The origin of brain macrophages in traumatic lesions, Wallerian degeneration, and retrograde degeneration.
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[Action potentials of the optic nerve in degeneration. II. Retrograde degeneration].
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Animals↗
Retrograde degeneration of the cochlear nerve.
Retrograde degeneration of the cochlear neurons has been studied in different types and degrees of peripheral cochlear damage such as acoustic trauma, intoxication, heredodegenerative deafness and others. It starts only when the peripheral dendrites to the inner hair cells are irreversibly damaged. About 10% of the neurons are not affected by retrograde degeneration. They correspond to the type II and III neurons, which also survive after transection of the cochlear nerve and are mainly associated with the outer hair cells. Cochlear damage due to vascular impairment usually leads to a complete loss of cochlear neurons. In hereditary abiotrophic deafness, neuronal degeneration is slower and its extent varies considerably according to the various genetic syndromes.
Animals↗
Thalamic retrograde degeneration following cortical injury: an excitotoxic process?
Traumatic or stroke-like injuries of the cerebral cortex result in the rapid retrograde degeneration of thalamic relay neurons that project to the damaged area. Although this phenomenon has been well documented, neither the basis for the relay neuron's extreme sensitivity to axotomy nor the mechanisms involved in the degenerative process have been clearly identified. Physiological and biochemical studies of the thalamic response to cortical ablation indicate that pathological overexcitation might contribute to the degenerative process. The responses of thalamic projection neurons, protoplasmic astrocytes, and inhibitory thalamic reticular neurons in adult mice were examined from one to 120 days following ablation of the somatosensory cortex as part of an investigation of the role of excitotoxicity in thalamic retrograde degeneration. The responses of thalamic neurons to cortical ablation were compared with those produced by intracortical injection of the convulsant excitotoxin kainic acid, since the degeneration of neurons in connected brain structures distant to the site of kainic acid injection is also thought to occur via an excitotoxic mechanism. Within two days after either type of cortical injury, protoplasmic astrocytes in affected regions of the thalamic ventrobasal complex and the medial division of the posterior thalamic nuclei became reactive and expressed increased levels of immunohistochemically detectable glial fibrillary acidic protein. Within the affected regions of the ventrobasal complex an increased intensity of puncta positive for glutamate decarboxylase immunoreactivity, presumably due to an increase in its content within the terminals of the reciprocally interconnected thalamic reticular neurons, was also evident. These immunohistochemically detectable alterations in the milieu of the damaged thalamic neurons preceded the disappearance of the affected relay neurons by at least two days following cortical ablation and by seven to 10 days following intracortical kainic acid injection. Regions of the thalamus containing reactive astrocytes corresponded very closely to the regions undergoing retrograde degeneration. Protoplasmic astrocytes in these areas remained intensely reactive up to 60 days after cortical injury. Levels of glutamate decarboxylase were only transiently elevated in the degenerating regions of the ventrobasal complex following cortical ablation and returned to normal by 14 days. Increased glutamate decarboxylase immunoreactivity was transiently seen through the entire ventrobasal complex following intracortical kainic acid injection but was markedly more intense in degenerating regions. These patterns of labeling did not return to normal until 50 days after intracortical kainic acid injection, well after the death of the relay neurons. Cortical ablation and intracortical kainic acid injection produce similar alterations in thalamic neuronal and glial populations.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
[Investigation on skin retrograde degeneration after tissue expansion].
OBJECTIVE: To study the effects of tissue expansion on tissue damage and retrograde degeneration. METHODS: 9 cases of conventional intermittent tissue expansion (CITE) and 9 cases of continuous pressure-controlled tissue expansion (CPTE) were chosen for the study. In creating of the expanded flaps, tissue samples were taken for histopathology, molecular biology and transmission electron microscope (TEM) examinations. RESULTS: Capillary bleeding, elastic and reticular fiber proliferation, arteriole thrombosis, fibroblast apoptosis and collagenolysis were observed after expansion. Retrograde degeneration was obvious in CITE group and acute lesion was obvious in CPTE group. CONCLUSION: Expansion stimulation induces tissue damage and retrograde degeneration, which indicates that the time for conventional intermittent expansion should be shortened and too fast continuous expansion is harmful.
Humans↗
[Surgical treatment for spinal canal stenosis of retrograde degeneration].
OBJECTIVE: To investigate the surgical effect on different types of spinal canal stenosis of retrograde degeneration. METHODS: The retrospective analysis was performed on 96 patients (85 males, 11 females; average age 54, range 39-71) admitted from September 2001 to January 2004 for spinal canal stenosis of retrograde degeneration. The patients were divided into five groups according to their clinical symptoms and signs and the imaging of the spinal cord. In group A, 39 patients had one segment of the spinal canal stenosis and they underwent the recessively expanding operation through the intervertebral canal by opening a window between the vertebral plates. In group B, 21 patients had stenosis of the central vertebral canal of one segment and they underwent excision of the intervertebral disc through the window opened between the vertebral plates and the recessively expanding operation. In group C, 18 patients had degenerative spinal derangement of one segment and they underwent decompression through the window opened between the bilateral vertebral plates and the recessively expanding operation, and then underwent the internal fixation and bone grafting. In group D, 11 patients had the mixed stenosis of the vertebral canal of more than 2 segments and they underwent the recessively expanding operation through the window opened bilaterally on the diseased segment and excision of the yellow ligament and the intervertebral disc. In group E, 7 patients had degenerative lateral curvature of the spine and they underwent the combined surgical procedures including decompression, internal fixation, and bone grafting. All the patients were followed up after operation. RESULTS: The follow-up of the 96 patients for 6-36 months with an average of 12.2 months showed that they had no postoperative complications. According to the JOA Scoring, 85 patients had an excellent result, 9 had a good result, 1 had a fair result, and only 1 had a poor result. The X-ray films revealed no mistaken placing of the nails on the vertebral arch, broken nails or loosened nails. CONCLUSION: The limited surgery and effective decompression can improve curative effects and reduce complications of spinal canal stenosis of retrograde degeneration. The imaging of the spinal cord has an important value in the choice of surgical protocols for spinal canal stenosis of retrograde.
Adult↗
[Retrograde degeneration of the neurons of the cerebellar nuclei after partial removal of the associative cerebral cortex].
Retrograde degeneration of the cerebellar nuclei cells has been studied after partial ablation of the associative parietal cerebral cortex in the cat. The material is stained after Nissl. Retrogradely degenerated and normal cells are counted. The "ghost-cells" in the cerebellar nuclei indicate that a direct axonal connection exists between some neurons and the cerebral cortex operated, while the cells that are at other stages of degeneration are, perhaps, connected with this part of the cortex by means of axonal collaterals.
Animals↗
Microglial reactions to retrograde degeneration of tracer-identified thalamic neurons after frontal sensorimotor cortex lesions in adult rats.
Thalamic neuronal degeneration after neocortical lesions involve both anterograde and retrograde components. This study deals with the thalamic microglial response after neocortical aspiration lesions, using fluorogold fluorescent prelabeling, to identify retrogradely degenerating thalamocortical neurons, combined with histochemical or immunohistochemical staining of microglial cells. Adult male Wistar rats were injected with the retrograde fluorescent tracer fluorogold, in the right sensorimotor cortex (forepaw area) in order to retrogradely label thalamic neurons projecting to this area. After 1 week, the fluorogold injection site was removed by aspiration, axotomizing at the same time the thalamic projection neurons now retrogradely labeled with fluorogold. After 3, 7, 14, and 28 days the animals were killed and processed for nucleoside diphosphatase histochemistry or complement type 3 receptor immuno-histochemistry and class I and II major histocompatibility complex immunohistochemistry using OX42, OX18, and OX6 antibodies. The histological analysis showed a prominent and progressive nucleoside diphosphatase-, OX42-, and OX6-positive microglial cell response in the ventrolateral, posterior, and ventrobasal thalamic nuclei with ongoing retrograde and anterograde neuronal degeneration. Initially the reactive microglia had a bushy morphology and were succeeded by ameboid microglia and microglial cluster cells as the reaction progressed. However, in the reticular thalamic nucleus, which suffered exclusively anterograde neuronal degeneration, a different picture was seen with only bushy microglia. The neurons undergoing retrograde degeneration in the ventrolateral, posterior, and ventrobasal thalamic nuclei were retrogradely labeled by the fluorogold tracer. Individual nucleoside diphosphatase-, OX42-, or OX6-positive microglial cells extended long cytoplasmic processes surrounding fluorogold-labeled neurons and had in some cases apparently phagocytized these. Several microglial cells were thus double-labeled with nucleoside diphosphatase or OX42 and fluorogold. In addition, small nucleoside diphosphatase-positive, fluorogold-labeled perivascular cells were observed in the neocortex near the fluorogold-injected and ablated neocortical areas and in the ipsilateral thalamus. This study demonstrates: (1) that the microglial response to thalamic degeneration after neocortical lesion is graded with a limited reaction to the well-known massive anterograde axonal degeneration and a more extended reaction to the axotomy-induced retrograde cell death; and (2) that also perivascular cells and possibly macrophages may contribute to this reaction, as seen by uptake of fluorogold from axotomized neurons in the degenerating thalamic nuclei.
Acid Anhydride Hydrolases↗
Retrograde degeneration of corticospinal axons following transection of the spinal cord in rats. A quantitative study with anterogradely transported horseradish peroxidase.
The extent of the retrograde degeneration of corticospinal axons following transection of the spinal cord was studied in rats by labeling corticospinal axons with anterogradely transported horseradish peroxidase injected in the sensorimotor cortex. Axotomized corticospinal axons underwent progressive and continuing retrograde degeneration. In specimens examined 5, 14, 28, and 56 days after trauma, the tips of the transected corticospinal axons were seen to terminate at 181 +/- 80 microns, 977 +/- 203 microns, 1751 +/- 344 microns, and 2559 +/- 466 microns (mean +/- standard deviation), respectively, from the site of transection. The rate of retrograde degeneration varied according to the interval after spinal cord transection, as follows: 36.2 microns/day during the first 5 days; 88.4 microns/day between 5 and 14 days; 55.3 microns/day between 14 and 28 days; and 28.8 microns/day between 28 and 56 days. These findings may serve as useful parameters for the objective assessment of therapeutic modalities in spinal cord injury research.
Animals↗
Axon end-bulb swellings and rapid retrograde degeneration after retinal lesions in young animals.
After making a lesion of the retina, anterograde (Wallerian) and retrograde degeneration of optic axons occurred more rapidly in newborn mice than in adults. Axon sprouting occurred only in adult mice, perhaps because retrograde degeneration may have been too rapid and severe for sprouting to occur in newborns. Retinal lesions in mice of any age produced end-bulb swellings initially on both sides of the lesion. In all animals, dense packing of lysosomes and other organelles occurred in end-bulbs on the side of Wallerian degeneration but did not occur in end-bulbs on the retrograde side, where accumulation of smooth endoplasmic reticulum was the most characteristic change. Retrograde end-bulbs appeared much like growth cones, which sprouted in adults, but degenerated in younger animals. Continuing daily enlargement of end-bulb swellings was noted on the Wallerian side of lesions in adults, but not in newborns. Such enlargement is believed to have resulted from retrograde axoplasmic transport and suggests that such transport may be greater in adults than in newborns.
Animals↗
Transneuronal retrograde degeneration of retinal ganglion cells following restricted lesions of striate cortex in the monkey.
Transneuronal retrograde degeneration of retinal ganglion cells follows extensive striate cortical removal in macaque monkeys. Its extent depends on the age of the monkey at operation, post-operative survival, species and retinal eccentricity. Some studies of human patients with occipital lobe injury have found no evidence for transneuronal retrograde degeneration, suggesting that either degeneration may not occur or, if present, it is caused directly by secondary damage impinging upon the underlying white matter or the blood supply to the dorsal lateral geniculate nucleus and optic tract. We therefore studied retinal ganglion cell degeneration in three macaques in which only the striate cortex corresponding to the macular retina had been removed, thereby sparing extrastriate cortex and precluding interruption of the vascular supply to the thalamus and optic tract. There was extensive loss of ganglion cells in the central retina, corresponding to the central 10 degrees of vision. As the cortical lesion was too small to affect the thalamus or optic tract directly, the retinal degeneration must be transneuronal. Quantitative analysis showed a 65-80% loss of ganglion cells in the corresponding perifoveal retinae along the horizontal meridian. The results confirm that the loss of retinal ganglion cells following striate cortical lesions is predominantly transneuronal.
Animals↗
Retrograde degeneration of the corticospinal tract associated with pontine infarction.
We report a 40-year-old man with myotonic dystrophy who survived for 5 years after pontine infarction. Serial MRI detected abnormal T2 elongation of the corticospinal tract at the cerebral peduncle 4 years after the infarction. An autopsy confirmed the existence of retrograde degeneration extending from the pons to the internal capsule, evidence that retrograde degeneration in the corticospinal tract occurs above the pontine level. MRI was suggested to be useful for detection of the degenerative process.
Adult↗
Up-regulated CNTF plays a protective role for retrograde degeneration in the axotomized rat retina.
Using reverse transcription-polymerase chain reaction and in situ hybridization, we investigated the expression and cellular localization of ciliary neurotrophic factor receptor alpha (CNTFRalpha) in the rat retina following optic nerve transection (ONT). Following ONT, a signal for CNTFRalpha mRNA appeared in a layer-specific and time-dependent manner. In the ganglion cell layer, the signal showed a peak value 1 day after ONT, and then gradually decreased. In the inner nuclear layer the signal reached a peak value at 14 days of about 500% of control level, but then decreased at 4 weeks. Our findings suggest that CNTF might play a protective role for the retrograde degeneration of retinal cells induced by ganglion cell death in the rat retina following ONT.
Animals↗
Proximal slowing in carpal tunnel syndrome resulting from either conduction block or retrograde degeneration.
In the carpal tunnel syndrome (CTS), decreased conduction velocity (CV) of the median nerve in the forearm segment has been ascribed to an electrodiagnostic artefact rather than pathophysiological changes. Standard CV of the forearm segment is calculated by subtracting the distal latency, which may not represent an exact assessment of CV in the proximal median nerve. A new technique modified from the method of Stoehr et al. and Pease et al. can exactly measure CV over the forearm. Using this new technique, the forearm nerve action potentials (FNAP) amplitude and forearm nerve conduction velocity (FNCV) proximal to the wrist can be directly determined. Normal subjects and patients with CTS were studied by both the standard and the new FNAP methods. Patients were divided into subgroups according to the severity derived from standard electro-diagnostic findings. By comparing the normal control and patient subgroups, the results show that there was a significant decrease in FNAP amplitudes proportional to severity, but FNCV was reduced to a lesser extent. In addition, the standard forearm median motor CV (MMCV) correlated well with severity, but the reduced MMCV did not correlate with the decreased FNCV. These findings suggest that retrograde degeneration of the median nerve does exist in CTS; however, retrograde degeneration contributes little to the reduced forearm MMCV which substantially results from the block of faster conduction fibres at the wrist. Therefore, technique artefact plays a major role in causing the proximal slowing in the standard electrodiagnosis.
Action Potentials↗
Anterograde vs. retrograde degeneration of the nucleus basalis medialis in Alzheimer's disease.
The evidence that degeneration in the basal forebrain cholinergic nuclei in Alzheimer's disease is a secondary phenomenon is reviewed. Experimental retrograde degeneration in these nuclei shares some common features with the degeneration actually observed in the disease, and can occur without direct damage to the cholinergic axons within the cortex. The neuroanatomical distribution of the pathological changes typical of Alzheimer's disease in the neocortex suggests a progression of the disease process, from the medial temporal cortex and amygdala out into the parieto-temporal association areas. Neurochemical evidence also points to the early and severe involvement of the amygdala in the disease. The close reciprocal relationship between the amygdala and the basal nucleus may underly the degeneration seen in the basal nucleus in Alzheimer's disease.
Alzheimer Disease↗
Thalamic retrograde degeneration in the congenitally hydrocephalic rat is attributable to apoptotic cell death.
Congenitally hydrocephalic HTX rats develop ventricular dilatation with extensive damage of the cerebral white matter. Recently, we have reported that neuronal cell death also occurs in the thalamus of HTX rats. To investigate the mechanism underlying this thalamic degeneration in these animals, we carried out a histopathological study of the brain at different phases of postnatal development. Eosinophilic neurons with condensed chromatin or fragmented nuclei were observed in the thalamus from postnatal day 17 onward. The incidence of cell death in the thalamus increased with the progression of hydrocephalus. Ultrastructurally, thalamic neurons occasionally had apoptotic features including nuclear chromatin condensation and marginalization. Immunohistochemically, single-stranded DNA-positive neuronal nuclei were found in the thalamus. They were also positively stained with the TUNEL method. Marked loss of myelin and axons with many TUNEL-positive oligodendrocytes were found in the cerebral white matter. These findings suggest that the neuronal cell death observed in the thalamus in hydrocephalic HTX rats is retrograde degeneration due to extensive damage of axons in the cerebral white matter and that the thalamic retrograde degeneration is attributable to apoptotic cell death.
Animals↗
Retrograde degeneration and colchicine protection of basal forebrain cholinergic neurons following hippocampal injections of an immunotoxin against the P75 nerve growth factor receptor.
Intracerebroventricular injection of 192 IgG antibody against the p75LNGFR rat low affinity nerve growth factor receptor conjugated with saporin, a ribosome inactivating protein, has been shown to destroy the p75LNGFR-expressing cholinergic neurons of the basal forebrain. We injected this immunotoxin into the hippocampus and studied its retrograde effect upon the cholinergic neurons of the medial septum and the vertical limb of the diagonal band of Broca. Seven days after injection, there was a nearly total depletion of cholinergic axons within the hippocampus. This depletion was associated with a marked and significant decrease in the number of cholinergic neurons of the ipsilateral medial septum and the vertical limb of the diagonal band of Broca. At longer survival times, these changes were more pronounced. Parvalbumin-positive, GABAergic neurons within the same areas of the basal forebrain were not affected by immunotoxin injections. Injections of saporin alone had no effect upon cholinergic neurons. Simultaneous injection of colchicine with the immunotoxin resulted in a significant reduction of retrograde degeneration of cholinergic neurons and relative preservation of hippocampal cholinergic axons. These observations suggest that 192 IgG-saporin is transported retrogradely from the hippocampus to the cholinergic neurons in the medial septum and the vertical limb of the diagonal band of Broca and provide a model for retrograde degeneration of basal forebrain cholinergic neurons following cortically based toxic-pathologic processes.
Animals↗
Factors inducing retrograde degeneration of the cochlear nerve.
The process of retrograde secondary degeneration is described and its mechanism, discussed. The extent of degeneration following transection of the central or peripheral axon and following various types of damage to the organ of Corti, including the time course of degeneration, is presented in animal experimentation and human temporal bones. Of greatest practical importance is secondary neuronal degeneration induced by alteration in the organ of Corti. The effect of damage to the outer hair cells, inner hair cells, supporting structures in the Corti, and nerve endings or peripheral dendrites is analyzed and related to different types of inner ear disease.
Acoustic Stimulation↗