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Objective: This study investigated how peripheral axonal excitability changes in ischemic stroke patients with hemiparesis or hemiplegia, reflecting the plasticity of motor axons due to corticospinal tract alterations along the poststroke stage.
Methods: Each subject received a clinical evaluation, nerve conduction study, and nerve excitability test. Nerve excitability tests were performed on motor median nerves in paretic and non-paretic limbs in the acute stage of stroke. Control nerve excitability test data were obtained from age-matched control subjects. Some patients underwent excitability examinations several times in subacute or chronic stages.
Results: A total of thirty patients with acute ischemic stroke were enrolled. Eight patients were excluded due to severe entrapment neuropathy in the median nerve. The threshold current for 50% compound muscle action potential (CMAP) was higher in paretic limbs than in control subjects. Furthermore, in the cohort with severe patients (muscle power ≤ 3/5 in affected hands), increased threshold current for 50% CMAP and reduced subexcitability were noted in affected limbs than in unaffected limbs. In addition, in the subsequent study of those severe patients, threshold electrotonus increased in the hyperpolarization direction: TEh (100-109 ms), and the minimum I/V slope decreased. The above findings suggest the less excitable and less accommodation in lower motor axons in the paretic limb caused by ischemic stroke.
Conclusion: Upper motor neuron injury after stroke can alter nerve excitability in lower motor neurons, and the changes are more obvious in severely paretic limbs. The accommodative changes of axons progress from the subacute to the chronic stage after stroke. Further investigation is necessary to explore the downstream effects of an upper motor neuron insult in the peripheral nerve system.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9531785 | PMC |
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0275450 | PLOS |
Ann Clin Transl Neurol
September 2025
Department of Neurology, Brain Centre Utrecht, University Medical Centre Utrecht, Utrecht, the Netherlands.
Objective: We investigated the effects of C9orf72 mutation carriership on peripheral nerve excitability in asymptomatic individuals from families with a history of C9orf72 amyotrophic lateral sclerosis (ALS) and patients.
Methods: We included 47 asymptomatic individuals from families with a history of C9orf72 ALS, of whom 23 were carriers (C9) and 24 were noncarriers (C9). In addition, 11 C9 and 110 C9 ALS patients and 50 healthy controls participated.
J Neurophysiol
September 2025
Shirley Ryan AbilityLab, Chicago, IL.
Spasticity results from upper motor neuron lesions and can create a deforming force, pain, and is often accompanied by contracture. While the origin of spasticity is neural, there is ample evidence of secondary muscle changes. Here we use direct measurement of the force-frequency relationship (FFR) to characterize human muscle's physiological properties.
View Article and Find Full Text PDFNeural Regen Res
September 2025
Department of Physiology, Army Medical University, Chongqing, China.
Injuries to the central nervous system can disrupt body functions and often cause excessive sympathetic activity, leading to immune suppression known as central nervous system injury- associated immunodepression syndrome. The connection between central nervous system injury and central nervous system injury-associated immunodepression syndrome is not fully clear. Gammaaminobutyric acid, an important inhibitory neurotransmitter, helps excitation-inhibition balance in the nervous system, especially after spinal cord injuries.
View Article and Find Full Text PDFNeural Regen Res
September 2025
Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Spinal V3 interneurons are glutamatergic neurons that are distributed among the dorsal, intermediate, and ventral spinal cord. They are involved in broad neural circuit connections in the central nervous system. Functionally, they play important roles in locomotion, such as the maintenance of robust and balanced gaits during walking.
View Article and Find Full Text PDFCase Rep Med
August 2025
Department of Medicine, Medical College Baroda, Vadodara, Gujarat, India.
Potassium is vital for cellular function, particularly in excitable tissues like nerves and muscles, which rely on potassium gradients to function normally. Hypokalemia can lead to severe issues such as muscle weakness and irregular heart rhythms. This case series presents four instances of hypokalemic paralysis, a neuromuscular condition that can be either periodic or isolated.
View Article and Find Full Text PDF