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12 Articles in this Series
Central Post-Stroke Pain – How Central Is It?
False-Positive Urine Drug Monitoring Results and Aspirin
Medical Marijuana & Pain
More Potential Uses for Low-Dose IV Naloxone
On the Horizon: A Brief Look at Potential Analgesics of the Future
Preview of PAINWeek 2018 - Know Before You Go
Stem Cells & Beyond
Underlying Causes of Small Fiber Neuropathies
Understanding Sexual Pain – A Physical Therapist’s Perspective
Video: Drs. Gudin & Fudin on PAINWeek 2018 and PPM's Future
Where Does the Patient-Centered Pain Practitioner Stand Today?
Why Interventional Tactics Should be Used for Chronic Pain Patients Now, Not Later

Central Post-Stroke Pain – How Central Is It?

For CPSP patients, medication and interventional approaches may provide relief, but also be aware of the role of sensory afferent input. A PAINWeek 2018 highlight with Michael Bottros, MD.

Michael Bottros, MD, associate professor of anesthesiology and chief of the Division of Pain Medicine at Washington University School of Medicine in St. Louis, began his talk at PAINWeek 2018 in Las Vegas by admitting that post-stroke pain patients are among some of the most difficult to treat. Half a million strokes are reported in the US every year and another 200,000 individuals have a recurrent stroke annually, he shared. Pain may be prevalent in 39 to 55% of post-stroke patients but not all cases involve central pain. The types of pain that may occur after a stroke include shoulder pain (the most common), headaches, spasticity, and lastly, central post-stroke pain (CPSP).

CPSP represents about 25% of post-stroke pain cases. In the US, approximately 100,000 individuals have stroke as their primary diagnosis and are living in a home healthcare facility as a result. This neuropathic pain condition is caused by the stroke-related lesion affecting the patient’s central somatosensory pathways. It is uncommon and hard to diagnose, said Dr. Bottros. For example, the time of pain onset is both gradual and variable; it may not occur right away, in some cases, emerging only after a recurrent stroke. In other cases, CPSP may disappear after a recurrent stroke. Most commonly, the pain onsets within the first few months after a stroke but can occur as late as one year after the attack. Dr. Bottros further described CPSP onset as similar to that of multiple sclerosis—it does not just occur with a massive force, he said. Any later onset of pain should therefore prompt an examination for other causes, such as a new stroke or spasticity, he advised. Below is a look at assessing the condition.

Diagnostic Criteria & Symptoms

There are four mandatory diagnostic criteria for CPSP:

  • Pain within an area of body that responds to a lesion of the central nervous system (CNS)
  • History suggestive of a stroke
  • Confirmation of a CNS legion by imaging or sensory signs confined to the area of the body corresponding to the lesion
  • Other causes of pain have been excluded.

There are no specific scales for rating CPSP but VAS and NRS may be useful, said Dr. Bottros. Clinically, CPRS may occur spontaneously (reported in 85% of patients) or be evoked, with an average NRS pain rating of 3 to 6 out of 10. Symptoms and severity in thalmic versus extrathalmic stroke do not differ, however. Intensity may increase with internal or external stimuli, and patient descriptions of the pain typically include continuous burning, aching, pricking, freezing, squeezing, or intermittent pain that is lacerating or shooting. Distribution of the pain may be restricted to a small area such as the hand or to one side of the body.

Although not common, Dr. Bottros said he has found quantitative sensory testing (QST) to be useful in assessing common or dissociated sensory findings as well. This type of research has been used elsewhere to document sensory findings, such as allodynia or hyperalgesia, which Dr. Bottros pointed out are not interchangeable conditions. QST uses graded physiological stimuli to mark a baseline, which then trials the application of a thermal stimulus, pressure, pinprick, and so forth.

"CPSP a very painful syndrome that we have a limited understanding of,” and the treatments currently used may not be enough, said Dr. Bottros. “Its important to get pain psychologists involved in the diagnosis as well,” he added, as central pain may affect sleep, mood, depression, and overall rehabilitation. As part of his presentation, he described five potential mechanisms for better understanding CPSP, including how the spinothalmic track (STT) may inhibit the lateral thalamus, which then disinhibits the medial thalamus. Another theory involves the STT directly impacting the thalamus, which may explain why calcium channel blockers, such as gabapentin, help to relieve central post-stroke pain. Below are details discussed by Dr. Bottros regarding potential treatment approaches.

Medication Management of CPSP

Front-line medications for CPSP include a range of options: antidepressants, anticonvulsants, antiarrhythmics, opioids, steroids, and intrathecal Baclofen, as well as rehabilitation and invasive approaches such as regional anesthesia, electrical stimulation, deep brain stimulation, neuroablation, and transcranial magnetic stimulation.


Tricyclic antidepressants (TCAs), in particular, are considered first-line, with amitriptyline (75 mg) being the drug of choice for consistent relief with mild-to-moderate side effects (primarily lethargy). Dr. Bottros said he asks his patients to take amitriptyline an hour or two before bed. He usually starts patients off at 25 mg and goes up to 50 mg a week later, and then up to 75 mg a week after that; it may take those 4 weeks for the patient to feel the effects as the dose is titrated up, he noted. Second-line selective serotonin reuptake inhibitors are mostly ineffective in this patient population, he added.


Anticonvulsants, such as gabapentin and pregabalin, have shown efficacy with central neuropathic pain but more severe side effects are possible, including dizziness, edema, nausea, and exacerbated depression. “These side effects are much more prevalent in higher doses,” explained Dr. Bottros, so he said he avoids prescribing over 300 mg. “Anything above that won’t provide enough significant relief to warrant the side effects,” he said. Instead, a clinician may try an ancillary medication at that point.

The anticonvulsant lamotrigine monotherapy may not be a favorite among pain practitioners, he said, but it has been moderately effective in 200 mg/day doses in a small trial of CPSP patients. Clinicians should be cautious of Stevens-Johnson syndrome and TENS when using lamotrigine. The anticonvulsant carbamazepine has been shown to improve symptoms at 3 weeks versus amitriptyline at up to 4 weeks in comparative placebo studies. Due to side effects, however, overall efficacy was limited, he said.


Opioids are generally considered ineffective in treating central post-stroke pain, but in one study described by Dr. Bottros, morphine helped to alter allodynia and thermal thresholds, reducing nociceptive pain and psychogenic influence. Morphine is usually discontinued due to side effects that occur from the high doses necessary for clinical benefit in this condition.


Interventional Management of CPSP

After failed medication management of CPSP, intravenous (IV) medications may be trialed in intractable cases. While many options exist, Dr. Bottros specifically focused on his experience with IV ketamine, lidocaine, and propofol. “Lidocaine in many ways has re-entered the fashion cycle, so to speak, with more uses for both chronic and acute pain,” he said. In fact, more and more, these local anesthetics are proving to alter cytokines in patients systemically, with infusion–based relief lasting as long as 3 to 6 weeks. He noted that some of his CPSP patients have only had success with lidocaine infusion. Ketamine, another current “it” pain medication, and propofol have shown to be beneficial as well but these treatments are not common in clinical settings just yet, said Dr. Bottros.

Other options, such as repetitive transcranial neurostimulation, may show benefit, and, if patients respond well to this method, they may also do well with a motor cortex stimulator. Also interesting, according to Dr. Bottros, is the emerging use of vestibular caloric stimulation, which demonstrated significant relief in two very small studies of CPSP patients.

He pointed out that despite the small trials in the literature to date for CPRS patients, it is important to keep in mind that this population is hard to find and trial to begin with. Thus, little successes may go a long way for these individuals as the syndrome becomes better understood.

In fact, Dr. Bottros’ recently published pilot study of ultrasound-guided peripheral nerve blocks with lidocaine in just 8 CPRS subjects is what led him to speak at PAINWeek 2018. He and his coauthors hypothesized that “CPSP is a result of misinterpretation of afferent sensory input by the sensitized neurons within the brain, rather than generated spontaneously by the damaged central nervous system neurons.” Next up? Dr. Bottros is applying for an NIH grant to study spinal cord stimulation for central nervous pain to block afferent input.

In the meantime, clinicians have a variety of options to consider for the treatment of intractable pain related to stroke, with new approaches potentially moving away from conventional central pain treatments and more toward interventional options. Stay tuned!

Next summary: False-Positive Urine Drug Monitoring Results and Aspirin
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