like kainic acid, exposure results in extensive hippocampal degeneration. The effect of domoic acid on other primate brain structures, however, is less resolved. In an attempt to clarify this issue, the present study applied a degeneration specific histochemical technique (de Olmos' cupric-silver method) to reveal degeneration within the brains of domoic acid-dosed cynomolgus monkeys. Degenerating neuronal cell bodies and terminals were found not only within the hippocampus, but also within a number of other 'limbic' structures including the entorhinal cortex, the subiculum, the piriform cortex, the lateral septum, and the dorsal lateral nucleus of the thalamus. Although the hippocampus is a component of the original limbic circuit of Papez, other components such as the mammillary bodies, the anterior nucleus of the thalamus and the cingulate cortex contained no degeneration, while a number of more recently documented efferent targets of the hippocampal formation revealed extensive degeneration. The pattern of degeneration generally correlated with those regions containing high densities of kainate receptors.

Animals↗
PubMed1998

Rhodopsin mutations as the cause of retinal degeneration. Classification of degeneration phenotypes in the model system Drosophila melanogaster.

Insight into the molecular basis of inherited photoreceptor cell degeneration has been rapidly evolving during the last decade. The Drosophila Rh1 rhodopsin gene was the first gene shown to cause retinal degeneration when mutated. Many more degeneration-causing mutations in genes encoding rhodopsin and other photoreceptor proteins have been isolated since then in both, Drosophila and humans. To date some 70 mutations of the Drosophila Rh1 gene have been isolated, most of them have been characterized at the molecular level, and more than 60% of them cause retinal degeneration. This review lists the known Rh1 mutations that cause retinal degeneration up to April 1998, gives an overview on the ultrastructural and biochemical correlates of photoreceptor cell degeneration, and suggests a system for the classification of degeneration-causing Rh1 mutations.

Amino Acid Sequence↗
PubMed1985

Degeneration of thalamic neurons in "Purkinje cell degeneration" mutant mice. II. Cytology of neuron loss.

The cytology of thalamocortical relay neuron degeneration in the ventral medial geniculate nucleus (vMG) of mice homozygous for the autosomal recessive Purkinje cell degeneration (pcd) mutation has been studied by light and electron microscopy. More limited sampling of the submedial and mediodorsal nuclei suggested that cytological alterations in the vMG were typical of all degenerating thalamic nuclei. The number of vMG neurons in pcd mutants was comparable to controls at and prior to postnatal day 40 (P40). By P60 seventy percent, and by P90 approximately 90%, of the original complement of vMG neurons had degenerated in mutant mice. At P30, the general cytological organization of vMG neurons closely resembled that of neurons in littermate (+/+ or +/pcd) controls, but neurons in mutants were distinguished by the presence of small aggregates of fine granules (approximately 9 nm in diameter) that were commonly associated with otherwise normal cisternae of rough endoplasmic reticulum; neither the number nor the size of these granular aggregates increased in older mutants. By P50 cytoplasmic organelles were curiously distributed in more severely affected neurons: large areas of cytoplasm were occupied exclusively by polysomes, while profiles of endoplasmic reticulum and the Golgi apparatus appeared to be reduced. Before frank degenerative changes were apparent (at P50), all classes of synaptic terminals identified in normal mice were found to have made morphologically normal synaptic contacts on mutant vMG neuron dendrites. In contrast to the homologous nuclear complex in the cat, presynaptic dendrites were not apparent in synaptic glomeruli in wild-type or mutant murine vMG. Cytopathological alterations in the neuropil of P50 and older mutants were dominated by degenerating dendritic profiles; there was no evidence that the loss of thalamic neurons in pcd mutants was associated with synaptic agenesis or dysgenesis or the prior or concurrent degeneration of afferent synaptic terminals.

Aging↗
PubMed1992

Calcium channel blockers inhibit retinal degeneration in the retinal-degeneration-B mutant of Drosophila.

Light accelerates degeneration of photoreceptor cells of the retinal degeneration B (rdgB) mutant of Drosophila. During early stages of degeneration, light stimuli evoke spikes from photoreceptors of the mutant fly; no spikes can be recorded from photoreceptors of the wild-type fly. Production of spike potentials from mutant photoreceptors was blocked by diltiazem, verapamil hydrochloride, and cadmium. Little, if any, effect of the (-)-cis isomer or (+)-cis isomer of diltiazem on the light response was seen. Further, the (+)-cis isomer was approximately 50 times more effective than the (-)-cis isomer in blocking the Ca2+ spikes, indicating that diltiazem action on the rdgB eye is mediated by means of blocking voltage-sensitive Ca2+ channels, rather than by blocking the light-sensitive channels. Application of the Ca(2+)-channel blockers (+)-cis-diltiazem and verapamil hydrochloride to the eyes of rdgB flies over a 7-day period largely inhibited light-dependent degeneration of the photoreceptor cells. Pulse labeling with [32P]phosphate showed much greater incorporation into eye proteins of [32P]phosphate in rdgB flies than in wild-type flies. Retarding the light-induced photoreceptor degeneration in the mutant by Ca(2+)-channel blockers, thus, suggests that toxic increase in intracellular Ca2+ by means of voltage-gated Ca2+ channels, possibly secondary to excessive phosphorylation, leads to photoreceptor degeneration in the rdgB mutant.

Action Potentials↗
PubMedDate not supplied

Degeneration of posterior column nucleus, inferior olivary nucleus and cerebellar cortex: system degeneration of paraneoplastic disease?

Degeneration of the posterior column nucleus, inferior olive, and cerebellar cortex is reported in a cancer patient. A 70-year-old man developed an ataxic gait and rapidly progressive disturbance of deep sensation over six months, followed by an abasic state. Early well-differentiated tubular adenocarcinoma was detected and total gastrectomy was performed. He died due to pulmonary tuberculosis about two years and nine months after the operation. Degeneration of the posterior column nuclei was found, explaining the disturbance of deep sensation noted in the clinical course, although there were few changes in the peripheral nerves, dorsal root ganglia, and spinal cord. Degeneration of the inferior olive and cerebellar corte was also found. Metastatic small cell carcinoma was present in the right pulmonary hilar and paratracheal lymph nodes at autopsy without any detectable primary focus. There was neither recurrence nor metastasis of the gastric carcinoma. This is the first case report of this type of central nervous system degeneration in a cancer patient, and its pathogenesis and etiology remain obscure. We discuss whether system degeneration or paraneoplastic degeneration was the etiology.

Adenocarcinoma↗