This article is intended for educational purposes only. It does not provide medical advice, diagnosis, or treatment. Readers should consult a qualified healthcare professional before starting, changing, or discontinuing any medication.
Neuropathic and related pain syndromes can look very different on the surface. A patient with diabetic neuropathy describes burning in the feet; another with shingles still feels searing pain long after the rash is gone; a third suffers electric-shock jolts of trigeminal neuralgia. Others live with restless legs, fibromyalgia, or focal seizures. What unites these seemingly distinct conditions is not the body region, but the wiring: nerve circuits that have become hyperexcitable, firing when they should be quiet, and amplifying signals that should fade.
Neuromodulators, which is an umbrella term for several drug classes, aim to calm these overactive networks. They do not simply “block pain” like an anesthetic. Instead, they restore balance by modulating calcium and sodium channels, enhancing inhibitory signals, or desensitizing peripheral fibers. This article takes a class-level view: how these medications work, where they fit across conditions, what they share, and how clinicians choose among them.
The Unifying Mechanism: Reducing Neural Hyperexcitability
Across neuropathic pain, restless legs syndrome, fibromyalgia, and focal seizures, the common thread is abnormal nerve signaling caused by hyperexcitable circuits. When nerves are injured or overstimulated, they may undergo central sensitization, where neurons amplify normal signals or fire spontaneously, explaining why a light touch can feel painful and why burning persists without a clear trigger.
Another factor is failure of descending inhibitory pathways, which normally use serotonin (5-HT) and norepinephrine (NE) to dampen overactive circuits. Drugs such as SNRIs and TCAs restore some of this lost braking effect. From the periphery, injured nerves can develop ectopic firing, suppressed by α2δ ligands (gabapentin, pregabalin) and sodium-channel modulators (carbamazepine, oxcarbazepine). Topical therapies silence overactive nociceptors locally, while dopamine agonists target disturbed dopaminergic tone in restless legs syndrome.
Despite differences in entry points, the goal is the same, i.e., reducing neural hyperexcitability. By acting at the periphery, spinal cord, descending tracts, or higher circuits, neuromodulators calm overactive networks rather than simply masking symptoms.
Neural hyperexcitability as the unifying mechanism of neuropathic conditions.
The Classes at a Glance
| Class | Representative Drugs | Primary Mechanism | Typical Niches | Advantages | Trade-Offs / Limitations | Monitoring Priorities |
|---|---|---|---|---|---|---|
| α2δ ligands | Gabapentin, Pregabalin, Gabapentin enacarbil | Bind to α2δ subunit of voltage-gated Ca²⁺ channels, reducing excitatory neurotransmitter release | Diabetic peripheral neuropathy (DPN), post-herpetic neuralgia (PHN), radiculopathy, RLS (off-label), fibromyalgia | Well tolerated in many; improve sleep quality; flexible use across pain + seizure spectrum | Sedation, dizziness, weight gain, edema; renal clearance needed; misuse potential in some populations | Renal function, weight/edema, fall risk |
| SNRIs | Duloxetine, Venlafaxine | Enhance serotonin & norepinephrine in descending inhibitory pathways | DPN, fibromyalgia, mixed neuropathic pain with depression/anxiety | Address mood disorders + pain; non-sedating for most | Nausea, hypertension, sweating; withdrawal if stopped abruptly | BP, mood/suicidality, hepatic function |
| TCAs | Amitriptyline, Nortriptyline, Desipramine | Block 5-HT & NE reuptake, plus sodium-channel and anticholinergic actions | PHN, radicular pain, fibromyalgia, migraine prevention, insomnia with pain | Low cost; broad analgesia; useful for insomnia (sedating) | Anticholinergic burden (dry mouth, constipation, urinary retention), QTc prolongation, weight gain, falls in elderly | ECG if cardiac risk, anticholinergic load, fall risk |
| Sodium-channel modulators | Carbamazepine, Oxcarbazepine, Lamotrigine (adjunct) | Stabilize voltage-gated Na⁺ channels, reducing ectopic firing | Trigeminal neuralgia, glossopharyngeal neuralgia, focal seizures | Strong evidence in trigeminal neuralgia; rapid efficacy | Hyponatremia, dizziness, rash (rare SJS / TEN); drug–drug interactions (enzyme induction) | Sodium levels, rash monitoring, drug interactions, hepatic function |
| Topical analgesics | Lidocaine 5% patch, Capsaicin 8% patch | Local peripheral desensitization of nociceptors | PHN, localized neuropathic pain, focal scar pain | Avoids systemic side effects; option in polypharmacy; applied directly to pain area | Local irritation, patch-site burning; limited efficacy in widespread pain | Skin integrity, correct application |
| Dopamine agonists (RLS context) | Pramipexole, Ropinirole | Stimulate dopamine receptors in basal ganglia circuits | Restless legs syndrome, especially when α2δ not tolerated | Rapid efficacy for many; target underlying dopaminergic deficit | Augmentation (worsening with long-term use), impulse control disorders, nausea | Monitor for augmentation, compulsive behaviors, daytime sleepiness |
Each class targets abnormal signaling differently, offering distinct benefits and trade-offs.
Condition-Driven Frameworks
Neuropathic Pain (DPN, PHN, Radicular, Post-Surgical)
Neuropathic pain syndromes such as diabetic peripheral neuropathy, post-herpetic neuralgia, radiculopathy, and post-surgical neuropathy are typically approached through three first-line building blocks: α2δ ligands, SNRIs, and TCAs. Each modulates hyperexcitability differently, affecting calcium-channel modulation, restoration of descending inhibition, or broad reuptake blockade. In practice, the choice of starting class often reflects patient phenotype and comorbidities, with the others reserved as sequential options. Topical agents (lidocaine or capsaicin patches) provide value for localized neuropathic pain where systemic therapy is not required. In partial responders, cross-mechanism combinations (e.g., α2δ plus SNRI) may improve outcomes, provided additive side effects are monitored.
α2δ ligands (gabapentin, pregabalin) as first-line agents for neuropathic pain.
SNRIs and TCAs restore descending inhibitory control.
Neuropathic pain syndromes are typically approached through three first-line building blocks: α2δ ligands, SNRIs, and TCAs.
Trigeminal Neuralgia & Cranial Neuropathies
These conditions remain the classic territory of sodium-channel modulators, which directly suppress the paroxysmal discharges that define trigeminal neuralgia. They act as the anchor of therapy, with α2δ ligands sometimes added as adjunctive agents if response is incomplete or tolerability is limited. The mechanistic match between sodium-channel stabilization and cranial neuropathic firing explains their distinctive efficacy.
Sodium-channel modulators anchor trigeminal neuralgia treatment.
These conditions remain the classic territory of sodium-channel modulators, which directly suppress the paroxysmal discharges.
Restless Legs Syndrome (RLS)
For RLS, α2δ ligands are often favored first because they reduce sensory hyperexcitability and improve sleep. Dopamine agonists offer rapid symptom relief but carry the risk of augmentation, a paradoxical worsening with earlier daytime onset and spread to other body parts. This risk shapes their use, often restricting them to second-line contexts. Importantly, iron deficiency or low ferritin is a modifiable factor, and correction of iron status can significantly reduce symptoms, sometimes obviating the need for pharmacotherapy.
Dopamine agonists play a role in restless legs syndrome but risk augmentation.
Dopamine agonists offer rapid symptom relief but carry the risk of augmentation, shaping their use as second-line.
Fibromyalgia & Centralized Pain
Fibromyalgia and related central sensitization syndromes involve dysregulated central processing rather than focal nerve damage. Here, SNRIs and α2δ ligands align best with the symptom constellation of widespread pain, sleep disturbance, and fatigue. However, their benefit is usually modest unless embedded within a multimodal approach that includes exercise, psychological strategies, and sleep hygiene. Neuromodulators are therefore one component of a broader treatment framework.
Fibromyalgia responds best to multimodal therapy including neuromodulators.
SNRIs and α2δ ligands align best with widespread pain and sleep disturbance but work best as part of a multimodal plan.
Focal Seizures (Adjunct Concepts)
In focal epilepsies, both sodium-channel modulators and α2δ ligands are used, typically as adjunctive therapies rather than monotherapy. Sodium-channel drugs stabilize cortical firing, while α2δ ligands can further reduce seizure burden. The principle is rational combination: engaging different mechanisms without stacking sedative or cognitive liabilities.
Choose by Phenotype: A Side-Effect–Led Selector (Matrix)
Selecting among neuromodulator classes often depends less on the exact diagnosis and more on the patient’s phenotype: sleep patterns, mood profile, comorbid conditions, and vulnerability to side effects. Instead of a “one best drug,” the decision is usually about matching mechanism to patient priorities while avoiding liabilities. The matrix below illustrates how goals and comorbidities can steer class choice.
| Patient Goal / Comorbidity | Classes to Consider | Classes to Use With Caution / Avoid | Rationale |
|---|---|---|---|
| Insomnia / poor sleep | Sedating options: TCAs at bedtime; α2δ ligands (gabapentin/pregabalin) | SNRIs (activating, may worsen sleep) | TCAs and α2δ agents can improve sleep continuity, while SNRIs may be alerting. |
| Daytime fatigue / need for alertness | SNRIs (duloxetine, venlafaxine) | TCAs, high-dose α2δ ligands | SNRIs are generally non-sedating or mildly activating; TCAs and α2δ ligands may increase daytime drowsiness. |
| Comorbid depression / anxiety | SNRIs, TCAs | α2δ ligands (do not address mood directly) | SNRIs and TCAs provide dual action on pain and mood symptoms. |
| Obesity / weight concerns | SNRIs (weight-neutral), topicals | α2δ ligands (edema/weight gain), TCAs (weight gain) | Weight gain can be limiting with α2δ or TCAs; SNRIs and topicals avoid this burden. |
| Fall risk / frailty | Topicals, cautious low-dose SNRI | α2δ ligands, TCAs (sedation, orthostasis) | Topicals minimize systemic CNS effects; sedating drugs heighten fall risk in older adults. |
| Renal impairment | SNRIs, TCAs, sodium-channel drugs | α2δ ligands (renally cleared) | Dose adjustments or avoidance required for α2δ ligands in renal dysfunction. |
| Hepatic impairment | α2δ ligands, topicals | SNRIs, TCAs, sodium-channel drugs (hepatic metabolism) | Gabapentinoids rely less on hepatic clearance; liver-metabolized drugs may accumulate. |
| Cardiac disease / QTc risk | α2δ ligands, SNRIs, topicals | TCAs (anticholinergic + QTc prolongation) | TCAs carry conduction / QT risks; safer alternatives available. |
| History of substance use | SNRIs, topicals | Caution with α2δ ligands (misuse potential), dopamine agonists (impulse control issues) | Some neuromodulators carry abuse or behavioral risks. |
Class choice depends on patient phenotype and comorbidities.
Selecting among neuromodulator classes often depends less on the exact diagnosis and more on the patient’s phenotype.
Principles Shared Across the Group: Initiation, Switching, Deprescribing
Across neuromodulators, the guiding rule is start low and go slow to limit sedation, dizziness, or gastrointestinal upset. Abrupt cessation is avoided, since sudden withdrawal can trigger rebound pain, withdrawal symptoms, or even lower seizure threshold.
When therapy changes are needed, clinicians usually favor cross-titration (tapering one agent while gradually introducing another) to maintain stability and avoid abrupt symptom shifts. Another shared principle is polypharmacy minimization. Combining multiple CNS depressants, whether neuromodulators, opioids, or benzodiazepines, sharply raises risks of falls, cognitive impairment, and respiratory suppression.
Finally, deprescribing is deliberate, not incidental. Periodic reassessment identifies when side effects outweigh benefits or when a patient can trial dose reduction. Careful tapering ensures that withdrawal harms are avoided.
Safety Themes & Monitoring (Class Clusters)
Across neuromodulator classes, safety profiles cluster around predictable patterns. The most frequent concerns involve sedation, dizziness, and cognitive slowing, which can compromise daily activities such as driving or working with machinery. These risks are dose-dependent and often most pronounced at initiation or dose escalation.
For α2δ ligands, additional issues include peripheral edema and weight gain, which may complicate management in patients with heart failure or metabolic syndrome. They are also renally cleared, so accumulation in impaired renal function can magnify adverse effects.
For tricyclic antidepressants (TCAs), the central limitation is anticholinergic burden (dry mouth, constipation, urinary retention, blurred vision), particularly problematic in older adults. They also prolong QTc interval and may exacerbate arrhythmia risk, requiring caution in cardiac disease.
For SNRIs, key safety considerations include blood pressure elevation, sweating, and gastrointestinal side effects such as nausea. Abrupt discontinuation can produce a recognizable withdrawal syndrome with dizziness, irritability, and flu-like symptoms, underscoring the need for tapering.
As for sodium-channel modulators, monitoring focuses on hyponatremia, dizziness, and dermatologic reactions. Rare but serious rashes such as Stevens–Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN) necessitate vigilance in the early weeks of therapy. These agents are also subject to enzyme induction or inhibition, raising interaction risks with other drugs.
Topical therapies avoid most systemic side effects, though they can cause localized irritation, erythema, or burning at the application site. Monitoring here is practical: skin integrity and adherence to application protocols. Overarching all classes is the need to remain alert to falls, driving impairment, and suicidality warnings attached to antiseizure-derived agents. These safety domains are not condition-specific but patient-specific, influenced by age, frailty, polypharmacy, and psychiatric history.
Safety monitoring focuses on sedation, falls, and organ-specific risks.
Across neuromodulator classes, safety profiles cluster around predictable patterns such as sedation, dizziness, and cognitive slowing.
Monitoring Checklist (Practical Highlights)
- Mood and suicidality screening (especially with antiseizure classes).
- Falls and gait stability at initiation and dose changes.
- Electrolytes (sodium) with carbamazepine/oxcarbazepine.
- Renal function for α2δ ligands.
- Hepatic function for SNRIs and TCAs.
- Cardiac monitoring (ECG/QTc) if TCAs are considered.
- Skin inspection for topical therapy adherence and tolerability.
Interaction Patterns That Matter
Since neuromodulators often affect central nervous system activity, their most important risks emerge when combined with other agents. The key is not just pharmacology but also real-world co-prescribing patterns, where opioids, benzodiazepines, or antidepressants are already common. One major category involves CNS depressants. Combining α2δ ligands, TCAs, or sodium-channel modulators with opioids, benzodiazepines, alcohol, or sedating antihistamines can magnify drowsiness, impair coordination, and increase risk of falls and respiratory suppression. This is particularly hazardous in older adults or those with sleep apnea.
A second pattern is serotonergic load. Both SNRIs and TCAs enhance serotonin. Adding triptans, MAO inhibitors, or certain opioids (tramadol, meperidine) raises the risk of serotonin syndrome, a rare but potentially life-threatening complication characterized by agitation, autonomic instability, and hyperreflexia.
A third interaction group stems from enzyme induction and inhibition. Carbamazepine and oxcarbazepine are strong inducers of CYP enzymes, lowering the effectiveness of oral contraceptives, anticoagulants, and many other drugs. Conversely, valproate and certain inhibitors can raise levels of lamotrigine or carbamazepine, increasing toxicity risk. Careful medication reconciliation is essential whenever sodium-channel modulators are prescribed. Even over-the-counter pitfalls deserve mention. First-generation antihistamines (diphenhydramine, hydroxyzine) can amplify sedation when paired with α2δ ligands or TCAs. NSAIDs may aggravate blood pressure issues in patients on SNRIs. Patients frequently overlook non-prescription items, making explicit inquiry a key part of safe prescribing.
Finally, Polypharmacy and drug interactions require careful review. It is not always one dangerous pairing but the cumulative effect of several mild depressants, each tolerated alone, that together cross the threshold into clinically significant impairment. This cumulative risk underscores the principle of minimizing unnecessary overlaps in therapy.
Special Populations
While neuromodulators share unifying principles, their risk–benefit balance shifts considerably in certain populations. Tailoring therapy to these groups is essential.
Older adults are particularly sensitive to sedation, dizziness, anticholinergic load, and fall risk. α2δ ligands and TCAs can cause unsteady gait, while TCAs also carry risks of urinary retention, constipation, and confusion. The guiding principle is lowest effective dose, slow titration, and frequent reassessment. Topical therapies often play an outsized role because they bypass systemic side effects.
Pregnancy and lactation pose special challenges. Most neuromodulators are not first-line during pregnancy, given associations with congenital malformations or neonatal adaptation syndromes, particularly for sodium-channel modulators and TCAs. Gabapentinoids and SNRIs also carry uncertainties. When necessary, therapy should be guided by a specialist with careful risk–benefit assessment, and patients should be offered preconception counseling whenever possible.
Renal impairment is critical for α2δ ligands, which are renally cleared and can accumulate, leading to excessive sedation, confusion, and edema. Dose adjustment or avoidance is mandatory at lower glomerular filtration rates. Conversely, SNRIs and TCAs depend more on hepatic metabolism, and thus can accumulate in hepatic impairment, with risks of toxicity and arrhythmia.
History of substance use is another dimension. Gabapentin and pregabalin have been reported in cases of misuse, especially when combined with opioids. Dopamine agonists can trigger impulse control disorders such as compulsive gambling or shopping. Patients with such histories require extra monitoring and clear boundaries around medication use.
The overarching principle across all special populations is individualized caution: starting lower, monitoring closer, and revisiting necessity more frequently than in the general population.
Older adults, pregnancy, renal impairment, and substance use history all require individualized caution and dose adjustment.
Evidence & Guidelines — How to Read Them
The evidence base for neuromodulators is substantial but also uneven. Most classes have been studied in multiple conditions, yet direct head-to-head trials are rare. This means that guideline recommendations often rely on indirect comparisons, network meta-analyses, and consensus panels rather than definitive superiority studies. For clinicians and patients, the key is learning how to interpret the numbers. Two metrics dominate in this field: Number Needed to Treat (NNT) and Number Needed to Harm (NNH). NNT expresses how many patients must be treated for one to benefit beyond placebo. NNH indicates how many must be treated before one withdraws due to side effects. In neuropathic pain, typical NNTs range from 4 to 7, meaning that only a subset achieves meaningful relief, while NNH values can be similar, reflecting the trade-off between benefit and tolerability.
Guidelines from organizations such as NICE, the American Academy of Neurology (AAN), and EFNS generally endorse α2δ ligands, SNRIs, and TCAs as first-line, with sodium-channel modulators or topicals added in specific niches. Importantly, they emphasize shared decision-making: matching the class to comorbidities, patient preferences, and risk profiles. Certainty levels vary, they are higher for diabetic neuropathy, lower for fibromyalgia or restless legs.
The bottom line is that guidelines offer probability estimates, not guarantees, and should be read as structured advice rather than rigid protocols.
Guidelines emphasize shared decision-making and realistic expectations.
FAQ
What do these drug classes have in common?
They all aim to reduce neural hyperexcitability. While their mechanisms differ and are represented by calcium-channel binding, serotonin/norepinephrine modulation, sodium-channel stabilization, or peripheral desensitization, the shared goal is to calm overactive nerve circuits rather than simply masking pain.
Can two different classes be combined safely?
Yes, combinations are sometimes used when single agents are insufficient, especially if they act on different mechanisms (for example, an α2δ ligand plus an SNRI). The main caution is to avoid stacking sedative effects or increasing fall and cognitive risks.
How long before I notice benefits?
Onset varies. Some people feel improvement in the first one to two weeks, while others may need four to six weeks at a stable dose before meaningful change is clear.
What if daytime sleepiness becomes a problem?
Options include dose adjustment, switching to an alternative class, or moving the dose to bedtime if appropriate. Discussing the problem early helps avoid unnecessary discontinuation.
When is a topical preferable?
Topical agents like lidocaine or capsaicin patches are particularly useful when pain is localized to a small area, or when systemic side effects make oral drugs impractical. They are less effective for widespread pain.
Practical Toolkit
To make sense of neuromodulators in everyday practice, structured aids can help bridge complex pharmacology with patient-centered care. The following resources are commonly used in clinic or adapted for educational settings.
Neuromodulator mechanism map
Phenotype-Based Selector (Quick Reference Matrix)
| Patient Goal / Comorbidity | Classes to Consider | Classes to Use With Caution / Avoid | Rationale |
|---|---|---|---|
| Insomnia / poor sleep | Sedating TCAs (bedtime), α2δ ligands | SNRIs (may worsen sleep) | TCAs and α2δ ligands can improve sleep; SNRIs may be alerting. |
| Daytime fatigue / need for alertness | SNRIs (mildly activating) | TCAs, high-dose α2δ ligands | SNRIs support daytime function; TCAs and α2δ ligands may sedate. |
| Comorbid depression / anxiety | SNRIs, TCAs | α2δ ligands (no direct mood effect) | SNRIs and TCAs relieve pain and mood symptoms simultaneously. |
| Obesity / weight concerns | SNRIs (weight-neutral), Topicals | α2δ ligands, TCAs (weight gain) | Avoid agents linked to weight gain; prefer neutral options. |
| Fall risk / frailty | Topicals, cautious low-dose SNRI | α2δ ligands, TCAs (sedation, orthostasis) | Topicals bypass systemic sedation; sedatives increase fall risk. |
| Renal impairment | SNRIs, TCAs, sodium-channel modulators | α2δ ligands (renally cleared) | Gabapentinoids accumulate in renal dysfunction. |
| Hepatic impairment | α2δ ligands, Topicals | SNRIs, TCAs, sodium-channel modulators | Most metabolized hepatically; α2δ ligands avoid liver metabolism. |
| Cardiac disease / QTc risk | α2δ ligands, SNRIs, Topicals | TCAs (QTc prolongation) | TCAs prolong QTc; safer classes avoid this liability. |
| History of substance use | SNRIs, Topicals | α2δ ligands (misuse potential), Dopamine agonists (impulse control issues) | Avoid drugs with misuse or behavioral risk. |
Shared-Decision Checklist for Clinic Visits
This checklist helps both patient and clinician align expectations, identify risks, and agree on a clear treatment plan.
- What is the main priority? Clarify whether the focus is pain relief, better sleep, improved mood, or functional gains such as mobility and daily activities. Knowing the top priority helps guide class choice.
- What side effects are least tolerable? Some patients are more concerned about weight gain, others about daytime sleepiness or cognitive fog. Ranking side effects makes it easier to avoid the wrong class from the start.
- What comorbidities could influence choice? Conditions such as cardiac disease, renal or hepatic impairment, depression, or fall risk can make some classes unsafe while steering preference toward others.
- Is a trial period and re-evaluation agreed upon? Emphasize that neuromodulator therapy is usually a time-limited trial. Benefits and harms should be re-assessed after a defined period (often 4–8 weeks), with a plan to continue, adjust, or taper.
“Switching Conversation” Scripts
Clear explanations reduce anxiety when changing therapies. Example clinician phrasing:
- “These medications act slowly, so it’s safest to overlap one while tapering the other. That way, we avoid withdrawal and give your body time to adjust.”
- “Switching too quickly can cause rebound pain, mood changes, or dizziness. A gradual cross-titration keeps you comfortable during the transition.”
- “Think of this as shifting gears smoothly rather than slamming the brakes and accelerating at once.”
Such framing helps patients understand why abrupt cessation is discouraged, and reinforces the idea that careful tapering is protective, not unnecessary delay.
Adherence Tips
Consistency is key when using neuromodulators. Taking the medication at the same time every day helps maintain steady levels in the body and makes it easier to remember. If the drug tends to cause drowsiness, it is best aligned with the sleep–wake cycle, often taken in the evening; if it is more activating, morning dosing may be preferable.
Medications work best when paired with supportive habits. Good sleep hygiene, gentle movement, and relaxation strategies can reinforce the benefits of neuromodulation, reducing reliance on higher doses. Patients are encouraged to keep a simple diary of pain intensity, sleep quality, and any side effects. This record not only empowers self-awareness but also gives the clinician a clear picture for making adjustments during follow-up visits.
In short, adherence is not only about taking the drug, but about integrating it into daily life in a way that maximizes benefit and minimizes burden.
References & Reviewer Box
- Attal, N., Bouhassira, D., & Baron, R. (2021). Diagnosis and assessment of neuropathic pain through questionnaires and clinical examination. The Lancet Neurology, 20(5), 406–417. https://doi.org/10.1016/S1474-4422(21)00042-1
- Finnerup, N. B., Kuner, R., & Jensen, T. S. (2021). Neuropathic pain: From mechanisms to treatment. Physiological Reviews, 101(1), 259–301. https://doi.org/10.1152/physrev.00045.2019
- NICE (2020). Neuropathic pain in adults: pharmacological management in non-specialist settings (CG173). National Institute for Health and Care Excellence. https://www.nice.org.uk/guidance/cg173
- American Academy of Neurology (AAN) Guideline Subcommittee. (2022). Treatment of painful diabetic neuropathy: Evidence-based guideline update. Neurology, 98(4), 285–299. https://doi.org/10.1212/WNL.0000000000013037
- Häuser, W., Sarzi-Puttini, P., & Tölle, T. (2021). Fibromyalgia syndrome and central sensitivity syndromes: Mechanism-oriented therapy. Arthritis Research & Therapy, 23(1), 50. https://doi.org/10.1186/s13075-021-02424-5
- Trenkwalder, C., et al. (2021). Restless legs syndrome: Pathophysiology, clinical presentation, and treatment. Nature Reviews Neurology, 17(8), 497–507. https://doi.org/10.1038/s41582-021-00523-5
This article was reviewed for clinical accuracy by Stephanie Chan, MD, Neurology & Pain Medicine Specialist.
Affiliation: Sunrise Hospital And Medical Center
Interests: Neuropathic pain, neuropharmacology, palliative neurology.
Disclosure: No financial conflicts of interest relevant to neuromodulators.