Axon reflex activation of Deiters neurones from the cerebellar cortex through collaterals of the cerebellar afferents

1969 ◽  
Vol 8 (3) ◽  
Author(s):  
M. Ito ◽  
N. Kawai ◽  
M. Udo ◽  
N. Mano
Keyword(s):  
Cerebellar Cortex ◽  
Axon Reflex ◽  
Cerebellar Afferents ◽  
Deiters Neurones ◽  
Reflex Activation

scholarly journals Towards a multi-function mapping of the cerebellar cortex

Brain ◽  
2017 ◽  
Vol 140 (3) ◽  
pp. 522-524 ◽  
Author(s):  
Maedbh King ◽  
Carlos Hernandez-Castillo ◽  
Jörn Diedrichsen
Keyword(s):  
Cerebellar Cortex ◽  
Function Mapping

scholarly journals Diagnosing small fiber neuropathy in clinical practice: a deep phenotyping study

2021 ◽  
Vol 14 ◽  
pp. 175628642110043
Author(s):  
Nadine Egenolf ◽  
Caren Meyer zu Altenschildesche ◽  
Luisa Kreß ◽  
Katja Eggermann ◽  
Barbara Namer ◽  
...  
Keyword(s):  
Neurological Examination ◽  
Punch Biopsy ◽  
Small Fiber Neuropathy ◽  
Fiber Density ◽  
Axon Reflex ◽  
Small Fiber ◽  
Corneal Confocal Microscopy ◽  
Intraepidermal Nerve Fiber Density ◽  
Number Of Patients ◽  
Skin Punch Biopsy

Background and aims: Small fiber neuropathy (SFN) is increasingly suspected in patients with pain of uncertain origin, and making the diagnosis remains a challenge lacking a diagnostic gold standard. Methods: In this case–control study, we prospectively recruited 86 patients with a medical history and clinical phenotype suggestive of SFN. Patients underwent neurological examination, quantitative sensory testing (QST), and distal and proximal skin punch biopsy, and were tested for pain-associated gene loci. Fifty-five of these patients additionally underwent pain-related evoked potentials (PREP), corneal confocal microscopy (CCM), and a quantitative sudomotor axon reflex test (QSART). Results: Abnormal distal intraepidermal nerve fiber density (IENFD) (60/86, 70%) and neurological examination (53/86, 62%) most frequently reflected small fiber disease. Adding CCM and/or PREP further increased the number of patients with small fiber impairment to 47/55 (85%). Genetic testing revealed potentially pathogenic gene variants in 14/86 (16%) index patients. QST, QSART, and proximal IENFD were of lower impact. Conclusion: We propose to diagnose SFN primarily based on the results of neurological examination and distal IENFD, with more detailed phenotyping in specialized centers.

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