An often overlooked condition, central neuropathic pain ensues directly when any type of central nervous system (CNS) lesion causes the dysfunction of somatosensory CNS pathways. It occurs most often after a stroke or as sequelae of multiple sclerosis or spinal cord injury, explained James C. Watson, MD, Associate Professor of Neurology, Mayo Clinic, Rochester, MN, at the 2016 American Academy of Pain Medicine meeting. Central neuropathic pain is challenging to diagnose and treat.
Central neuropathic pain is differentiated from any type of central sensitization leading to allodynia or hyperalgesia, as well as from spasticity. It has obligatory demonstrable sensory dysfunction. Dr Watson noted that central neuropathic pain is also separate from musculoskeletal pain secondary to immobility after stroke, gait disorders, and spinal cord injury in wheelchair-bound patients, including the latter’s upper extremity overuse syndromes.
“Distinguishing musculoskeletal from neuropathic pain may not be straightforward, because neurologically impaired patients may have impaired sensory discrimination,” Dr Watson said. Pain descriptors and localization may be vague, and pain triggers may be poorly defined. In cases of paraplegia or quadiparesis, positioning for office examination can be challenging. Furthermore, the various characterizations of deep and superficial pain do not serve to discriminate central pain from peripheral pain.
Central poststroke pain is the most common form of central neuropathic pain, and develops in 2% to 8% of patients with stroke. The onset of central poststroke pain is most often delayed and can manifest months to years after a stroke. It is a presenting feature in only 5.5% to 10% of patients with multiple sclerosis, and when it does occur as such, future central pain is more likely.
Spinal cord injury has the longest average latency, and although 50% of patients experience central pain within 3 months, latency can be up to 5 years. “To classify as central pain syndrome, pain must occur in the body region clinically affected by the CNS insult.” Also obligatory is neuronal hyperexcitability in surviving spinothalamic tract neurons. Although spinothalamic tract dysfunction is obligatory for the diagnosis of central pain, not all patients with spinothalamic tract dysfunction develop central pain.
Treating Central Neuropathic Pain
“Unfortunately, the pharmacological options for central neuropathic pain syndromes are not many,…and successes with single agents are almost nil,” said Paola Sandroni, MD, PhD, Professor of Neurology, Mayo Clinic, Rochester, MN.
A common pattern is that a study on a new drug will find that it works, and 2 months later another study emerges undermining the validity of the first study, Dr Sandroni added. Huge interpatient variability is among the factors responsible for making consistent testing very challenging. Hard evidence from good, controlled studies on opioid efficacy is also lacking, she said. “It is really an unchartered territory.”
In addition, tolerability is an issue among patients whose pathology may include compromised cognition (stroke and multiple sclerosis, especially).
Some evidence of drug efficacy has been demonstrated with lamotrigine and amitriptyline for central poststroke pain (mixed results with pregabalin); with pregabalin and lamotrigine for spinal cord injury central pain (mixed results with gabapentin and amitriptyline); and with duloxetine and cannabinoids for multiple sclerosis central pain.
With respect to surgical options for central neuropathic pain, Dr Sandroni noted that destructive lesions are applied most often to the spine via commissurotomy, cordotomy, and cordectomy. She emphasized that because these procedures are neither benign nor reversible, and because pain often returns or evolves into a different type of pain (such as anesthesia dolorosa), these procedures are typically reserved for patients with terminal disease.
Neuromodulation with dorsal cord stimulation can be helpful in patients with spinal cord injury, but whether creating plasticity improves recovery and reduces pain remains uncertain.
Transcranial Magnetic Stimulation
Noninvasive brain stimulation with transcranial electrical stimulation produces radial flow of current and is painful in itself. Transcranial magnetic stimulation (TMS), however, induces current influx perpendicular to the plane of the coil, with various coil shapes allowing the control of stimulation depth and strength, and with modified stimulation parameters facilitating the activation or the inhibition of cortical excitability. TMS can induce or modulate neuroplasticity after a stroke. Furthermore, TMS can counteract disease effects on cortical excitability in dystonia, Parkinson’s disease, and cerebellar disorders.
TMS carries a low seizure risk (<1:1000; 0.1%). In addition, it can cause readily treated headache and neck pain (3%-10%), and transient hearing threshold shifts or tinnitus (approximately 10%), which is preventable with the recommended use of earplugs. Cognitive disruption can occur during the TMS procedures, but without short-term neuropsychiatric effects. TMS is contraindicated in the presence of various electrically based or metal medical devices and in individuals with a history of seizures.
Turning to an incidental but relevant finding, Dr Sandroni noted that electroconvulsive therapy is beneficial in refractory pain states and in depression. Likewise, TMS is FDA approved for adults with depression. In a 2011 clinical trial of repetitive TMS for depression and borderline personality disorder, patients with concomitant fibromyalgia had pain resolution independent of and often sooner than their psychiatric improvement. Pathways for pain, emotions, and mood overlap, noted Dr Sandroni.
She asked, if repetitive TMS and electroconvulsive therapy help similarly in depression, “why not for pain? You do not need anesthesia, and you do not have the memory changes that occur with ECT [electroconvulsive therapy].”