Changes in leg muscle biopsies appear to be common in children and teenagers with JIA. The presence of inflammatory cells in the muscle and expression of MHC class II on muscle fibres may be a sign of inflammatory myopathy. There are no findings of type II muscle fibre hypotrophy or neuropathy, as in adults with RA.
The aim of this study was to investigate to what extent women with superficial dyspareunia can be diagnosed for both partial vaginismus (PaV) and vulvar vestibulitis (VVS) and to discover to what extent surface electromyography (sEMG) of the pelvic floor muscles (PFM) can distinguish between women with PaV solely, PaV+ VVS, and asymptomatic women. A total of 224 consecutive women with superficial dyspareunia were examined clinically for both PaV and VVS diagnoses. We examined 47 women with PaV+/-VVS and 27 asymptomatic women with sEMG of the PFM. The results showed that 102/224 women with superficial dyspareunia and 33/47 women with PaV in the sEMG part of the study had both PaV and VVS. All women with VVS had vaginismus, while 42/224 had PaV but not VVS. sEMG measurements revealed no significant differences between the three groups of women (PaV solely, PaV + VVS, and asymptomatic). Almost half of the women with superficial dyspareunia referred to our clinic have both the diagnosis PaV and VVS. sEMG was not a method of any value to distinguish between women with PaV solely, PaV + VVS, or asymptomatic women. The increased tone found clinically in the PFM of women with PaV+/-VVS may be of other origin than electrogenic contractions.
Optic neuritis (ON) causes axonal loss as reflected by thinning of retinal nerve fiber layer (RNFL) and can be tracked by optical coherence tomography (OCT) about 6 months after ON onset, when swelling of optic nerve head (ONH) has vanished. Changes of macular ganglion cell layer (GCL) thickness provide another window to track the disease process in ON. GCL thinning over time in relation to RNFL change after ON remains elusive. Using OCT, we followed 4 patients with acute unilateral isolated ON for more than 9 months. A diagnosis of multiple sclerosis (MS) was established in all 4 patients. First follow-up was 2-3 weeks after ON onset, and thereafter every 2-3 months. RNFL swelling peaked during first month after acute ON, followed by rapidly reduced swelling (pseudoatrophy) during following 2 months, and thereafter successively vanished 6 months after ON onset. GCL thinning was observed 1-3 months after ON onset, i.e. already during optic disk swelling and before real RNFL thinning. The results imply that quantifying GCL thickness provides opportunities to monitor early axonal loss and ON-to-MS progression, and facilitates distinguishing real atrophy from pseudoatrophy of RNFL after acute ON.
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