Post-stroke sarcopenia as a neuromuscular disorder: a mini review of neural mechanisms and clinical implications

Post-stroke sarcopenia represents a distinct neuromuscular disorder characterized by progressive muscle loss and functional decline. Unlike age-related sarcopenia, stroke-induced muscle wasting involves specific neural mechanisms originating from central nervous system injury.

To systematically review the neural mechanisms underlying post-stroke sarcopenia and synthesize evidence on its clinical implications, diagnostic approaches, and therapeutic interventions.

A mini review of the literature was conducted, synthesizing evidence from key studies addressing neural mechanisms, pathophysiology, diagnosis, or treatment of post-stroke sarcopenia.

Post-stroke sarcopenia affects 11%-67% of stroke survivors, with paretic limbs losing >30% muscle mass within 6 months. The pathophysiology involves a cascade from corticospinal tract damage to motor neuron degeneration, neuromuscular junction dysfunction, and muscle fiber atrophy. Key mechanisms include denervation-induced neurogenic atrophy, inflammatory dysregulation (IL-6, TNF-α, myostatin upregulation), and impaired IGF-1/Akt/mTOR signaling. Asymmetric muscle loss patterns distinguish this condition from primary sarcopenia. Diagnostic approaches combine imaging (DXA, BIA, CT), functional assessments (grip strength, gait speed, SPPB), and stroke-specific criteria. Multimodal interventions including neuromuscular electrical stimulation, resistance training, nutritional support, and spasticity management show promise.

Post-stroke sarcopenia is a neurogenic disorder requiring distinct diagnostic criteria and targeted interventions. Early recognition and multidisciplinary management are essential for optimizing functional recovery and reducing disability burden.