Focal slowing of nerve conduction velocity in leprosy patients unveiled through multisegmented nerve analysis.

BACKGROUND AND AIMS: Leprosy is a chronic infectious disease caused by Mycobacterium leprae (M. leprae), an intracellular bacillus that systematically invades the peripheral nerves. Diagnosing leprosy neuropathy is still a defying skill, and late diagnosis and treatment are still a reality. Based on the biological characteristics of M. leprae, particularly its preference for invading the Schwann cells localized at the coldest areas of human body, we hypothesized that these areas have focal demyelination that may escape detection through standard nerve conduction studies (NCSs) protocols. METHODS: Twenty-five patients with confirmed multibacillary leprosy and 14 controls were accessed. A multisegmented NCS protocol (MP) was performed, targeting short segments through the coldest areas, to identify focal areas of slowed conduction velocity. The effectiveness of this multisegmented protocol was compared to the standard protocol (SP) to detect abnormalities. RESULTS: All leprosy patients presented an abnormal study with the MP, contrasting to 19 with the SP. The most frequent NCS pattern was an asymmetric neuropathy with focal slowing of conduction velocity, found in 23 out of 25 leprosy patients. Significant differences favoring the proposed method were observed when comparing the MP with the SP. Notably, the MP increased the sensitivity to detect abnormalities by 122%, 133%, and 257% for the median, peroneal, and tibial nerves, respectively. MP also increases sensitivity to detect focal abnormalities in the ulnar nerve. INTERPRETATION: The MP protocol significantly increases the sensitivity of NCSs to detect neurophysiological abnormalities in leprosy neuropathy.

Vocal Parameters and Self-Perception in Individuals With Adductor Spasmodic Dysphonia.

OBJECTIVE: The study aimed to compare and correlate perceptual-auditory analysis of vocal parameters and self-perception in individuals with adductor spasmodic dysphonia before and after the application of botulinum toxin. STUDY DESIGN: This is a prospective cohort study. METHODS: Sixteen individuals with a diagnosis of adductor spasmodic dysphonia were submitted to the application of botulinum toxin in the thyroarytenoid muscle, to the recording of a voice signal, and to the Voice Handicap Index (VHI) questionnaire before the application and at two time points after application. Two judges performed a perceptual-auditory analysis of eight vocal parameters with the aid of the Praat software for the visualization of narrow band spectrography, pitch, and intensity contour. RESULTS: Comparison of the vocal parameters before toxin application and on the first return revealed a reduction of oscillation intensity (P = 0.002), voice breaks (P = 0.002), and vocal tremor (P = 0.002). The same parameters increased on the second return. The degree of severity, strained-strangled voice, roughness, breathiness, and asthenia was unchanged. The total score and the emotional domain score of the VHI were reduced on the first return. There was a moderate correlation between the degree of voice severity and the total VHI score before application and on the second return, and a weak correlation on the first return. CONCLUSIONS: Perceptual-auditory analysis and self-perception proved to be efficient in the recognition of vocal changes and of the vocal impact on individuals with adductor spasmodic dysphonia under treatment with botulinum toxin, permitting the quantitation of changes along time.