Introduction

Spasticity is one of the most common secondary complications following a complete or incomplete spinal cord injury (SCI). After SCI, the prevalence of spasticity ranges from 65% to 78%, and 35% to 49% have problematic spasticity ( ; ). Currently, problematic spasticity is managed through a combination of therapeutic modalities, oral medications, botulinum toxin injections, phenol neurolysis, and surgical procedures ( Table 1 ). Pharmaceutical options include medications delivered orally, via local injections, or through intrathecal baclofen (ITB) pumps. Botulinum toxin injections and chemical neurolysis with phenol or alcohol are the first-line treatment options for problematic focal spasticity. However, after the introduction of botulinum toxins for the treatment of spasticity, the use of phenol/alcohol chemical neurolysis for spasticity management declined over the period. Potential causes of the decline in neurolysis use include laborious techniques that required more precise skill in the pre-ultrasound era. There is a concern for the risk of loss of sensation, dysesthesias, and weakness. However, a review of existing evidence suggests that chemical neurolysis with phenol and alcohol has demonstrated effectiveness in eliminating clonus, decreasing spasticity, improving joint range of motion, decreasing painful spasms, and improving function ( ; ; ; ; ). In our experience, ultrasound guidance and electrical stimulation improved these procedures’ efficiency and quality.

Poorly controlled severe spasticity after SCI can result in multiple complications, including the development of joint contractures ( Fig. 1 ), inability to participate in therapy, skin breakdown, decreased function, poor sleep, and poor quality of life ( ; ; ). In people with cervical SCI, we are often faced with managing problematic spasticity in all four extremities. In this scenario, a combination of treatment approaches, including phenol or alcohol neurolysis, may help manage spasticity effectively and prevent complications due to poorly controlled spasticity ( ; ). Besides, there are many other case scenarios where neurolysis can be a very useful tool to manage spasticity effectively. Such scenarios include patient refusal of ITB therapy, contraindications to ITB therapy due to ongoing infectious process, hypersensitivity to baclofen, and insufficient resources to pursue botulinum toxin injections or ITB therapy.

Joint contracture and deformities due to delayed spasticity management.

Additionally, botulinum toxin and intrathecal baclofen therapies are not available in many parts of the world to date. Untreated spasticity can lead to significant limitations in function and limit recovery ( ; ). Therefore, it is essential to incorporate cost-effective alternative therapies such as phenol neurolysis to treat spasticity. This chapter will describe the following with regard to phenol neurolysis: mechanism, techniques, dosing, risks, and benefits. It will demonstrate the procedure’s application in people with SCI with a case study. These procedures are similar to those for alcohol neurolysis.

Phenol or alcohol neurolysis history

The usefulness of chemical neurolysis or nerve block was first recognized in 1863 by Luton to treat pain due to phenol’s and alcohol’s ability to block nerve conduction ( ). There were many reports of loss of motor function after intrathecal injections of phenol for pain management in the 1950s ( ; ). Between 1964 and 1967, Khalili et al. published their experience of performing peripheral nerve blocks in patients diagnosed with a stroke, cerebral palsy, and spinal cord injury ( ). They reported improved spasticity in the muscles following nerve block by a 2%–3% phenol solution to mixed or motor nerves ( ). They also reported several unanticipated side effects, including loss of sensation in < 1% instances following a nerve block. Subsequently, peripheral motor point blocks were performed to minimize sensory side effects under electromyography (EMG) and electrical stimulation guidance ( ; ).

Mechanism of action

Phenol, also known as carbolic acid (C ₆ H ₅ OH), is a benzene ring. In a solid state, it exists as a crystal. It is water-soluble at room temperature at ≤ 6.7% concentration. Phenol is typically used in 3%–6% concentration ( ). When injected at a concentration of 5% and above, phenol denatures protein, which results in tissue necrosis and axonal degeneration ( ; ; ). The effects of neurolysis last longer with 5%–6% concentration. Phenol at < 3% concentration causes demyelination and some axonal destruction, resulting in shorter-lasting effects ( ). The phenol application to the nerve trunk or motor point results in a short-term anesthetic effect that lasts for few hours. Short-term and immediate local anesthetic effects result in instant spasticity relief ( ; ). However, long-term and full effects may take 7–9 days after injections due to the time required for axonal degeneration ( ). The duration of effects is dependent on the site of injection and concentration of phenol used ( ; ). Following injection at the proximal portion of a nerve using a higher concentration of phenol, the nerve takes 6–9 months to re-generate, whereas injections at the nerve’s distal portion takes 3–4 months to recover. Repeated neurolysis can result in permanent nerve damage and muscle atrophy ( ).

Phenol neurolysis technique and dose

Extensive knowledge of the anatomy of mixed, motor, and sensory nerve pathways and muscles innervated by individual motor branches is essential to prevent serious side effects and improve outcomes. Phenol neurolysis can be performed with anatomic localization, electrical stimulation guidance, or ultrasound guidance. Often, these techniques are combined to maximize the efficiency of the procedure and minimize errors in localizing targets. In some cases, first performing a temporary nerve block with 1% lidocaine prior to phenol neurolysis may help assess the efficacy and potential loss of function that can be expected with the long-lasting procedure. The injection technique and materials required for performing a motor point block and peripheral neurolysis are similar. Teflon-coated electromyography needles of 25- to 27-gauge, surface electrodes, and a portable electrical stimulator are required for performing injections with electrical stimulation guidance. Anatomical localization along with electrical stimulation allows rapid localization of motor points or peripheral nerves. The use of a lower amount of current (≤ 1 mA) and stronger contractions suggests closer proximity to motor points or target nerve branches. Ultrasound guidance combined with electrical stimulation can decrease side effects and improve procedure efficiency and efficacy. In a study, injections performed under combined ultrasound and electrical stimulation guidance resulted in a lower phenol dose compared to electrical stimulation guidance alone ( ; ; ). Motor points typically require multiple injection sites for a reduction in spasticity. Phenol neurolysis of proximal nerve trunk requires injection at one to two sites, and electrical stimulation results in stronger muscle contraction. However, ultrasound guidance requires additional equipment and skill. Typically, at each injection site, 0.2–0.5 mL of 5%–6% phenol is injected. However, the phenol amount per nerve or site may vary based on the practitioner’s expertise and guidance used for injections ( ).

Immediate spasticity relief experienced due to phenol’s anesthetic effect during the procedure can be used to titrate the dose when injecting motor points. There are no clear studies about the target recommended dose, but the current literature recommends no more than 1.0–1.2 g in total (e.g., 20 mL of 5%–6% concentration) ( ; ; ). However, a study reported safe use of up to 30 mL of 6% phenol ( ). Systemic doses of 8.5 g and above can result in serious side effects, including cardiovascular and central nervous system dysfunction ( ; ).

The decision to inject the proximal portion of nerve vs distal motor points depends on various factors, including time from injury, complete vs incomplete injury, spasticity management goals, and current functional status. A careful evaluation and discussion of the risks and benefits of various options for spasticity management should be discussed. Before neurolysis, evaluate for any potential for nerve transfers to improve function. It is also essential to remember that while preserving motor points is vital for potential neurorecovery, poorly controlled spasticity can prevent participation in therapies, result in joint contractures, and significantly limit recovery. Current evidence suggests a significant improvement in spasticity in the upper and lower extremity muscles following chemical neurolysis ( ; ; ; ; ; ; ; ; ; ; ).

Upper extremity targets

A list of the phenol neurolysis of upper extremity targets in people with SCI is presented in Table 2 . Our center’s data suggest that medial and lateral pectoral nerve neurolysis and musculocutaneous motor point block are the most common upper extremity targets for phenol neurolysis in people with SCI. Spasticity of shoulder adductors and shoulder internal rotators muscles can be very severe and challenging in people with spinal cord injury. Stretching is often limited due to pain in the shoulder and inadequate response to botulinum toxin injections. Phenol neurolysis to medial and lateral pectoral and thoracodorsal nerves can successfully decrease spasticity in these muscle groups and improve shoulder range of motion. The pectoral nerves can be easily located with ultrasound guidance between the pectoralis major and pectoralis minor ( Fig. 2 ). Due to the proximity of these nerves to the lungs and pleura, ultrasound guidance is recommended. The musculocutaneous nerve is a mixed nerve and supplies sensation to the lateral forearm by its terminal branch known as the lateral cutaneous nerve of the forearm. The musculocutaneous nerve can be localized near the pectoralis major tendon’s distal insertion between the coracobrachialis and the short head of the biceps on the arm’s medial side ( ). In people with incomplete injury, a motor point block to target muscle is recommended to prevent weakness of the elbow flexors and loss of sensation over the forearm ( ). The motor point block to distal muscle groups (finger flexors and wrist flexors) of the upper extremity or mixed nerves can be targeted with ultrasound or electrical stimulation guidance. However, we must isolate the target motor branches or perform motor point blocks to prevent unintended sensory loss and weakness in other muscle groups supplied by the target nerve ( ; ).

Table 2

Upper extremity targets for phenol neurolysis.

Spasticity pattern	Main target muscles	Nerve block or motor point block
Shoulder adduction and internal rotation	Pectoralis major, Latissimus dorsi	Medial and lateral pectoral nerves, thoracodorsal nerves
Elbow flexors	Brachialis, Biceps brachii, BCR	Musculocutaneous motor points to brachialis and biceps Radial motor branches to BCR
Elbow extensors	Triceps lateral head, long head, and medial head	Radial motor branches to triceps
Pronation	Pronator teres	Median motor points to pronator teres
Wrist flexors	FCR and FCU	Median nerve motor branches to FCR and ulnar motor branches to FCU
Finger flexors	FDS and FDP	Respective median and ulnar motor branches to FDS and FDP

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