Botulinum Toxin Type A for the Treatment of Neuropathic Pain in Neuro-Rehabilitation

Pain is a natural protective mechanism and has a warning function signaling imminent or actual tissue damage. Neuropathic pain (NP) results from a dysfunction and derangement in the transmission and signal processing along the nervous system and it is a recognized disease in itself. The prevalence of NP is estimated to be between 6.9% and 10% in the general population. This condition can complicate the recovery from stroke, multiple sclerosis, spinal cord lesions, and several neuropathies promoting persistent disability and poor quality of life. Subjects suffering from NP describe it as burning, itching, lancing, and numbness, but hyperalgesia and allodynia represent the most bothersome symptoms. The management of NP is a clinical challenge and several non-pharmacological and pharmacological interventions have been proposed with variable benefits. Botulinum toxin (BTX) as an adjunct to other interventions can be a useful therapeutic tool for the treatment of disabled people. Although BTX-A is predominantly used to reduce spasticity in a neuro-rehabilitation setting, it has been used in several painful conditions including disorders characterized by NP. The underlying pharmacological mechanisms that operate in reducing pain are still unclear and include blocking nociceptor transduction, the reduction of neurogenic inflammation by inhibiting neural substances and neurotransmitters, and the prevention of peripheral and central sensitization. Some neurological disorders requiring rehabilitative intervention can show neuropathic pain resistant to common analgesic treatment. This paper addresses the effect of BTX-A in treating NP that complicates frequent disorders of the central and peripheral nervous system such as spinal cord injury, post-stroke shoulder pain, and painful diabetic neuropathy, which are commonly managed in a rehabilitation setting. Furthermore, BTX-A has an effect in relief pain that may characterize less common neurological disorders including post-traumatic neuralgia, phantom limb, and complex regional pain syndrome with focal dystonia. The use of BTX-A could represent a novel therapeutic strategy in caring for neuropathic pain whenever common pharmacological tools have been ineffective. However, large and well-designed clinical trials are needed to recommend BTX-A use in the relief of neuropathic pain

Botulinum Toxin Type A for the Treatment of Neuropathic Pain in Neuro-Rehabilitation

Pain is a natural protective mechanism and has a warning function signaling imminent or actual tissue damage. Neuropathic pain (NP) results from a dysfunction and derangement in the transmission and signal processing along the nervous system and it is a recognized disease in itself. The prevalence of NP is estimated to be between 6.9% and 10% in the general population. This condition can complicate the recovery from stroke, multiple sclerosis, spinal cord lesions, and several neuropathies promoting persistent disability and poor quality of life. Subjects suffering from NP describe it as burning, itching, lancing, and numbness, but hyperalgesia and allodynia represent the most bothersome symptoms. The management of NP is a clinical challenge and several non-pharmacological and pharmacological interventions have been proposed with variable benefits. Botulinum toxin (BTX) as an adjunct to other interventions can be a useful therapeutic tool for the treatment of disabled people. Although BTX-A is predominantly used to reduce spasticity in a neuro-rehabilitation setting, it has been used in several painful conditions including disorders characterized by NP. The underlying pharmacological mechanisms that operate in reducing pain are still unclear and include blocking nociceptor transduction, the reduction of neurogenic inflammation by inhibiting neural substances and neurotransmitters, and the prevention of peripheral and central sensitization. Some neurological disorders requiring rehabilitative intervention can show neuropathic pain resistant to common analgesic treatment. This paper addresses the effect of BTX-A in treating NP that complicates frequent disorders of the central and peripheral nervous system such as spinal cord injury, post-stroke shoulder pain, and painful diabetic neuropathy, which are commonly managed in a rehabilitation setting. Furthermore, BTX-A has an effect in relief pain that may characterize less common neurological disorders including post-traumatic neuralgia, phantom limb, and complex regional pain syndrome with focal dystonia. The use of BTX-A could represent a novel therapeutic strategy in caring for neuropathic pain whenever common pharmacological tools have been ineffective. However, large and well-designed clinical trials are needed to recommend BTX-A use in the relief of neuropathic pain

A multi-centric observational study on heterotopic ossification in severely brain injured patients with disorders of consciousness: preliminary data

Aims: to identify occurrence of neurogenic heterotopic ossification (NHO) in patients with prolonged disorder of consciousness (DoC) and possible risk factors. Design: Multi-center observational study. Setting: twenty-three intensive neurorehabilitation units. Subjects: two hundred and seventy-eight patients with prolonged disorder of consciousness (DoC; 150 in vegetative state and 128 in minimally conscious state) of different aetiology (vascular 125, traumatic=83; anoxic=56 brain injury and other brain aetiologies=14). Main Measures: at study entry: clinical evaluation by the Coma Recovery Scale-Revised (CRS-R), Disability Rating Scale (DRS), Early Rehabilitation Barthel Index (ERBI), Clinical Feature Scale (CFS); presence of ventilator support, spasticity, bone fractures. Within 3 months after admission: clinical evidence of NHO (i.e. limited range of motion and/or joint pain and/or local inflammation) confirmed by standard radiological and/or sonographic evaluation and presence of paroxysmal sympathetic hyperactivity (PSH). Results: Thirty-one patients (11.2%) developed NHO. Presence of abnormal ossifications was significantly higher in patients in VS than in patients in MCS and in patients with traumatic brain injury. Moreover patients with NHO showed higher DRS category and total score, higher occurrence of limb spasticity and bone fractures at study entry than patients without NHO. Patients with NHO did not differ from patients without NHO for sex, age, time post-injury, CRS-R and ERBI total scores, presence of non-invasive ventilator support at study entry and presence of PSH. Conclusions: Our findings suggest a relation between development of NHO and clinical diagnosis, functional disability status and aetiology in patients with DoC. Moreover, we identified spasticity and bone fractures as possible risk factors for occurrence of NHO in patients with severe brain injury and DoC