Phenol neurolysis for spasticity management in people with spinal cord injury

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.

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 ( ).