Search

IntroductionAnimal and human studies of diabetes have shown significant alterations in nerve blood flow (NBF), which may also play a role in the development of neuropathy. However, the non-invasive assessment of NBF in human subjects has remained elusive until the recent technological advancements in ultrasound (US) technology. We undertook sonographic assessment of NBF in 75 patients with type 2 diabetes and correlated the findings with neuropathy severity scores and electrophysiological parameters.MethodsBlinded median and tibial nerve ultrasound scans were performed at non-entrapment sites using a high-resolution linear probe. NBF was quantified using power Doppler techniques to obtain the vessel score (VSc) and maximum perfusion intensity (MPI). Routine nerve conduction studies were performed, and neuropathy severity was assessed using the total neuropathy score (TNS). Aged- and gender-matched controls were enrolled.ResultsDiabetic nerves had higher rates of NBF detection (28%) compared to the control group (p2 vs. 7.2 ± 0.1 mm2, p2 vs. 12. 8 ±0.5 mm2, pConclusionsPeripheral nerve hypervascularity is detectable by US in moderate to severe diabetic neuropathy with prominent sensory dysfunction. Consistent with previous studies, the sonographic detection of NBF is a pathological finding.

Carpal tunnel syndrome (CTS) is a common entrapment neuropathy. Electrodiagnostic testing (EMG) is used to confirm the diagnosis. It is not known what the diagnostic accuracy of high-resolution sonography is in comparison to EMG.The aim of this study was to compare the diagnostic accuracy of both tests in CTS patients.A prospective cohort of 207 patients with possible CTS underwent high-resolution sonography and EMG. The diagnosis of CTS was based on clinical signs and symptoms. The cross-sectional area of the median nerve at the carpal tunnel inlet and at the distal one-third level of the forearm was assessed by an investigator, blinded to the clinical and EMG data. Normal sonographic values were obtained from 137 controls. All patients and 40 controls underwent a standardised nerve conduction study. The kappa coefficient was used to evaluate the relationship between sonography, EMG and clinical diagnosis.The cross-sectional area at the distal one-third of the forearm was not significantly different between the controls and patients (p = 0.59), whereas the cross-sectional area at the carpal tunnel inlet was significantly increased in the patient group (p0.0001). The kappa coefficient for EMG using the median-ulnar distal sensory latency difference versus clinical evaluation was 0.64 and, for sonography, this coefficient was 0.69; these were not statistically different (p = 0.37). Combining the two tests resulted in a kappa coefficient of 0.72, which was not significantly different from sonography alone (p = 0.73).In patients with a clinical diagnosis of CTS, the accuracy of sonography is similar to that for EMG. Sonography is probably preferable because it is painless, easily accessible and preferred by the patients.

The risk factors for treatment related clinical fluctuations, relapses occurring after initial therapeutic induced stabilisation or improvement, were evaluated in a group of 172 patients with Guillain-Barre syndrome. Clinical, laboratory, and electrodiagnostic features of all 16 patients with Guillain-Barre syndrome with treatment related fluctuations, of whom 13 were retreated, were compared with those who did not have fluctuations. No significant differences were found between patients with Guillain-Barre syndrome treated with plasma exchange and patients treated with intravenous immune globulins either alone or in combination with high dose methylprednisolone. None of the patients with Guillain-Barre syndrome with preceding gastrointestinal illness, initial predominant distal weakness, acute motor neuropathy, or anti-GM1 antibodies showed treatment related fluctuations. On the other hand patients with fluctuations showed a trend to have the fluctuations after a protracted disease course. It is therefore suggested that treatment related clinical fluctuations are due to a more prolonged immune attack. There is no indication that the fluctuations are related to treatment modality. The results of this study may help the neurologist to identify patients with Guillain-Barre syndrome who are at risk for treatment related fluctuations.