RESUMO
Upper limb nerve injuries are common, and their treatment poses a challenge for physicians and surgeons. Experimental models help in minimum exploration of the functional characteristics of peripheral nerve injuries of forelimbs. This study was conducted to characterize the functional recovery (1, 3, 7, 10, 14, and 21 days) after median and ulnar nerve crush in mice and analyze the histological and biochemical markers of nerve regeneration (after 21 days). Sensory-functional impairments appeared after 1 day. The peripheral nerve morphology, the nerve structure, and the density of myelin proteins [myelin protein zero (P0) and peripheral myelin protein 22 (PMP22)] were analyzed after 21 days. Cold allodynia and fine motor coordination recovery occurred on the 10th day, and grip strength recovery was observed on the 14th day after injury. After 21 days, there was partial myelin sheath recovery. PMP22 recovery was complete, whereas P0 recovery was not. Results suggest that there is complete functional recovery even with partial remyelination of median and ulnar nerves in mice.
Assuntos
Nervo Mediano/fisiopatologia , Recuperação de Função Fisiológica , Remielinização , Nervo Ulnar/fisiopatologia , Animais , Masculino , Nervo Mediano/lesões , Nervo Mediano/metabolismo , Camundongos , Proteína P0 da Mielina/metabolismo , Proteínas da Mielina/metabolismo , Compressão Nervosa , Nervo Ulnar/lesões , Nervo Ulnar/metabolismoRESUMO
OBJECTIVE: Some case reports have suggested primary hyperparathyroidism (PHPT) and peripheral polyneuropathy (PPN) are associated; however, there are no reports of studies examining this possible relationship. The aim of this study was to evaluate peripheral nerve conduction in subjects with PHPT. METHODS: The study involved 17 patients with PHPT. Mean patient age was 60.5 ± 12.9 years, serum calcium concentration was 11.5 ± 1.0 mg/dL, and the serum parathyroid hormone (PTH) level was 315 ± 569 pg/dL. The control group comprised 17 individuals without PHPT. The mean age of controls was 60.8 ± 12.5 years and the serum calcium concentration was 9.8 ± 0.3 mg/dL. Motor and sensory nerve conduction was assessed by electroneurography (ENG). RESULTS: The following ENG parameters differed significantly between the PHPT and control groups: right (R) sural sensory nerve action potential conduction velocity (52.7 ± 6.3 m/s versus 58.0 ± 8.0 m/s; P = .041); R median compound muscle action potential (CMAP) amplitude (7.4 ± 1.6 mV versus 8.9 ± 1.7 mV; P = .002); R median CMAP latency (4.3 ± 1.2 ms versus 3.6 ± 0.6 ms; P = .032); R tibial CMAP latency (4.2 ± 1.1 ms versus 3.3 ± 0.4 ms; P = .001). The neurological examination was normal in all patients. CONCLUSION: Our data demonstrate an association between PHPT and peripheral neurological alterations, consistent with subclinical sensory-motor PPN.
Assuntos
Hiperparatireoidismo Primário/fisiopatologia , Sistema Nervoso Periférico/fisiopatologia , Polineuropatias/etiologia , Potenciais de Ação , Idoso , Cálcio/sangue , Estudos Transversais , Feminino , Humanos , Hipercalcemia/etiologia , Hiperparatireoidismo Primário/sangue , Hiperparatireoidismo Primário/metabolismo , Masculino , Nervo Mediano/metabolismo , Nervo Mediano/fisiopatologia , Pessoa de Meia-Idade , Neurônios Motores/metabolismo , Condução Nervosa , Hormônio Paratireóideo/sangue , Sistema Nervoso Periférico/metabolismo , Polineuropatias/fisiopatologia , Células Receptoras Sensoriais/metabolismo , Índice de Gravidade de Doença , Nervo Sural/metabolismo , Nervo Sural/fisiopatologia , Nervo Tibial/metabolismo , Nervo Tibial/fisiopatologiaRESUMO
Nerve conduction is profoundly affected in Spinocerebellar ataxia 2 (SCA2) even before the onset of the disease, but there is no information regarding its progression to the final stage of SCA2. In order to study the progression patterns of nerve conduction abnormalities in SCA2 we performed a prospective follow up evaluation of sensory and motor conduction in 21 SCA2 mutation carriers-initially presymptomatics- and 19 non-SCA2 mutation carriers during 20years. The earliest electrophysiological alterations were the reduction of sensory amplitudes in median and sural nerves, which could be found 8 to 5years prior disease onset and in the last 4years of the preclinical stage respectively. These abnormalities were followed by the increase of sensory latencies and decrease of conduction velocities. Sensory amplitudes progressively decreased during the follow-up clinical stage, rendering almost all patients with abnormal amplitudes and lack of sensory potentials, with faster progression rates in patients with larger CAG repeat lengths. Peripheral motor nerves showed the later involvement. These findings were used to define three distinct stages that describe the progression of the peripheral neuropathy. We suggest that sensory amplitudes could be useful biomarkers to assess the progression of peripheral nerve involvement and therefore to evaluate future clinical trials of therapeutic agents.
Assuntos
Doenças do Sistema Nervoso Periférico/diagnóstico , Doenças do Sistema Nervoso Periférico/fisiopatologia , Ataxias Espinocerebelares/diagnóstico , Ataxias Espinocerebelares/fisiopatologia , Adolescente , Adulto , Ataxinas , Biomarcadores/análise , Criança , Estudos de Coortes , Progressão da Doença , Eletrodiagnóstico , Feminino , Seguimentos , Humanos , Masculino , Nervo Mediano/metabolismo , Nervo Mediano/fisiopatologia , Pessoa de Meia-Idade , Proteínas do Tecido Nervoso/genética , Condução Nervosa/genética , Doenças do Sistema Nervoso Periférico/genética , Valor Preditivo dos Testes , Estudos Prospectivos , Tempo de Reação/genética , Sensibilidade e Especificidade , Células Receptoras Sensoriais/fisiologia , Índice de Gravidade de Doença , Ataxias Espinocerebelares/genética , Nervo Sural/metabolismo , Nervo Sural/fisiopatologia , Fatores de TempoRESUMO
Denatured muscle grafts obtained by freeze thawing have been proposed to replace losses in the peripheral nerves. In the present report, we compare the performance of such grafts with fresh grafts in the rat median nerve. A long-term effect of muscle interposition on reinnervation was studied by behavioral assessment, muscle ATPase histochemistry, and retrograde labeling of motoneurons. There was no difference in grasping strength recovery between fresh and denatured 10-mm-long muscle grafts. Recovery was delayed and incomplete. Twelve months after surgery, only 50% of the normal grasping strength was attained. Grasping recovery was not observed in the 20-mm-long graft groups. Pathway reinnervation was non-specific with a huge amount of motor fiber misdirection. A decrease in the number of misdirected motor fibers occurred with time and activity recovery. Muscle reinnervation was not specific with disturbance of the mosaic pattern and type-grouping formation. Preference of type I axons for reinnervating deeper zones was observed. Type I aberrant reinnervation was demonstrated in the muscle periphery. The mosaic distribution of type I and II muscle fibers was not stable, and readjustments were observed with time, correlating with grasping improvement. During grasping strength recovery, there was a decrease in the number of type I fibers peripherally located and an increase of those deeply disposed. A time- and activity-related recovery was associated with readjustment in the pathways and muscle fiber rearrangement. We suggest that muscle activity generates specificity.