T Cell–mediated ganglionitis associated with acute sensory neuronopathy

Hainfellner, J.; Kristoferitsch, Wolfgang; Lassmann, Hans; Bernheimer, H.; Neisser, A.; Drlicek, M.; Beer, Franz; Budka, Herbert

doi:10.1002/ana.410390418

Cited by 26 publications

(17 citation statements)

References 17 publications

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“…In human idiopathic SN, both T cell-mediated immune response and autoantibody against spinal ganglion neurons were involved on its pathogenesis [1,9,16,18]. However, a previous report of human acute SN [10] described that CD8 positive-T cell-mediated immunity against ganglion neurons might mostly contribute the pathologic events and humoral immunity had only a limited role. Some forms of human SN have been associated with lung or breast cancers called as "paraneoplastic syndromesh" [7,9].…”

Section: Discussionmentioning

confidence: 98%

“…Regardless of whether the distal peripheral nerve lesions are primary or secondary changes, the lesions have clinical utility for the diagnosis using biopsy of the distal peripheral sensory nerves. In fact, biopsy specimens of the sural nerve mostly consisting of sensory nerves have been used for pathological evaluations of acute SN in humans [8,10].…”

Section: Discussionmentioning

confidence: 99%

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Pathological Features of Ganglioradiculitis (Sensory Neuropathy) in Two Dogs

Funamoto

Nibe

Morozumi

et al. 2007

The Journal of Veterinary Medical Science

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ABSTRACT. Canine ganglioradiculitis (sensory neuropathy) was examined pathologically in two dogs (dog Nos. 1 and 2). The affected dogs had 1 and 2 years clinical courses from the onset, respectively. As common clinical signs, both cases showed progressive ataxia, difficulty in prehending food, visual deficit, and several sensory abnormalities. Gross observation after tissue fixation revealed whitish discoloration in the dorsal column of the spinal cords. The histological lesions were mainly distributed in the spinal dorsal roots, ganglions, and dorsal columns. In the spinal dorsal roots and ganglions, there were striking myelin loss, mild infiltration of mononuclear cells, and proliferation of small spindle cells. In the dorsal funiculus, there were moderate to severe diffuse myelin-loss and axonal degeneration. Immunohistochemistry for substance P (SP) revealed marked reduction of SP-immunopositive granules in the spinal substantia gelatinosa of affected dogs. By immunohistochemistry, CD3-positive cells were observed in the dorsal roots of dog No. 2, while CD3-positive cells were rare in those of dog No. 1. In the spinal ganglion of dog No. 1 there were many CD3-and MHC class II-positive cells. By indirect immunofluorescence assay using sera from affected dogs, no autoantibodies against canine nerve tissues were detected. The clinicopathological features of the present cases are almost consistent with those in previous reports of canine sensory neuropathies, while the etiology remains unclear.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Pathological Features of Ganglioradiculitis (Sensory Neuropathy) in Two Dogs

Funamoto

Nibe

Morozumi

et al. 2007

The Journal of Veterinary Medical Science

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“…This has been pathologically demonstrated with paraneoplastic SNN (Graus et al ., 1990; Dalmau et al ., 1991; Wanschitz et al ., 1997), HIV infection (Scaravilli et al ., 1992; Esiri et al ., 1993), Sjögren's syndrome, unclassified connective diseases and rare idiopathic cases (Okajima et al ., 1983; Sobue et al ., 1988; Griffin et al ., 1990; Hainfellner et al ., 1996; Kurokawa et al ., 1998; Colli et al ., 2008). Interestingly, in all of these circumstances, dorsal root ganglia degeneration was associated with an inflammatory T-cell reaction suggesting that the disorder is mainly driven by a cell-mediated immune response.…”

Section: Introductionmentioning

confidence: 99%

The pattern and diagnostic criteria of sensory neuronopathy: a case-control study

Camdessanché¹,

Jousserand²,

Férraud³

et al. 2009

Brain

213

176

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Acquired sensory neuronopathies encompass a group of paraneoplastic, dysimmune, toxic or idiopathic disorders characterized by degeneration of peripheral sensory neurons in dorsal root ganglia. As dorsal root ganglia cannot easily be explored, the clinical diagnosis of these disorders may be difficult. The question as to whether there exists a common clinical pattern of sensory neuronopathies, allowing the establishment of validated and easy-to-use diagnostic criteria, has not yet been addressed. In this study, logistic regression was used to construct diagnostic criteria on a retrospective study population of 78 patients with sensory neuronopathies and 56 with other sensory neuropathies. For this, sensory neuronopathy was provisionally considered as unambiguous in 44 patients with paraneoplastic disorder or cisplatin treatment and likely in 34 with a dysimmune or idiopathic setting who may theoretically have another form of neuropathy. To test the homogeneity of the sensory neuronopathy population, likely candidates were compared with unambiguous cases and then the whole population was compared with the other sensory neuropathies population. Criteria accuracy was checked on 37 prospective patients referred for diagnosis of sensory neuropathy. In the study population, sensory neuronopathy showed a common clinical and electrophysiological pattern that was independent of the underlying cause, including unusual forms with only patchy sensory loss, mild electrical motor nerve abnormalities and predominant small fibre or isolated lower limb involvement. Logistic regression allowed the construction of a set of criteria that gave fair results with the following combination: ataxia in the lower or upper limbs + asymmetrical distribution + sensory loss not restricted to the lower limbs + at least one sensory action potential absent or three sensory action potentials <30% of the lower limit of normal in the upper limbs + less than two nerves with abnormal motor nerve conduction study in the lower limbs.

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“…20 In fact, pathologic studies in SSN have confirmed the site of pathology by demonstrating inflammation and cellular loss in the dorsal root ganglia, which are thought to reflect the immune-mediated inflammatory process causing the syndrome. 12,17,21 In a few cases, autopsy studies in patients with paraneoplastic SSN have also revealed degeneration of the posterior columns of the spinal cord, suggesting that inflammation is not limited to the peripheral sensory nerves, and the central nervous system may also be involved. 13 However, radiographic evidence (e.g., MRI) of central nervous system involvement in SSN has not been reported.…”

Section: Discussionmentioning

confidence: 99%