Vagner Wilian Batista E Sá1, Maria Katia Gomes2, Maria Luíza Sales Rangel3, Tiago Arruda Sanchez2, Filipe Azaline Moreira2, Sebastian Hoefle4, Inaiacy Bittencourt Souto2, Antônio José Ledo Alves da Cunha2, Ana Paula Fontana2, Claudia Domingues Vargas5. 1. Núcleo de Pesquisas em Fisioterapia, Universidade Castelo Branco, Rio de Janeiro, Rio de Janeiro, Brazil; Programa de Pós-Graduação em Clínica Médica, Hospital Universitário Clementino Fraga Filho e Departamento de Medicina de Família e Comunidade/Faculdade de Medicina da Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil; Laboratório de Neurobiologia II, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil. 2. Programa de Pós-Graduação em Clínica Médica, Hospital Universitário Clementino Fraga Filho e Departamento de Medicina de Família e Comunidade/Faculdade de Medicina da Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil. 3. Laboratório de Neurobiologia II, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil. 4. Laboratório de Neurobiologia II, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil; Cognitive and Behavioral Neuroscience Unit and Neuroinformatics Workgroup, D'Or Institute for Research and Education, Rio de Janeiro, Brazil. 5. Laboratório de Neurobiologia II, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil; Instituto de Neurologia Deolindo Couto da Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Abstract
BACKGROUND: Leprosy is an endemic infectious disease caused by Mycobacterium leprae that predominantly attacks the skin and peripheral nerves, leading to progressive impairment of motor, sensory and autonomic function. Little is known about how this peripheral neuropathy affects corticospinal excitability of handgrip muscles. Our purpose was to explore the motor cortex organization after progressive peripheral nerve injury and upper-limb dysfunction induced by leprosy using noninvasive transcranial magnetic stimulation (TMS). METHODS: In a cross-sectional study design, we mapped bilaterally in the primary motor cortex (M1) the representations of the hand flexor digitorum superficialis (FDS), as well as of the intrinsic hand muscles abductor pollicis brevis (APB), first dorsal interosseous (FDI) and abductor digiti minimi (ADM). All participants underwent clinical assessment, handgrip dynamometry and motor and sensory nerve conduction exams 30 days before mapping. Wilcoxon signed rank and Mann-Whitney tests were performed with an alpha-value of p<0.05. FINDINGS: Dynamometry performance of the patients' most affected hand (MAH), was worse than that of the less affected hand (LAH) and of healthy controls participants (p = 0.031), confirming handgrip impairment. Motor threshold (MT) of the FDS muscle was higher in both hemispheres in patients as compared to controls, and lower in the hemisphere contralateral to the MAH when compared to that of the LAH. Moreover, motor evoked potential (MEP) amplitudes collected in the FDS of the MAH were higher in comparison to those of controls. Strikingly, MEPs in the intrinsic hand muscle FDI had lower amplitudes in the hemisphere contralateral to MAH as compared to those of the LAH and the control group. Taken together, these results are suggestive of a more robust representation of an extrinsic hand flexor and impaired intrinsic hand muscle function in the hemisphere contralateral to the MAH due to leprosy. CONCLUSION: Decreased sensory-motor function induced by leprosy affects handgrip muscle representation in M1.
BACKGROUND:Leprosy is an endemic infectious disease caused by Mycobacterium leprae that predominantly attacks the skin and peripheral nerves, leading to progressive impairment of motor, sensory and autonomic function. Little is known about how this peripheral neuropathy affects corticospinal excitability of handgrip muscles. Our purpose was to explore the motor cortex organization after progressive peripheral nerve injury and upper-limb dysfunction induced by leprosy using noninvasive transcranial magnetic stimulation (TMS). METHODS: In a cross-sectional study design, we mapped bilaterally in the primary motor cortex (M1) the representations of the hand flexor digitorum superficialis (FDS), as well as of the intrinsic hand muscles abductor pollicis brevis (APB), first dorsal interosseous (FDI) and abductor digiti minimi (ADM). All participants underwent clinical assessment, handgrip dynamometry and motor and sensory nerve conduction exams 30 days before mapping. Wilcoxon signed rank and Mann-Whitney tests were performed with an alpha-value of p<0.05. FINDINGS: Dynamometry performance of the patients' most affected hand (MAH), was worse than that of the less affected hand (LAH) and of healthy controls participants (p = 0.031), confirming handgrip impairment. Motor threshold (MT) of the FDS muscle was higher in both hemispheres in patients as compared to controls, and lower in the hemisphere contralateral to the MAH when compared to that of the LAH. Moreover, motor evoked potential (MEP) amplitudes collected in the FDS of the MAH were higher in comparison to those of controls. Strikingly, MEPs in the intrinsic hand muscle FDI had lower amplitudes in the hemisphere contralateral to MAH as compared to those of the LAH and the control group. Taken together, these results are suggestive of a more robust representation of an extrinsic hand flexor and impaired intrinsic hand muscle function in the hemisphere contralateral to the MAH due to leprosy. CONCLUSION: Decreased sensory-motor function induced by leprosy affects handgrip muscle representation in M1.
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