Hand Surgeon Guide to Peripheral Nerve Injury Rehabilitation
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This document discusses the stages of recovery following peripheral nerve injury and the management approach at each stage. It describes 3 stages: 1) degeneration, 2) regeneration, and 3) reinnervation and maturation. Stage 1 management focuses on protecting the repair site, preventing adhesions, and monitoring recovery. Stage 2 addresses complications like stiffness and pain management. Stage 3 involves tendon transfers and strengthening exercises. An intensive, long-term rehabilitation program tailored to the recovery stage is key to achieving good functional outcomes.
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Hand Surgeon Guide to Peripheral Nerve Injury Rehabilitation
- 1. Dr Andrew Yam MBBS, MRCS, MMed (Surg), FAMS (Hand Surgery) Hand and Peripheral Nerve Surgeon Hand Surgery Associates www.handsurgerysingapore.com
- 2. Protect the repair! ◦ SPLINT for 2-3 weeks in position of minimal tension ◦ Block movements that stretch nerve, allow those that slacken nerve Prevent adhesions ◦ NERVE GLIDING exercises during and after period of splinting Monitor for recovery Formal rehabilitation programme
- 3. Stage I Degeneration (First 2-3 weeks) Wallerian degeneration Loss of nerve function Cortical rearrangement starts
- 4. Stage I Degeneration (First 2-3 weeks) Wallerian degeneration Loss of nerve function Cortical rearrangement starts Stage II Regeneration (2-18 months depending on distance to target organ) Axonal regeneration after successful repair Chronic denervation changes, end-organ atrophy Decreased motor and sensory cortical representation
- 5. Stage I Degeneration (First 2-3 weeks) Wallerian degeneration Loss of nerve function Cortical rearrangement starts Stage II Regeneration (2-18 months depending on distance to target organ) Axonal regeneration after successful repair Chronic denervation changes, end-organ atrophy Decreased motor and sensory cortical representation Stage III Reinnervation and maturation (Up to 5 years) Function returns but impaired due to denervation atrophy, immature and decreased axons and cortical representation Increasing function with maturation and cortical reorganisation
- 6. Surgical Therapy STAGE I (Degenerative stage) Diagnosis Assess severity Nerve repair/recon Sensory and motor assessment Prevent complications of denervation Sensory re-education Pain control
- 7. Stiffness Injury and infection Neuropathic pain syndromes
- 8. Abnormal joint postures due to imbalanced forces across joints joint contractures Myostatic contracture Tendon adhesions Oedema -Dependent limb -Loss of muscle pump -Loss of sympathetic tone
- 9. PATIENTS TEND TO NEGLECT OR AVOID MOVING AND TOUCHING THE DENERVATED LIMB Median and ulnar nerve – MCPJ extension and PIPJ flexion contractures Radial nerve – flexion contractures Brachial plexus – shoulder, elbow, wrist, finger contractures
- 10. Joint stiffness is a contraindication for tendon transfers Reinnervated muscles will not overcome stiffness ALL JOINTS MUST BE KEPT SUPPLE IN ANTICIPATION OF FUNCTIONAL RECOVERY BY REINNERVATION OR MUSCLE TRANSFER
- 11. Management of joints post nerve injury Passive mobilization through full range as early as possible Patient education and compliance – prevent neglect Splinting with caution in insensate hands No heat therapy in insensate hands Surgical release as necessary
- 12. Secondary injury and infection Insensate limbs prone to serious injury - no withdrawal reflex Paralyzed limbs cannot be moved out of danger Neuropathic ulcers Burns Neglected cuts Severe infection with delayed treatment
- 13. Preventing secondary injury and infection Awareness of danger of insensate limb Avoid exposure to hot, cold or sharp objects Frequent inspection for injury Keep flail limbs in sling Avoid prolonged pressure including splints
- 14. Most major nerve injuries Up to 80% of brachial plexus avulsion injuries NEUROPATHIC PAIN MAY BE THE MOST CRIPPLING ASPECT OF NERVE INJURY CRPS Type II Avulsion/deafferentation pain Neurostenalgia Abnormal perception of stimuli – allodynia, dysaesthesia
- 15. Pharmacological Physical Behavioural Psychological Surgical AGGRESSIVE EARLY MULTI-MODALITY TREATMENT OF NEUROPATHIC PAIN IMPORTANT TO DECREASE RISK OF DEVELOPING CHRONIC PAIN SYNDROME
- 16. Gate-control theory Melzack Non-painful stimulus ◦ To border of hyperaesthetic area ◦ To territory of other nerves in same dermatome ◦ To adjacent dermatome Gradual increase in intensity of stimulus
- 17. CORTICAL PLASTICITY Decreased afferent transmission to cortex decreased cortical representation of denervated area Early (immediate) re-education to maintain cortical representation Substitute touch sense with visual or auditory
- 18. Surgical Therapy STAGE I (Degenerative stage) Diagnosis Assess severity Nerve repair/recon Prevent complications of denervation Sensory re-education Pain management STAGE II (Regeneration) Manage contractures, adhesions and other complications of denervation Monitor recovery (advancing Tinel’s sign) Adaptive techniques Assistive devices Pain management Strengthen and isolate donor muscles
- 19. PERIPHERAL NERVE INJURIES RARELY INCAPACITATE COMPLETELY! Assistive devices and coping strategies Avoid inactivity and reinforcement of “helplessness”
- 20. Assistive devices Training uninjured limb to compensate Train to do things differently to compensate Change of mindset - motivational talks, acceptance of limitation, hope for recovery, employment ENCOURAGE USE OF THE INJURED LIMB AS MUCH AS POSSIBLE
- 21. Radial nerve – finger and wrist extension Median nerve – thumb abduction/opposition Ulnar nerve – claw hand correction
- 22. Radial nerve Median nerve Ulnar nerve
- 23. Upper type BPI Flail arm Gauntlet with attachments
- 24. Strengthening and Isolating Donor Muscles All potential donor muscles for transfer identified Physical exercises to increase strength Visualisation of new function while activating donor muscle Physical activity decreases neuropathic pain and increases sense of well-being EARLY TRAINING OF DONOR MUSCLES FACILITATES RE-EDUCATION AFTER TRANSFER
- 25. Surgical Therapy STAGE I (Degenerative stage) Diagnosis Assess severity Nerve repair/recon Prevent complications of denervation Sensory re-education Desensitisation STAGE II (Regeneration) Manage contractures, adhesions and other complications of denervation Monitor recovery (advancing Tinel’s sign) Adaptive techniques Assistive devices Desensitisation Strengthen and isolate donor muscles Stage III (Post-reinnervation or reconstruction) Tendon transfers Functioning free muscle Protected mobilisation Re-training of transferred nerve or muscle Strengthening, dexterity
- 26. Graduated strengthening exercises - gravity eliminated exercises - resistance exercises - functional use and work hardening Neuromuscular electrical stimulation Biofeedback
- 27. Gravity eliminated exercises for shoulder and elbow Muscle power M2-M3
- 28. Resistance training Work hardening with BTE Muscle power M3 and above
- 29. Surface electrodes stimulate reinnervated muscle end plates augmenting active contraction High intensity, short duration Beware of muscle fatigue and injury
- 30. Surface electrode EMGs Visual/auditory feedback ◦ Increase contraction of agonist muscles ◦ Decrease contraction of antagonists Useful for managing co- contractions and training tendon/muscle transfers
- 31. Intensive structured rehabilitation program is essential to achieve good functional results after nerve injury and reconstruction Rehabilitation starts immediately post-injury to minimize cortical reorganization and encourage ongoing use of the denervated upper limb Program tailored to different stages of recovery Patient motivation is essential until reinnervation and maturation (up to 2 YEARS for higher lesions, BPI) Pain management is vital – the patient will not use a painful limb Emphasis on early return to function while accepting limitations and learning to adapt
Editor's Notes
- To effectively reconstruct and rehabilitate a patient with nerve injuries, it is necessary to understand the biology of nerve injuries and recovery. The biological process can be divided into three stages, and a rehabilitation programme designed around each stage. The first stage is DEGENERATION. The injured nerve undergoes wallerian degeneration over the first 2-3 weeks. Loss of nerve function is evident, but what is not so obvious is that changes start to occur in the brain as well. The denervated area’s representation in the cortex starts to shrink, and synapses start to disappear.
- The second stage is REGENERATION. In an axonotmesis, axonal regeneration occurs at a rate of 1-2 mm a day from the proximal end of the injured nerve and moves towards the target organs. In a neurotmesis, this cannot occur because of the gap between the ends, and a neuroma forms. A successful nerve repair that bridges the gap is required to allow regeneration. The target organ atrophies and displays chronic and progressive denervation changes until it is reinnervated by the regenerating axons. In the brain, the sensory and motor areas representing the denervated area becomes progressively smaller.
- The third stage, REINNERVATION AND MATURATION begins once the regenerating axons reach the target organ. The previous denervation changes are reversed. How much function returns after successful reinnervation depends on the duration of denervation. Initially, the function is impaired by atrophy of the end-organ, immaturity and decreased axon numbers, and decreased and deranged cortical representation. Function can continue to improve for several years, with ongoing maturation of the reinnervated organ, regenerated axons and cortical reorganisation.
- Each stage presents a different challenge to the reconstructive surgeon and the therapist. In the first stage, the surgeon must diagnose the location, nature and severity of the lesion, and do neurolysis, nerve repair, grafting or nerve transfer as appropriate. The therapist must accurately assess sensory and motor function to determine the functional loss and remaining function. The patient must be educated to avoid complications of denervation. Sensory re-education is started to minimise the impact of cortical reorganisation, and neuropathic pain must be controlled.
- Complications of denervation are stiffness, injury and infection, and neuropathic pain.
- Denervated limbs easily become stiff. Prolonged abnormal joint postures due to imbalanced forces across the joints result in joint contractures. Myostatic contractures occur in unopposed muscles that are continually contracted. Tendon adhesions and dependent limb oedema also contribute to stiffness.
- Typically, the MCPJs become stiff in extension and the PIPJs stiff in flexion in median and ulnar nerve injuries, while in radial nerve injuries, flexion contractures occur. In brachial plexus injuries, shoulder, elbow, wrist and finger stiffness are common. The main cause of stiffness is the patient’s tendency to neglect or avoid moving and touching the denervated limb.
- As stiffness prevents successful tendon transfer and prevents reinnervated muscle from moving the joints, it is critical to keep all joints supple in anticipation of functional recovery either by reinnervation or by muscle transfer.
- The patient, working with the therapist, has the main responsibility. Passive mobilisation through the full range is taught as soon as it is safe to do so, pending healing of concomitant injuries to bone and tendon. The patient is taught to perform the exercises at least 20 times every hour, and monitored weekly for compliance. Splinting is used with caution in insensate hands, as pressure ulcers may develop. Heat therapy is contraindicated in denervated hands. If contractures develop that are resistant to stretching and splinting, surgical release may be needed.
- Another problem with denervated limbs is injury and infection. Insensate limbs are prone to serious injury as there is no withdrawal reflex. Paralyzed limbs cannot be moved out of danger. Denervated skin is soft and dry and does not heal well. The classic example is the patient with leprosy, who develops neuropathic ulcers, severe burns, neglected cuts ultimately resulting in severe infection that is not noticed and treated late, resulting in loss of the extremity.
- It is important to educate the patient on the dangers of the insensate limb, to avoid hot, cold or sharp objects, to inspect frequently for injury, and to keep flail limbs in a sling close to the body. Prolonged pressure must be avoided, including from splints and tools.
- Neuropathic pain, while not so common, is probably the most crippling aspect of nerve injury. It is most common in avulsion injuries of the plexus, but may occur in traction lesions, partial nerve lacerations, and with neuroma formation. The pain is characteristic – stabbing, shooting, pins and needles, “numb”, burning, throbbing, and electric-shocks. Managing this pain is crucial in restoring the patient to useful function, as the patient will not use the limb even if muscle power and sensation is restored if the pain is too severe.
- Multi-modal treatment must be started early and aggressively. This involves drugs like pregabalin, physical techniques, behavioural techniques, and psychological techniques. Surgical neurolysis may be effective in some cases. In some centres like the Peripheral Nerve Injuries Unit at the Royal National Orthopaedic Hospital in Stanmore, patients with severe neuropathic pain are admitted for a week to the rehabilitation ward for intensive pain management involving all modalities, especially physical therapy.
- Desensitisation and TENS works via the gate-control theory of pain. A non-painful stimulus is applied to the border of the hypersensitive area, or to the territory of other nerves in a same dermatome or an adjacent dermatome. This sensory signal travels by fast nerve fibres and inhibits pain signals travelling in slower fibers. The stimulus is gradually increased in the hypersensitive area until the patient is able to tolerate pressure compatible with daily contact when using the limb.
- Early sensory re-education is advocated by Rosen and Lundborg. They found that cortical plasticity results in reorganisation of the cortical representation of the denervated limb soon after the nerve injury. Early re-education using the eyes or ears to substitute for the sense of touch, and “mirror therapy” helps to maintain the cortical representation of the denervated limb. This facilitates return of function once reinnervation occurs.
- In the second stage, the surgeon must manage contractures, adhesions, and other complications of denervation while monitoring for signs of recovery. The therapist should help the patient to function independently via adaptive techniques and assistive devices. Pain management continues. Donor muscles should be trained and strengthened in anticipation of possible transfers.
- It is important to restore the patient to independent function early, despite the limitations imposed by the denervated limb. Peripheral nerve injuries rarely incapacitate completely. The exception is a bilateral total brachial plexus injury, which is extremely rare. Attitudes are the real disability: the attitudes of the patient, their family and their employers. Each should be engaged to help the patient avoid inactivity and reinforcement of helplessness.
- Numerous methods can be used to augment any existing function. The goal is always to encourage the patient to use the denervated limb as much as possible and to function independently.
- Some assistive devices we commonly use are the dynamic finger and wrist extension splint for radial nerve, opposition strap for median nerve and anti-claw splint for ulnar nerve
- More complex devices are also used for brachial plexus injuries, such as a locked elbow splint for upper type BPI to position the functioning hand, a flail arm splint in total BPI to allow some control of the limb using the contralateral scapulothoracic movements, and a gauntlet that can be fitted with various attachments to allow the limb to assist in bimanual tasks. These are cumbersome and difficult to fit and train. However, a motivated patient will find them useful. At the Peripheral Nerve Injuries unit in Stanmore, two patients with BPI with poor recovery are employed in the orthotics department and work using these devices.
- Strengthening and isolating donor muscles helps facilitate re-education after transfer, and also decreases neuropathic pain by encouraging the patient to use the limb.
- In the final stage, reinnervation or lack of reinnervation is seen. If function is not adequate, tendon and muscle transfers may be useful. Protected mobilisation is started after the transfers, followed by re-training and strengthening. If nerve transfers were done in the first stage, then these must be trained to perform their new function. Sensory re-education now aims to improve tactile gnosis.
- Muscle strengthening and training is done by graduated strengthening exercises, aided by neuromuscular electrical stimulation and biofeedback
- Gravity eliminated exercises are started once M2 power returns. Slings and low friction devices are used to allow patient to move the limb actively. Exercising in a swimming pool or hydrotherapy pool is also useful.
- Resistance training starts with M3 power, followed by work hardening
- Neuromuscular electrical stimulation helps to augment muscle contractions by delivering high intensity, short duration bursts of current to the motor end plates. It is important not to overuse this, as muscle fatigue and injury can occur it contractions are too strong or frequent.
- Biofeedback provides useful visual or auditory feedback indicating when the agonist and antagonist muscles are activated. This can help the patient to increase contraction of agonists and decrease those of antagonists. It is most useful for managing co-contractions and training tendon or muscle transfers.