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Journal articles on the topic 'Neurology; Wallerian degeneration'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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1

PEARCE, J. M. S. "Wallerian degeneration." Journal of Neurology, Neurosurgery & Psychiatry 69, no. 6 (December 1, 2000): 791. http://dx.doi.org/10.1136/jnnp.69.6.791.

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2

Kim, Muwoong, Hyosun Kim, Dogyeong Kim, Dokyoung Kim, Youngbuhm Huh, Chan Park, Hyung-Joo Chung, Junyang Jung, and Na Young Jeong. "Heme Oxygenase 1 in Schwann Cells Regulates Peripheral Nerve Degeneration Against Oxidative Stress." ASN Neuro 11 (January 2019): 175909141983894. http://dx.doi.org/10.1177/1759091419838949.

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During Wallerian degeneration, Schwann cells lose their characteristic of myelinating axons and shift into the state of developmental promyelinating cells. This recharacterized Schwann cell guides newly regrowing axons to their destination and remyelinates reinnervated axons. This Schwann cell dynamics during Wallerian degeneration is associated with oxidative events. Heme oxygenases (HOs) are involved in the oxidative degradation of heme into biliverdin/bilirubin, ferrous iron, and carbon monoxide. Overproduction of ferrous iron by HOs increases reactive oxygen species, which have deleterious effects on living cells. Thus, the key molecule for understanding the exact mechanism of Wallerian degeneration in the peripheral nervous system is likely related to oxidative stress-mediated HOs in Schwann cells. In this study, we demonstrate that demyelinating Schwann cells during Wallerian degeneration highly express HO1, not HO2, and remyelinating Schwann cells during nerve regeneration decrease HO1 activation to levels similar to those in normal myelinating Schwann cells. In addition, HO1 activation during Wallerian degeneration regulates several critical phenotypes of recharacterized repair Schwann cells, such as demyelination, transdedifferentiation, and proliferation. Thus, these results suggest that oxidative stress in Schwann cells after peripheral nerve injury may be regulated by HO1 activation during Wallerian degeneration and oxidative-stress-related HO1 activation in Schwann cells may be helpful to study deeply molecular mechanism of Wallerian degeneration.
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3

Nagata, Kiyoshi, Yuji Nikaido, Takashi Yuasa, Kenta Fujimoto, Yong Jin Kim, and Masazumi Inoue. "Germinoma causing wallerian degeneration." Journal of Neurosurgery 88, no. 1 (January 1998): 126–28. http://dx.doi.org/10.3171/jns.1998.88.1.0126.

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✓ Germinomas occurring in the thalamus and basal ganglia sometimes cause atrophy of the cerebral hemisphere on the affected side. The authors present the case of a 12-year-old girl with a germinoma that developed in the basal frontal lobe and cerebral basal ganglia. Magnetic resonance imaging showed atrophy not only of the cerebrum but also of the brainstem. A T2-weighted image revealed an area of high intensity that proved to be wallerian degeneration extending from the corona radiata and internal capsule to the brainstem. The authors suggest that this pathological change may be involved in the development of the symptoms and hemiatrophy associated with germinomas in this region of the brain.
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4

Dräger, B., W. Schwindt, S. Evers, and S. Knecht. "Immediate Wallerian Degeneration after Stroke." Klinische Neurophysiologie 36, no. 03 (September 2005): 147–48. http://dx.doi.org/10.1055/s-2005-867023.

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5

Olsson, Y., M. Jarild, L. Malmgren, and C. Tengvar. "Early axonal changes during Wallerian degeneration." Acta Neurologica Scandinavica 63, no. 2 (January 29, 2009): 142–43. http://dx.doi.org/10.1111/j.1600-0404.1981.tb00763.x.

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6

Watanabe, Toru, Yoshiho Honda, Yukihiko Fujii, Miyako Koyama, Hitoshi Matsuzawa, and Ryuichi Tanaka. "Three-dimensional anisotropy contrast magnetic resonance axonography to predict the prognosis for motor function in patients suffering from stroke." Journal of Neurosurgery 94, no. 6 (June 2001): 955–60. http://dx.doi.org/10.3171/jns.2001.94.6.0955.

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Object. The purpose of this study was to assess how early wallerian degeneration in the corticospinal tracts of patients who had suffered from stroke was detected using three-dimensional anisotropy contrast (3D-AC) magnetic resonance (MR) axonography and to explore the possibility of predicting the prognosis for motor function in these patients. Methods. Ten healthy volunteers and 16 stroke patients with hemiparesis were studied using MR images including 3D-AC MR axonography images obtained using a 1.5-tesla MR imaging system. The axonography was performed using an echoplanar imaging method. All patients underwent MR studies 2, 3, and 10 weeks after stroke onset. To detect wallerian degeneration, the diffusion anisotropy in the corticospinal tracts at the level of the upper pons was evaluated on axial images. These MR findings were compared with the patients' motor functions, which were classified according to the Brunnstrom criteria 12 weeks after the onset of stroke. In all patients with poor recovery (Brunnstrom Stages I–IV), wallerian degeneration, which was demonstrated as a reduction in diffusion anisotropy on axonography images, could be observed in the corticospinal tracts; this degeneration was not found in patients with good recovery (Stages V and VI). Axonography could be used to detect degeneration between 2 and 3 weeks after stroke onset. On conventional T2-weighted MR images, hyperintense areas indicating wallerian degeneration were not detected until 10 weeks after stroke onset. Conclusions. With the aid of 3D-AC MR axonography, wallerian degeneration can be detected in the corticospinal tracts during the early stage of stroke (2–3 weeks after onset), much earlier than it can be detected using T2-weighted MR imaging. The procedure of 3D-AC MR axonography may be useful in predicting motor function prognosis in stroke patients.
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7

Carroll, Steven L., Michele L. Miller, Paul W. Frohnert, Susanne S. Kim, and John A. Corbett. "THE NEUREGULINS IN WALLERIAN DEGENERATION." Journal of Neuropathology and Experimental Neurology 55, no. 5 (May 1996): 631. http://dx.doi.org/10.1097/00005072-199605000-00116.

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8

Chaudhry, Vinay, Jonathan D. Glass, and John W. Griffin. "Wallerian Degeneration in Peripheral Nerve Disease." Neurologic Clinics 10, no. 3 (August 1992): 613–27. http://dx.doi.org/10.1016/s0733-8619(18)30200-7.

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9

Moldovan, M., S. Alvarez, and C. Krarup. "Motor axon excitability during Wallerian degeneration." Brain 132, no. 2 (June 20, 2008): 511–23. http://dx.doi.org/10.1093/brain/awn332.

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10

Scheidt, P., and R. L. Friede. "Myelin phagocytosis in Wallerian degeneration." Acta Neuropathologica 75, no. 1 (1987): 77–84. http://dx.doi.org/10.1007/bf00686796.

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11

Domi, Trish, Gabrielle deVeber, Manohar Shroff, Elizabeth Kouzmitcheva, Daune L. MacGregor, and Adam Kirton. "Corticospinal Tract Pre-Wallerian Degeneration." Stroke 40, no. 3 (March 2009): 780–87. http://dx.doi.org/10.1161/strokeaha.108.529958.

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12

Ludwin, S. K. "Oligodendrocyte survival in Wallerian degeneration." Acta Neuropathologica 80, no. 2 (June 1990): 184–91. http://dx.doi.org/10.1007/bf00308922.

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13

Ma, Marek, Toby A. Ferguson, Kathleen M. Schoch, Jian Li, Yaping Qian, Frances S. Shofer, Kathryn E. Saatman, and Robert W. Neumar. "Calpains mediate axonal cytoskeleton disintegration during Wallerian degeneration." Neurobiology of Disease 56 (August 2013): 34–46. http://dx.doi.org/10.1016/j.nbd.2013.03.009.

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14

Jimenez-Gomez, Andres, and Robert Clinton Stowe. "Teaching NeuroImages: Wallerian degeneration in evolving pediatric stroke." Neurology 89, no. 13 (September 25, 2017): e166-e167. http://dx.doi.org/10.1212/wnl.0000000000004422.

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15

West, Norman R., and George H. Collins. "Relationship of Wallerian Degeneration to Regrowing Axons." Journal of Neuropathology & Experimental Neurology 50, no. 6 (November 1991): 693–703. http://dx.doi.org/10.1097/00005072-199111000-00002.

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16

Ludwin, S. K. "THE BEHAVIOUR OF OLIGODENDROCYTES DURING WALLERIAN DEGENERATION." Journal of Neuropathology and Experimental Neurology 48, no. 3 (May 1989): 364. http://dx.doi.org/10.1097/00005072-198905000-00197.

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17

Liang, Zhijian, Jinsheng Zeng, Cuimei Zhang, Sirun Liu, Xueying Ling, Fang Wang, Li Ling, Qinghua Hou, Shihui Xing, and Zhong Pei. "Progression of Pathological Changes in the Middle Cerebellar Peduncle by Diffusion Tensor Imaging Correlates With Lesser Motor Gains After Pontine Infarction." Neurorehabilitation and Neural Repair 23, no. 7 (February 25, 2009): 692–98. http://dx.doi.org/10.1177/1545968308331142.

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Background. Wallerian degeneration in pyramidal tract following supratentorial stroke has been detected by some studies using diffusion tensor imaging (DTI), but the Wallerian degeneration in middle cerebellar peduncle after pontine infarction and its potential clinical significance remain to be confirmed. Methods. Seventeen patients with a recent focal pontine infarct underwent 3 DTIs at week 1 (W1), week 4 (W4), and week 12 (W12) after onset. Seventeen age-matched and gender-matched controls underwent DTI one time. Mean diffusivity and fractional anisotropy (FA) were measured in the basis pontis and bilateral middle cerebellar peduncles. Neurological deficit, motor deficit, functional independence, and limbs ataxia were assessed with the National Institutes of Health (NIH) Stroke Scale, Fugl-Meyer scale, Barthel Index, and the second part of International Cooperative Ataxia Rating Scale. Results. FA values at the bilateral middle cerebellar peduncles decreased significantly from W1 to W12 progressively ( P < .01). The patients improved on the NIH Stroke Scale, Fugl-Meyer scale, and Barthel Index over time ( P < .01). Greater absolute value of percentage reduction of FA at the bilateral middle peduncles, however, was associated with the less absolute value of percentage reduction of the NIH Stroke Scale and less increase in the Fugl-Meyer scale, as well as greater ataxia over time. Conclusions. Wallerian degeneration in the middle cerebellar peduncle revealed by DTI may hinder the process of neurological recovery following a focal pontine infarct.
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18

Alvarez, Susana, Mihai Moldovan, and Christian Krarup. "Acute energy restriction triggers Wallerian degeneration in mouse." Experimental Neurology 212, no. 1 (July 2008): 166–78. http://dx.doi.org/10.1016/j.expneurol.2008.03.022.

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19

Sea, Tia, Martis L. Ballinger, and George D. Bittner. "Cooling of Peripheral Myelinated Axons Retards Wallerian Degeneration." Experimental Neurology 133, no. 1 (May 1995): 85–95. http://dx.doi.org/10.1006/exnr.1995.1010.

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20

Brück, Wolfgang. "The Role of Macrophages in Wallerian Degeneration." Brain Pathology 7, no. 2 (April 1997): 741–52. http://dx.doi.org/10.1111/j.1750-3639.1997.tb01060.x.

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21

Br�ck, W., Y. Br�ck, B. Maruschak, and R. L. Friede. "Mechanisms of macrophage recruitment in Wallerian degeneration." Acta Neuropathologica 89, no. 4 (March 1, 1995): 363–67. http://dx.doi.org/10.1007/s004010050258.

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22

Br�ck, W., Y. Br�ck, B. Maruschak, and R. L. Friede. "Mechanisms of macrophage recruitment in Wallerian degeneration." Acta Neuropathologica 89, no. 4 (April 1995): 363–67. http://dx.doi.org/10.1007/bf00309630.

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23

Abe, Yoshinori, Teiji Yamamoto, Yasuji Sugiyama, Takako Watanabe, Naoshi Saito, Hisae Kayama, and Tomohiro Kumagai. ""Anoikis" of Oligodendrocytes Induced by Wallerian Degeneration: Ultrastructural Observations." Journal of Neurotrauma 21, no. 1 (January 2004): 119–24. http://dx.doi.org/10.1089/089771504772696002.

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24

TASKINEN, HANNA-STIINA, and MATIAS RÖYTTÄ. "Cyclosporin A Affects Axons and Macrophages During Wallerian Degeneration." Journal of Neurotrauma 17, no. 5 (May 2000): 431–40. http://dx.doi.org/10.1089/neu.2000.17.431.

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25

Chaballe, Linda, Pierre Close, Maxime Sempels, Stéphanie Delstanche, Julien Fanielle, Lieve Moons, Peter Carmeliet, Jean Schoenen, Alain Chariot, and Rachelle Franzen. "Involvement of placental growth factor in Wallerian degeneration." Glia 59, no. 3 (December 6, 2010): 379–96. http://dx.doi.org/10.1002/glia.21108.

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26

Koliatsos, Vassilis E., and Athanasios S. Alexandris. "Wallerian degeneration as a therapeutic target in traumatic brain injury." Current Opinion in Neurology 32, no. 6 (December 2019): 786–95. http://dx.doi.org/10.1097/wco.0000000000000763.

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27

Gräβel, David, Thomas M. Ringer, Clemens Fitzek, Sabine Fitzek, Matthias Kohl, Werner A. Kaiser, Otto W. Witte, and Hubertus Axer. "Wallerian Degeneration of Pyramidal Tract after Paramedian Pons Infarct." Cerebrovascular Diseases 30, no. 4 (2010): 380–88. http://dx.doi.org/10.1159/000319573.

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28

Fregni, Felipe, Adriana Bastos Conforto, Maria da Graça Morais Martin, Claudia da Costa Leite, Fábio Iuji Yamamoto, and Milberto Scaff. "Magnetic Resonance Imaging of Wallerian Degeneration in Stroke." Archives of Neurology 60, no. 10 (October 1, 2003): 1466. http://dx.doi.org/10.1001/archneur.60.10.1466.

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29

Eather, Terry F., and Martin Pollock. "Collagenosis in Wallerian degeneration depends on peripheral nerve type." Experimental Neurology 100, no. 3 (June 1988): 524–30. http://dx.doi.org/10.1016/0014-4886(88)90036-2.

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30

Patel, Arpan, Prateeka Koul, and Asaff Harel. "Wallerian degeneration as a mimic of recurrence of myelitis." Practical Neurology 21, no. 3 (March 18, 2021): 235–36. http://dx.doi.org/10.1136/practneurol-2020-002911.

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A middle-aged woman with idiopathic longitudinally extensive myelitis underwent repeat MR scan of cervical spine at 5-month follow-up, which showed new non-enhancing T2 hyperintensities, initially reported as myelitis recurrence. However, the hyperintensities involved both lateral corticospinal tracts caudal to the initial lesion and both dorsal columns rostral to the initial lesion and were therefore compatible with Wallerian degeneration. This radiological mimic should be considered in the differential of recurrence of myelitis.
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31

Delgado-Lezama, Rodolfo, and E. J. Mun˜oz-Marti´nez. "The influence of peripheral connections on wallerian degeneration." Brain Research 525, no. 1 (August 1990): 152–54. http://dx.doi.org/10.1016/0006-8993(90)91332-b.

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32

Abe, Y., T. Yamamoto, Y. Sugiyama, H. Kayama, T. Watanabe, N. Saito, and T. Kumagai. ""ANOIKIS" OF OLIGODENDROCYTES INDUCED BY WALLERIAN DEGENERATION: ELECTRON MICROSCOPIC OBSERVATIONS." Journal of Neurotrauma 15, no. 10 (October 1998): 853–906. http://dx.doi.org/10.1089/neu.1998.15.853.

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33

Chaudhry, Vinay, and David R. Cornblath. "Wallerian degeneration in human nerves: Serial electrophysiological studies." Muscle & Nerve 15, no. 6 (June 1992): 687–93. http://dx.doi.org/10.1002/mus.880150610.

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34

Kakulas, Byron A. "Spinal Cord Injuries the Facts of Neuropathology: Opportunities and Limitations." Current Neuropsychiatry and Clinical Neuroscience Reports 1, no. 1 (July 4, 2019): 1–5. http://dx.doi.org/10.33702/cncnr.2019.1.1.1.

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It is essential for research projects which are undertaken to find a “cure” for human spinal cord injury (SCI) to be consistent with the neuropathological facts of the disorder. In this respect there are three main points to be taken into account. Firstly, the researcher should be aware that simple transection of the spinal cord is not a feature of human SCI. The usual lesion is one of compression and disruption with haemorrhage. The second and most important aspect of human SCI is to understand that Wallerian degeneration inevitably ensues following disruption of the axon. Wallerian degeneration is progressive and inexorable and unlike the peripheral nervous system CNS axons do not regenerate. The third and more helpful fact is that in the majority (71%) of SCI autopsies a small amount of white matter, myelin and axons, was found to be preserved at the level of injury. Re-activation of these dormant, axons offers the opportunity for improvement of the SCI patient’s neurological status by means of restorative neurology (RN).
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35

RAEDER, Mariana Trombetta de Lima, Eduardo Pontes REIS, Brunno Machado CAMPOS, Igor Aloísio Garcez ZAMILUTE, Marcondes Cavalcante FRANÇA JÚNIOR, and Fabiano REIS. "Transaxonal degenerations of cerebellar connections: the value of anatomical knowledge." Arquivos de Neuro-Psiquiatria 78, no. 5 (May 2020): 301–6. http://dx.doi.org/10.1590/0004-282x20200021.

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ABSTRACT Transaxonal degenerations result from neuronal death or the interruption of synaptic connections among neuronal structures. These degenerations are not common but may be recognized by conventional magnetic resonance imaging. Objective: The learning objectives of this review include recognition of the imaging characteristics of transaxonal degenerations involving cerebellar connections, the identification of potential encephalic lesions that can lead to these degenerations and correlation of the clinical manifestations with imaging findings that reflect this involvement. Methods: In this report, we review the neuroanatomical knowledge that provides a basis for identifying potential lesions that can result in these degenerations involving cerebellar structures. Results: Hypertrophic olivary degeneration results from an injury that interrupts any of the components of the Guillain-Mollaret triangle. In this work, we describe cases of lesions in the dentate nucleus and central tegmental tract. The crossed cerebellar diaschisis presents specific imaging findings and clinical correlations associated with its acute and chronic phases. The Wallerian degeneration of the middle cerebellar peduncle is illustrated by fiber injury of the pontine cerebellar tracts. A T2-hyperintensity in the dentate nucleus due to a thalamic acute lesion (in ventral lateral nuclei) is also described. Each condition described here is documented by MRI images and is accompanied by teaching points and an anatomical review of the pathways involved. Conclusion: Neurologists and radiologists need to become familiar with the diagnosis of these conditions since their presentations are peculiar and often subtle, and can easily be misdiagnosed as ischemic events, degenerative disease, demyelinating disease or even tumors.
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36

Brück, W., and R. L. Friede. "The role of complement in myelin phagocytosis during PNS wallerian degeneration." Journal of the Neurological Sciences 103, no. 2 (June 1991): 182–87. http://dx.doi.org/10.1016/0022-510x(91)90162-z.

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37

Konno, Hidehiko, Teiji Yamamoto, Yuzo Iwasaki, Hiroyoshi Suzuki, Tasuku Saito, and Hiroshi Terunuma. "Wallerian degeneration induces Ia-antigen expression in the rat brain." Journal of Neuroimmunology 25, no. 2-3 (December 1989): 151–59. http://dx.doi.org/10.1016/0165-5728(89)90132-x.

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38

Sunio, Arisa, and George D. Bittner. "Cyclosporin A Retards the Wallerian Degeneration of Peripheral Mammalian Axons." Experimental Neurology 146, no. 1 (July 1997): 46–56. http://dx.doi.org/10.1006/exnr.1997.6484.

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39

Ahdab, Rechdi, Raghid Kikano, Hiba Saade, and Naji Riachi. "Early corticospinal tract Wallerian degeneration versus mesencephalic substantia nigra degeneration secondary to striatal stroke." Clinical Neurology and Neurosurgery 118 (March 2014): 101–2. http://dx.doi.org/10.1016/j.clineuro.2013.12.005.

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40

Levenson, D., and J. Rosenbluth. "Electrophysiologic changes accompanying Wallerian degeneration in frog sciatic nerve." Brain Research 523, no. 2 (July 1990): 230–36. http://dx.doi.org/10.1016/0006-8993(90)91491-x.

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41

Glass, Jonathan D., Deborah G. Culver, Allan I. Levey, and Norman R. Nash. "Very early activation of m-calpain in peripheral nerve during Wallerian degeneration." Journal of the Neurological Sciences 196, no. 1-2 (April 2002): 9–20. http://dx.doi.org/10.1016/s0022-510x(02)00013-8.

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42

Wagner, Rochelle, Heidi M. Heckman, and Robert R. Myers. "Wallerian degeneration and hyperalgesia after peripheral nerve injury are glutathione-dependent." Pain 77, no. 2 (August 1998): 173–79. http://dx.doi.org/10.1016/s0304-3959(98)00091-8.

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43

Winder, Toni R., and Roland N. Auer. "Sensory Neuron Degeneration in Familial Kugelberg-Welander Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 16, no. 1 (February 1989): 67–70. http://dx.doi.org/10.1017/s0317167100028535.

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ABSTRACT:A 53 year old man developed symptoms of motor neuron disease in childhood. There was a family history of a similar disorder and it was felt to represent a form of Kugelberg-Welander disease. In addition to the motor deficits, sensory abnormalities in his legs were documented during life. Autopsy revealed anterior horn cell loss throughout the length of the spinal cord, with preservation of the phrenic nucleus. The lumbar dorsal root ganglia showed active degeneration of sensory neurons, with nuclear changes exceeding cytoplasmic ones. The fasciculus gracilis showed Wallerian degeneration. The findings provide direct evidence that sensory neurons can degenerate in some forms of motor neuron disease, and that the “demyelination” or “degeneration” of posterior columns sometimes seen in the various forms of motor neuron disease may actually be secondary to cell body disease in the dorsal root ganglia.
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44

Krinke, G., A. P. Grieve, and K. Schnider. "The role of Schmidt-Lanterman incisures in Wallerian degeneration." Acta Neuropathologica 69, no. 1-2 (1986): 168–70. http://dx.doi.org/10.1007/bf00687055.

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45

Lu, Jian-Qiang, Han Kyu Lee, Alim P. Mitha, Gernot Neumayer, and Minh Dang Nguyen. "α-synuclein in activated microglias during infarct-induced Wallerian degeneration." Journal of Neuropathology and Experimental Neurology 66, no. 5 (May 2007): 429–30. http://dx.doi.org/10.1097/01.jnen.0000268849.12854.9e.

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46

George, R., and J. W. Griffin. "ACCELERATED HACROPHAGE RESPONSE TO WALLERIAN DEGENERATION IN THE LEWIS STRAIN." Journal of Neuropathology and Experimental Neurology 52, no. 3 (May 1993): 286. http://dx.doi.org/10.1097/00005072-199305000-00103.

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47

RAO, D. G., and P. R. LYONS. "Wallerian degeneration of the pyramidal tract after a thrombotic stroke." Journal of Neurology, Neurosurgery & Psychiatry 65, no. 6 (December 1, 1998): 944. http://dx.doi.org/10.1136/jnnp.65.6.944.

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48

Wang, Min-Sheng, Yue Wu, Deborah G. Culver, and Jonathan D. Glass. "The Gene for Slow Wallerian Degeneration (Wlds) Is Also Protective against Vincristine Neuropathy." Neurobiology of Disease 8, no. 1 (February 2001): 155–61. http://dx.doi.org/10.1006/nbdi.2000.0334.

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49

Paul, Jennifer A., and Norman A. Gregson. "An immunohistochemical study of phospholipase A2 in peripheral nerve during Wallerian degeneration." Journal of Neuroimmunology 39, no. 1-2 (July 1992): 31–47. http://dx.doi.org/10.1016/0165-5728(92)90172-h.

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50

Bignami, Amico, Hussein Mansour, and Doris Dahl. "Glial hyaluronate-binding protein in Wallerian degeneration of dog spinal cord." Glia 2, no. 5 (1989): 391–95. http://dx.doi.org/10.1002/glia.440020511.

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