Poststroke pain may be controlled by targeting neuropathic symptoms

 This is after the fact, WHOM will be doing the research that will prevent post stroke pain?

Poststroke pain may be controlled by targeting neuropathic symptoms

LAS VEGAS — Central neuropathic pain can be challenging to treat, but several pharmacologic and nonpharmacologic options are available, according to a presenter at BRAINWeek 2022.

“Central neuropathic pain is one of the most difficult pain syndromes to treat,” Michael Bottros, MD, associate professor of anesthesiology and clinical operations and medical director of pain services at Keck School of Medicine the University of Southern California, Los Angeles, said during his presentation. “There are a number of reasons for developing central neuropathic pain syndromes, and stroke is just one of them.”

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Bottros explained that pain is among the most common complications of stroke, with an estimated prevalence between 39% and 55%, and tends to appear in central locations like the head, shoulders and upper extremities. Central poststroke pain (CPSP) is neuropathic in origin and affects sensory pathways, accounting for roughly 25% of poststroke pain cases, he said.

Onset of poststroke pain, Bottros stated, can develop immediately following stroke in some patients, 3 to 6 months after stroke in others and up to several years in some. However, CPSP onset within a few months is most common, with later onset a possible sign of stroke recurrence.

“Pain is the most common complication,” Bottros said. “The majority of pain described by people who have a stroke is musculoskeletal.”

To make an accurate pain assessment, clinicians should work around emotional response in their patients, he noted, and find an accurate and objective alternative to pain scales, particularly in cases of CPSP.

Bottros cited the Quantitative Sensory Testing (QST) method as the most objective, as CPSP encompasses a range of pain sensations, locations and emotions within patients that can interfere with diagnosis.

First-line treatment for CPSP is pharmacologic, Bottros said, and includes antidepressants such as amitriptyline, while anticonvulsants like gabapentin and pregabalin are good second-line choices. Lamotrigine monotherapy also is moderately effective and generally well tolerated, although this treatment comes with more serious potential side effects. And while opioids are considered generally ineffective in treating CPSP, Bottros reported that IV ketamine provided relatively rapid pain relief, which lasted 2 to 3 hours, in a double-blind, placebo-controlled study.

In the realm of nonpharmacologic treatment, various forms of neurostimulation (motor cortex, transcranial magnetic stimulation, deep brain and vestibular caloric) demonstrated beneficial pain reducing effects.

Regional blocking of nerves, Bottros added, resulted in fairly rapid pain reduction as a result of signals from the brain being cut off before reaching the locus of pain. This, he said, may be an indicator that pain may not be generated and perceived in the central nervous system.

“CPSP has variable timetable to onset following stroke,” Bottros said. “Sensory afferent input could play an important role in patients hiding the effects of poststroke pain.”