関: Ganglionopathy, sensory

WordNet

involving or derived from the senses; "sensory experience"; "sensory channels" (同)sensorial

PrepTutorEJDIC

感覚の
(光・温度・放射能などの)感知器

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1. 感覚消失患者へのアプローチ approach to the patient with sensory loss
2. 脊髄および後根神経節に影響を与える腫瘍随伴性症候群 paraneoplastic syndromes affecting the spinal cord and dorsal root ganglia
3. 銅欠乏性脊髄神経障害 copper deficiency myeloneuropathy
4. 脊髄に影響を与える疾患 disorders affecting the spinal cord
5. 免疫誘導性神経障害 immune mediated neuropathies

English Journal

Mice with a deletion of the major central myelin protein exhibit hypersensitivity to noxious thermal stimuli: involvement of central sensitization.

Petit B1, Giraudet F2, Béchon C1, Bardin L3, Avan P2, Boespflug-Tanguy O4, Bégou M5.Author information 1Clermont Université, Université d'Auvergne, Faculté de Médecine, BP 10448, F-63000 Clermont-Ferrand, France; Inserm U676, Hôpital Robert-Debré, Faculté de médecine Denis-Diderot, Université Paris-7, 75205 Paris cedex 13, France.2Clermont Université, Université d'Auvergne, Laboratoire de Biophysique, BP 10448, F-63000 Clermont-Ferrand, France; Inserm U1107, NEURO-DOL, F-63001 Clermont-Ferrand, France.3Division of Neurobiology 2, Pierre Fabre Research Center, 81106 Castres, France.4AP-HP, Hôpital Robert Debré, Service de Neurologie Pédiatrique, Centre de référence "leukodystrophies", 75019 Paris, France; Inserm U676, Hôpital Robert-Debré, Faculté de médecine Denis-Diderot, Université Paris-7, 75205 Paris cedex 13, France.5Clermont Université, Université d'Auvergne, Faculté de Médecine, BP 10448, F-63000 Clermont-Ferrand, France; Inserm U676, Hôpital Robert-Debré, Faculté de médecine Denis-Diderot, Université Paris-7, 75205 Paris cedex 13, France. Electronic address: melina.begou@udamail.fr.AbstractNull mutations in the gene encoding the major myelin protein of the central nervous system, proteolipid protein 1 (PLP1), cause an X-linked form of spastic paraplegia (SPG2) associated with axonal degeneration. While motor symptoms are the best known manifestations of this condition, its somatosensory disturbances have been described but poorly characterized. We carried out a longitudinal study in an animal model of SPG2 - mice carrying a deletion of the Plp1 gene (Plp-null mice). Plp-null mice exhibited severe early-onset thermal hyperalgesia, in the absence of thermal allodynia. We first performed an electrophysiological testing which showed an early decrease in peripheral and spinal conduction velocities in Plp null mice. Such as the abnormal sensitive behaviors, this slowing of nerve conduction was observed before the development of myelin abnormalities at the spinal level, from 3months of age, and without major morphological defects in the sciatic nerve. To understand the link between a decrease in nerve velocity and an increased response to thermal stimuli before the appearance of myelin abnormalities, we focused our attention on the dorsal horn of the spinal cord, the site of integration of somatosensory information. Immunohistochemical studies revealed an early-onset activation of astrocytes and microglia that worsened with age, associated later in age with perturbation of the expression of the sensory neuropeptides calcitonin-gene-related peptide and galanin. Taken together, these results represent complementary data supporting the hypothesis that Plp-null mice suffer from ganglionopathy associated with late onset central demyelination but with few peripheral nerve alterations, induced by the glial-cell-mediated sensitization of the spinal cord. The mechanism suggested here could underlie pain experiments in other leukodystrophies as well as in other non-genetic demyelinating diseases such as multiple sclerosis.
Neurobiology of disease.Neurobiol Dis.2014 May;65:55-68. doi: 10.1016/j.nbd.2014.01.005. Epub 2014 Jan 11.
Null mutations in the gene encoding the major myelin protein of the central nervous system, proteolipid protein 1 (PLP1), cause an X-linked form of spastic paraplegia (SPG2) associated with axonal degeneration. While motor symptoms are the best known manifestations of this condition, its somatosenso
PMID 24423646

Dorsal root ganglionopathy is responsible for the sensory impairment in CANVAS.

Szmulewicz DJ1, McLean CA, Rodriguez ML, Chancellor AM, Mossman S, Lamont D, Roberts L, Storey E, Halmagyi GM.Author information 1From the University of Melbourne (D.J.S.), Royal Victorian Eye & Ear Hospital, Melbourne, Australia; Department of Anatomical Pathology (C.A.M.), Alfred Hospital, Melbourne, Australia; Department of Forensic Medicine (M.L.R.), New South Wales Pathology, New South Wales, Australia; Department of Medicine (A.M.C.), Tauranga Hospital, Wellington, New Zealand; Department of Neurology (S.M.), Capital Coast Health, Wellington, New Zealand; Pathology (D.L.), Waikato Hospital, Hamilton, Waikato, New Zealand; Department of Neuroscience (L.R.), St Vincent's Hospital, Melbourne, Australia; Department of Neuroscience (E.S.), Monash University, Melbourne, Australia; and Department of Neurology (G.M.H.), Royal Prince Alfred Hospital, Sydney, Australia.AbstractOBJECTIVE: To elucidate the neuropathology in cerebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome (CANVAS), a novel cerebellar ataxia comprised of the triad of cerebellar impairment, bilateral vestibular hypofunction, and a peripheral sensory deficit.
Neurology.Neurology.2014 Mar 28. [Epub ahead of print]
OBJECTIVE: To elucidate the neuropathology in cerebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome (CANVAS), a novel cerebellar ataxia comprised of the triad of cerebellar impairment, bilateral vestibular hypofunction, and a peripheral sensory deficit.METHOD: Brain and spina
PMID 24682971

The neurology of Sjogren's syndrome and the rheumatology of peripheral neuropathy and myelitis.

Berkowitz AL1, Samuels MA.Author information 1Department of Neurology, Brigham and Women's Hospital, , Boston, Massachusetts, USA.AbstractNeurological symptoms occur in approximately 20% of patients with Sjögren's syndrome, and may be the presenting manifestations of the disease. Here, we review several neurological conditions that can occur in Sjögren's syndrome: sensory ganglionopathy, painful small fibre neuropathy, and transverse myelitis (independently or as part of neuromyelitis optica). We present the symptoms, signs, differential diagnoses, recommended diagnostic evaluation, and treatment of each of these, highlighting the features that should alert neurologists to consider Sjögren's syndrome.
Practical neurology.Pract Neurol.2014 Feb;14(1):14-22. doi: 10.1136/practneurol-2013-000651. Epub 2013 Dec 4.
Neurological symptoms occur in approximately 20% of patients with Sjögren's syndrome, and may be the presenting manifestations of the disease. Here, we review several neurological conditions that can occur in Sjögren's syndrome: sensory ganglionopathy, painful small fibre neuropathy, and transvers
PMID 24307005

Japanese Journal

免疫性自律性ニューロパチー : Autoimmune autonomic ganglionopathy と acute autonomic and sensory neuropathy の比較

小池春樹,児矢野繁,冨田稔,両角佐織,川頭祐一,飯島正博,祖父江元
末梢神経 = Peripheral nerve 20(2), 232-233, 2009-12-01
NAID 10027268112

急性自律性感覚性ニューロパチーの臨床病理学的検討

小池春樹,熱田直樹,足立弘明,冨田稔,両角佐織,川頭祐一,飯島正博,服部直樹,安田武司,深田育代,安井建一,中島健二,堀内正浩,塩見一剛,福居和人,高嶋修太郎,森田ゆかり,国吉和昌,長谷川康博,鳥邉泰久,祖父江元
末梢神経 = Peripheral nerve 19(2), 324-326, 2008-12-01
NAID 10025625514