Background:Carpal tunnel syndrome (CTS) is a common entrapment neuropathy. Diagnosis of CTS is usually based on a combination of clinical symptoms and electrodiagnostic study (EDS). Ultrasonography (US) also has been shown to be a useful diagnostic tool in CTS and is based on an increase in the median nerve cross-sectional area (CSA) at the level of the pisiform bone. In this study we assessed findings in US in correlation with severity of CTS.Materials and Method:This was a cross-sectional case-control study, which was carried out on November 2012 to July 2013. Subjects were chosen from patients who referred to the Alzahra Hospital (Isfahan, Iran). Patients were classified as having mild, moderate, and severe CTS according to EDS and high-resolution US was performed for CSA measurement at the tunnel inlet.Results:A total of 87 individuals screened and 52 subjects (81 hands) met all inclusion and no exclusion criteria. The mean ± SD of the CSA was 0.12 ± 0.03 cm2 (range, 0.08–0.18) in mild, 0.15 ± 0.03 cm2 (range, 0.08–0.19) in moderate, and 0.19 ± 0.06 cm2 (range, 0.11–0.32) in severe CTS. We detected a significant correlation between MN CSA and the severity of CTS (P < 0.001).Conclusion:In conclusion it is expected that sonography may serve as an additional or complementary method which is useful and reliable in assessing the severity of CTS.
Nonneoplastic demyelinating processes of the brain with mass effect on magnetic resonance imaging can cause diagnostic difficulties. It requires differential diagnosis between the tumefactive demyelinating lesion and the coexistence of neoplasm. We document the case of 41-year-old woman with clinical and radiological findings suggestive of multiple sclerosis. Additional investigations confirmed the coexistence of astrocytoma. This report emphasizes the importance of considering brain tumors in the differential diagnosis of primary demyelinating disease presenting with a cerebral mass lesion.
Background: Multiple sclerosis (MS) may have atypical presentations, one of whom being migraine-like headaches. This could be explained as following: the demyelination process in MS may involve brain structures or signaling pathways involved in migraine physiopathology, and therefore, simulate migraine headaches.
Case presentation: This case report is about a middle-aged male who developed a new-onset severe headache with migraine properties accompanied with vertigo, and was finally diagnosed with MS.
Conclusions: MS may have atypical presentations like severe headaches accompanied by additional symptoms, indicating the involvement of various brain structures; when working up such headaches, MS should be kept in mind besides other etiologies like vascular, infectious, and neoplastic conditions, and even primary migraine.
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