From the Guidelines
Disuse atrophy in stroke patients is the deterioration of muscle tissue that occurs when muscles aren't regularly used following a stroke, and it can be prevented and treated with early mobilization, physical therapy, and proper nutritional support, as emphasized in the most recent guidelines 1.
Definition and Causes
Disuse atrophy in stroke patients develops when paralysis or weakness on one side of the body prevents normal movement, causing muscles to shrink and weaken over time. The process begins within days of immobility, with patients potentially losing 1-3% of muscle strength daily during complete bed rest. This condition is a significant concern in stroke rehabilitation, as it can impede rehabilitation progress and functional recovery.
Manifestations and Consequences
Disuse atrophy manifests as visible muscle wasting, decreased strength, reduced endurance, and limited range of motion. It occurs because lack of muscle contraction leads to protein breakdown exceeding protein synthesis, resulting in decreased muscle fiber size and number. This atrophy can significantly impact a stroke patient's functional outcomes and quality of life, making it essential to address promptly.
Prevention and Treatment
Prevention and treatment of disuse atrophy focus on:
- Early mobilization
- Physical therapy with passive and active exercises
- Neuromuscular electrical stimulation
- Proper positioning
- Nutritional support with adequate protein intake As noted in recent guidelines, early intervention is crucial, and a multidisciplinary approach to rehabilitation can significantly improve a stroke patient's functional outcomes and quality of life 1.
Importance of Early Intervention
Addressing disuse atrophy promptly is vital, as it is easier to prevent muscle loss than to rebuild atrophied muscle. Proper intervention can significantly improve a stroke patient's functional outcomes and quality of life, highlighting the need for timely and effective rehabilitation strategies 1.
From the Research
Definition of Disuse Atrophy in Stroke Patients
Disuse atrophy in stroke patients refers to the loss of skeletal muscle mass due to inactivity or lower than 'normal' use, often resulting from hemiparesis or immobilization after a stroke [ 2 ]. This condition can lead to weakness, metabolic comorbidities, and a decline in functional outcomes.
Causes and Mechanisms
The decline in muscle mass is attributed largely to a decline in postabsorptive and postprandial muscle protein synthesis rates [ 3 ]. Disuse muscle atrophy occurs even in healthy subjects as early as 4 days after bed rest immobilization and progresses further correlating with the duration of immobilization [ 2 ]. Free radical scavengers are known to play an important role in the development of disuse muscle atrophy [ 2 ].
Key Features
- Loss of skeletal muscle mass due to inactivity or lower than 'normal' use
- Often results from hemiparesis or immobilization after a stroke
- Leads to weakness, metabolic comorbidities, and a decline in functional outcomes
- Can be prevented or alleviated with interventional strategies, including exercise (mimetics) and appropriate nutritional support [ 3 ]
- Free radical scavengers may play a role in preventing disuse atrophy [ 2 ]
Related Concepts
- Muscle atrophy and weakness occur as a consequence of disuse after musculoskeletal injury (MSI) [ 4 ]
- Skeletal muscle disuse atrophy can be attenuated with dietary protein or free amino acid-based supplementation [ 4 ]
- Exercise sensitizes skeletal muscle to the anabolic effect of protein ingestion, and early rehabilitation may act synergistically with dietary protein to protect muscle mass and function during postinjury disuse conditions [ 4 ]