Sensory Ganglionopathy

2020 ◽  
Vol 383 (17) ◽  
pp. 1657-1662
Author(s):  
Anthony A. Amato ◽  
Allan H. Ropper
Author(s):  
David Campo‐Caballero ◽  
Ana Vinagre‐Aragón ◽  
Javier Ruiz‐Martinez ◽  
Laura Naranjo ◽  
Raquel Ruiz‐García ◽  
...  

2020 ◽  
Vol 30 (8) ◽  
pp. 701-706
Author(s):  
Stela Lefter ◽  
Bernadette Monaghan ◽  
Brian McNamara ◽  
Michael J. Regan

Author(s):  
Taimour Alam ◽  
Alexander StJ.E. Barker ◽  
James J.P. Alix ◽  
Marios Hadjivassiliou ◽  
Dasappaiah G. Rao

AbstractBackground: Sensory ganglionopathy (SG) is characterised by asymmetrical sensory fibre degeneration, with the primary pathology occurring at the level of the dorsal root ganglion. It is seen in the context of autoimmune, paraneoplastic, and degenerative disorders. There is limited literature examining the electrophysiological correlate of the trigeminal ganglion and associated pathways, the blink reflex (BR), in cases of SG. Previous work has suggested that the BR is preserved in cases of SG associated with paraneoplasia. Methods: The local clinical neurophysiology database was searched for patients diagnosed with SG from peripheral nerve conduction studies in whom the BR was performed. Twenty-six patients were included in the final analysis. Results: Sjögren’s syndrome constituted the most common SG aetiology (8/26), followed by idiopathic cases (7/26) and paraneoplasia (5/26). BR abnormalities were seen in 9 of the 26 patients (34.6%) across all aetiologies. No patients reported sensory disturbance in the distribution of the trigeminal nerve, indicating that the changes noted are subclinical. Three patients showed abnormality of the R1 response; in the remaining six patients, only R2 responses were affected. Conclusions: Subclinical abnormalities of both R1 and R2 can be seen in the context of SG of varying aetiologies, including paraneoplasia. Performing the BR in patients with suspected of having SG may be helpful in providing additional evidence of patchy sensory fibre involvement that is characteristic of the disease.


1998 ◽  
Vol 64 (4) ◽  
pp. 561-561 ◽  
Author(s):  
M. SATAKE ◽  
Y. NAKAGAWA ◽  
S. YAMASHITA ◽  
E. HASHIGUCHI ◽  
N. FUJII ◽  
...  

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