Quadriplegic Hands: Spinal Levels, Joint Changes, and Function
Explore how spinal cord injury affects hand function, muscle control, joint structure, and sensation in individuals with quadriplegia.
Explore how spinal cord injury affects hand function, muscle control, joint structure, and sensation in individuals with quadriplegia.
The hands are essential for daily activities, but for individuals with quadriplegia, their function is significantly altered based on the level of spinal cord injury. Movement, strength, and sensation vary widely, impacting independence and requiring adaptations.
Understanding how spinal levels affect hand function provides insight into changes in muscle control, joint structure, and sensory perception.
Hand function in quadriplegia depends on the level of spinal cord injury, as different segments control specific muscle groups. Injuries at or above C5 result in severe impairment, as wrist and finger muscles receive little or no input. Individuals with C5 injuries retain shoulder and elbow flexion due to biceps brachii function but lack wrist extensors and intrinsic hand muscles, severely restricting grasping. Wrist-driven orthoses are often necessary for functional use.
At C6, partial wrist extension is possible due to extensor carpi radialis activation, enabling tenodesis grasp—a biomechanical mechanism where passive finger flexion occurs with wrist extension. This movement allows for object manipulation despite the lack of active finger flexion. Training in tenodesis techniques improves independence in self-care tasks, emphasizing the importance of rehabilitation strategies that optimize residual function.
C7 injuries improve hand use with functional triceps brachii and additional wrist and finger extensors. Active elbow extension enhances stability for reaching and weight-bearing, while partial finger extension aids object release. However, fine motor control remains limited due to the lack of intrinsic hand muscle activation, governed by C8-T1. Research in neurorehabilitation has explored functional electrical stimulation (FES) to improve grasp and release, showing promising outcomes.
Injuries at C8-T1 preserve most intrinsic hand muscle function. C8-level injuries allow active finger flexion, enabling a more coordinated grip, though intrinsic muscle weakness can affect precision tasks. T1 injuries primarily impact small hand muscles, leading to subtle fine motor deficits but generally allowing near-normal grasping. Functional recovery at these levels is influenced by spasticity, muscle imbalances, and compensatory movement patterns.
Spinal cord damage disrupts neural signals controlling muscle activation, leading to characteristic changes in hand function. The degree of impairment depends on which motor neurons remain intact. In quadriplegia, movement patterns shift, often requiring compensatory strategies for grasping and object manipulation.
At C5, the absence of wrist and finger extensor activation forces reliance on passive flexion and external support to secure objects. Without voluntary control of the flexor digitorum profundus and superficialis, grasping is limited. Individuals with C5 injuries often compensate by increasing shoulder and elbow movement, which contributes to fatigue. Targeted rehabilitation can help optimize residual motor control.
With C6 injuries, wrist extension due to partial extensor carpi radialis function introduces the tenodesis effect, allowing passive finger flexion with wrist extension. Training in tenodesis grasp significantly improves independence in utensil handling, dressing, and wheelchair propulsion. However, the lack of active finger extension makes object release difficult, requiring adaptive tools or assistance.
C7 injuries bring greater muscle function, with triceps brachii activation stabilizing arm movements and improving force generation. Additional wrist and finger extensors, such as extensor digitorum, enhance hand opening and coordination. Despite these gains, intrinsic hand muscle function remains absent, limiting fine motor control. Neuromuscular stimulation has shown potential for improving dexterity, with some individuals demonstrating better grip precision.
At C8, voluntary finger flexion is restored, improving grip strength and coordination. However, intrinsic muscle weakness affects tasks requiring rapid finger adjustments or sustained precision. Individuals with C8 injuries often exhibit reduced pinch force and fine motor endurance, impacting activities like writing or buttoning clothing. Hand therapy focusing on strengthening residual muscle function has been beneficial.
Quadriplegia leads to significant changes in joint and structural integrity, as immobility and altered muscle function create imbalances in force distribution. Without normal neural input, wrist and finger muscles undergo atrophy and spasticity, affecting joint positioning and stability. Over time, these changes contribute to contractures, deformities, and soft tissue alterations.
A common structural adaptation is joint stiffness due to prolonged positioning in flexed or extended states. Connective tissue shortening, especially in the flexor tendons, can lead to fixed contractures. In higher cervical injuries, weak extensors and relatively stronger flexors promote a curled hand posture, limiting object manipulation. Early intervention with splinting and range-of-motion exercises helps preserve joint mobility and reduce complications.
The wrist undergoes structural changes, particularly in individuals relying on the tenodesis effect for grasping. Repeated use of passive finger flexion during wrist extension places stress on the carpometacarpal and metacarpophalangeal joints, leading to ligamentous laxity. This can reduce the efficiency of tenodesis grasp. Custom orthotic support is often recommended to stabilize the wrist, especially for individuals with C6 injuries who depend on this mechanism.
Thumb positioning is also affected, as intrinsic muscle dysfunction impacts pinch grasp. The adductor pollicis and thenar muscles, primarily innervated by C8-T1, are essential for thumb opposition and stability. When these muscles lose function, the thumb may drift into adduction, reducing dexterity. Surgical interventions, such as tendon transfers, have been explored to restore thumb mobility, with some procedures improving lateral pinch strength.
Sensory function in quadriplegia depends on the level of spinal cord injury, as touch, temperature, and proprioception rely on intact neural pathways. Disruptions lead to partial or complete sensory loss, making it difficult to detect pressure, texture, and pain. This increases the risk of injury, such as burns from hot surfaces or pressure sores from prolonged contact with rigid materials.
Loss of proprioception—awareness of hand and finger positioning without visual input—complicates hand use. Without internal feedback, movements become less coordinated, requiring greater reliance on vision. Studies suggest the brain adapts by enhancing reliance on other senses, such as vision or auditory cues, to guide movements. Functional MRI scans show increased activity in visual and auditory processing areas corresponding to sensory loss.
Partial sensation may result in altered perceptions, including tingling, hypersensitivity, or neuropathic pain. These sensations stem from abnormal nerve signaling and vary in intensity. Neuropathic pain, often described as burning or electric shock-like, is a common complication. Management strategies, including neuromodulatory therapies and medications like gabapentinoids, have been explored to alleviate discomfort, with varying results based on individual nerve recovery patterns.