Accurate Education – Nutraceutical Protocols:  Central Post-Stroke Pain (CPSP)

Nutraceutical Protocols: 

Central Post-Stroke Pain (CPSP)

See:  

Nutraceutical Protocols: 

• Nutraceutical Protocols: Central Post-Stroke Pain (CPSP)
• Nutraceutical Protocols: Chemotherapy-Induced Peripheral Neuropathy (CIPN)
• Nutraceutical Protocols: Chronic Low Back Pain
• Nutraceutical Protocols: Complement Chronic Opioid Therapy
• Nutraceutical Protocols: Complex Regional Pain Syndrome (CRPS)
• Nutraceutical Protocols: Diabetic Peripheral Neuropathy (DPN)
• Nutraceutical Protocols: Fibromyalgia
• Nutraceutical Protocols: Inflammatory Bowel Diseases (IBD)
• Nutraceutical Protocols: Migraine Headaches
• Nutraceutical Protocols: Multiple Sclerosis (MS)-associated pain
• Nutraceutical Protocols: Myofascial Pain Syndrome
• Nutraceutical Protocols: Preventing the Transition From Acute to Chronic Pain After Trauma or Surgery

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Definitions and Terms Related to Pain

Central Post-Stroke Pain (CPSP)

Central post-stroke pain (CPSP) is a neuropathic pain condition affecting 8–35% of stroke patients, classically associated with thalamic stroke (Dejerine-Roussy syndrome) but can result from lesions anywhere along the spinothalamic and thalamocortical tracts.[1][2]

• Symptoms: Burning, freezing, aching, or tearing sensations, frequently accompanied by cold or light touch triggering severe pain (allodynia).
• Causes: A lesion in the brainstem, thalamus, or cortex, leading to hyperexcitability of neurons in the central nervous system
• Diagnosis: Primarily based on clinical history (pain beginning shortly after stroke) and MRI/CT confirmation of a stroke in the sensory pathway.

   Pathophysiology Targeted:

• Central disinhibition
• Thalamocortical pathway dysfunction
• Neuroinflammation
• Microglial Activation
• Oxidative stress
• NMDA receptor dysregulation
• TNF-α/NLRP3 inflammasome activation
• GABAergic disinhibition

Pain is typically described as burning or aching with allodynia to touch, cold, or movement, usually beginning within days to weeks after stroke.[2] CPSP is notoriously treatment-resistant, with pharmacological therapy showing only a small effect size in meta-analysis.[1]

First-line treatments include:

• Duloxetine (Cymbalta)
• Amitriptyline
• Lamotrigine
• Neuromodulation (rTMS) showing moderate effects.[1][3]

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MECHANISTIC RATIONALE FOR NUTRACEUTICAL APPROACH

The pathophysiology of CPSP involves several mechanisms that are targetable by nutraceuticals:

1. Neuroinflammation and microglial activation: Microglia activation in the perilesional site and remote areas (thalamus) drives CPSP through proinflammatory cytokine release (TNF-α, IL-6, IL-1β).[4][5][6]

2. Oxidative stress: Excessive ROS, matrix metalloproteinases (MMPs), and peroxynitrite contribute to CPSP development.[7][8]

3. Central disinhibition: P2X4R/TNF-α/TNFR1 pathway causes GABAa receptor endocytosis, reducing inhibitory tone.[6]

4. NMDA receptor dysregulation: Glutamatergic hyperexcitability contributes to central sensitization.[9]

5. BDNF/TrkB pathway disruption: Altered synaptic plasticity and monoamine levels contribute to pain and comorbid depression.[4]

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NUTRACEUTICAL PROTOCOL FOR CPSP

Tier 1: Core Agents (Strongest Mechanistic Rationale)

[4][21][22][23][14][24][25][17][26][27][28]

PEA + Luteolin Evidence for CPSP: A preclinical study directly evaluated co-ultramicronized PEA + luteolin (PEALut) in a mouse model of thalamic hemorrhage-induced CPSP. Repeated administration significantly reduced mechanical hypersensitivity by reducing early microglial activation in the perilesional site. PEALut also prevented depressive-like behavior (common comorbidity in CPSP), restored synaptic plasticity in the lateral entorhinal cortex-dentate gyrus pathway, normalized monoamine levels, and restored MED1/TrkB/BDNF expression. Notably, MED1 overexpression was confirmed in human autoptic brain specimens after stroke, indicating translational potential.[4]

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Tier 2: Anti-Neuroinflammatory and Antioxidant Agents

[29][30][31][32][33][34][35][36][37]

   Animal Studies

• Resveratrol in Stroke: A systematic review and meta-analysis of 75 rodent studies found resveratrol significantly reduced infarct size, edema, BBB impairment and neurofunctional impairment through reduction of oxidative stress, inflammation, and apoptosis.[36]
• Omega-3 in Stroke Recovery: Post-stroke administration of omega-3 PUFAs promotes neurovascular restoration, enhances angiogenesis, oligodendrogenesis, neuron survival, and white matter restoration in both young and aged mice.[37] Omega-3 supplementation also accelerates nerve regeneration and prevents neuropathic pain behavior.[34][35]

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Tier 3: Supporting Agents

[29][30][33]

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PHASED IMPLEMENTATION PROTOCOL

Phase 1: Acute/Subacute Post-Stroke (0–4 Weeks After Stroke)

Goal: Neuroprotection, reduce neuroinflammation, prevent CPSP development

• PEA 600 mg BID (ultramicronized formulation)
• Omega-3 2–3 g daily (if not contraindicated by anticoagulation status)
• Magnesium 400 mg daily (check renal function)
• Melatonin 3–5 mg QHS
• Vitamin D3 optimization (check levels; supplement to achieve 40–60 ng/mL)
• Consider Citicoline 500–1000 mg daily for neuroprotection

Phase 2: Early CPSP Development (1–3 Months Post-Stroke)

Goal: Address established neuroinflammation, central sensitization

• PEA + Luteolin (co-ultramicronized) 600 mg + 70 mg BID
• Magnesium 400–500 mg daily
• Melatonin 5–10 mg QHS
• Resveratrol 500 mg daily
• Curcumin 500 mg TID (high-bioavailability)
• Omega-3 2–3 g daily
• Mantain Vitamin D3 optimization

Phase 3: Established/Refractory CPSP (>3 Months)

Goal: Multimodal approach targeting multiple pathways

• Continue all Phase 2 agents
• Add NAC 600 mg BID
• Add ALA 600 mg daily
• Add Quercetin 500 mg BID
• Consider higher Melatonin doses (10–15 mg QHS)
• Consider IV Magnesium 500 mg–1 g for acute flares (if tolerated)

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INTEGRATION WITH PHARMACOTHERAPY

CPSP typically requires pharmacological treatment. Nutraceuticals should be used as adjunctive therapy to enhance efficacy and potentially reduce medication doses/side effects.

[1][2][38][3][23]

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MONITORING AND ASSESSMENT

Baseline Assessment:

• Pain intensity, pain quality assess for neuropathic features)
• Mood assessment – depression/anxiety common in CPSP
• Sleep quality assessment
• Functional status (Barthel Index, modified Rankin Scale)
• Laboratory: 25(OH)D, magnesium, renal function, liver function

Follow-up (Monthly for 3 months, then quarterly):

• Pain scores and quality
• Medication requirements (track any dose reductions)
• Adverse effects
• Mood and sleep
• Functional status

Expected Timeline:

• Weeks 1–2: Sleep improvement with melatonin

• Weeks 2–4: Initial anti-inflammatory effects; possible modest pain reduction

• Weeks 4–8: More substantial pain reduction if responding

• Weeks 8–12: Full assessment of efficacy; consider protocol adjustments

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SPECIAL CONSIDERATIONS FOR CPSP

Stroke-Related Factors:

• Anticoagulation: If on warfarin, monitor INR with omega-3 initiation (may potentiate anticoagulation); generally safe with DOACs at standard doses
• Dysphagia: Consider liquid or powder formulations if swallowing impaired
• Cognitive impairment: Simplify regimen; use pill organizers; involve caregivers
• Polypharmacy: Review for interactions; prioritize agents with strongest evidence

Comorbid Depression:

• Depression is common in CPSP and shares pathophysiological mechanisms

• PEA + Luteolin specifically prevented depressive-like behavior in CPSP model[4]

• Melatonin, omega-3, and resveratrol also have antidepressant properties

• Consider prioritizing these agents in patients with comorbid depression

Thalamic vs. Non-Thalamic CPSP:

• Thalamic CPSP (Dejerine-Roussy syndrome) may be more severe and treatment-resistant
• Consider more aggressive multimodal approach for thalamic lesions
• PEA + Luteolin evidence is specifically from thalamic hemorrhage model[4]

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PATIENT EDUCATION HANDOUT

Managing Central Post-Stroke Pain: Your Supplement Guide

Understanding Central Post-Stroke Pain

Central post-stroke pain (CPSP) is a type of nerve pain that can develop after a stroke. It occurs because the stroke damaged parts of your brain that process pain signals. This can cause your brain to misinterpret normal sensations as painful.

CPSP is often described as:

– Burning, aching, or freezing sensations

– Pain triggered by light touch, cold, or movement

– Pain in the area of your body affected by the stroke

This type of pain can be challenging to treat, but a combination of medications and natural supplements may help improve your symptoms.

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Why Natural Supplements May Help

After a stroke, inflammation and oxidative stress in your brain can contribute to pain. The supplements your healthcare provider has recommended target these specific problems:

– Reducing brain inflammation that keeps pain signals active

– Protecting nerve cells from further damage

– Calming overactive pain pathways in your brain

– Improving sleep, which is essential for pain management

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Your Supplement Program

Core Supplements

PEA with Luteolin (Palmitoylethanolamide + Luteolin)

– Take 600 mg PEA + 70 mg Luteolin twice daily for the first 4 weeks, then once daily

– This combination has been specifically studied for stroke-related pain

– It helps calm inflammation in the brain and protects nerve cells

– It may also help with mood, which is often affected after stroke

Magnesium – 400–500 mg daily

– Helps calm overactive nerve signals

– Has protective effects on the brain

– Take with food to reduce stomach upset

Melatonin – 5–10 mg at bedtime

– Helps improve sleep, which is often disrupted by pain

– Has natural pain-relieving properties

– Works with your body’s own pain-control systems

Additional Supplements

Resveratrol – 500 mg daily

– A powerful antioxidant found in grapes

– Helps reduce brain inflammation

– Protects brain cells from damage

Curcumin – 500 mg three times daily

– An anti-inflammatory compound from turmeric

– Use a high-absorption form as recommended

– Take with food for best absorption

Omega-3 Fish Oil – 2–3 grams daily

– Supports brain healing after stroke

– Reduces inflammation

– May help with mood and cognitive function

– If you take blood thinners, discuss with your doctor first

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What to Expect

Central post-stroke pain is challenging to treat, and improvement may be gradual:

– Weeks 1–2: You may notice improved sleep

– Weeks 2–4: Some people begin to notice slight pain reduction

– Weeks 4–8: More noticeable improvement if the supplements are helping

– Weeks 8–12: Full assessment of how well the program is working

Be patient – these supplements work gradually by addressing the underlying causes of your pain, not just masking symptoms.

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Important Safety Information

– Continue all medications prescribed by your doctor

– Tell your healthcare provider about all supplements you take

– If you take blood thinners (warfarin, aspirin, or others), discuss omega-3 fish oil with your doctor

– Most side effects are mild (stomach upset, drowsiness with melatonin)

– Take supplements with food to reduce stomach discomfort

When to Contact Your Healthcare Provider

– If your pain significantly worsens

– If you experience unusual bleeding or bruising

– If you have new neurological symptoms

– If you experience severe side effects

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Tips for Success

1. Be consistent: Take supplements at the same time each day

2. Use a pill organizer: This helps track multiple supplements

3. Keep a pain diary: Note your pain levels, sleep quality, and mood

4. Stay engaged in rehabilitation: Supplements work best alongside physical therapy and other treatments

5. Address mood: Depression and anxiety are common after stroke and can worsen pain – let your provider know if you’re struggling

6. Be patient: Nerve pain takes time to improve

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Working With Your Healthcare Team

These supplements are meant to work alongside your prescribed medications, not replace them. Your healthcare team may adjust your medications over time based on your response. Always discuss any changes with your provider before stopping or changing any treatment.

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Clinical Implementation Notes

The evidence for nutraceuticals in CPSP is primarily mechanistic and preclinical, with PEA + Luteolin having the most direct evidence from a thalamic hemorrhage-induced CPSP model.[4] This study demonstrated that PEALut reduced mechanical hypersensitivity, prevented depression, and restored synaptic plasticity through microglial modulation and BDNF pathway restoration. The finding of MED1 overexpression in human autoptic brain specimens after stroke provides translational support.

Magnesium has neuroprotective properties in stroke through NMDA receptor antagonism and has shown some efficacy in cancer-related neuropathic pain poorly responsive to opioids.[24][25] However, clinical trials in adult stroke have been disappointing for acute neuroprotection.[25]

Melatonin has strong preclinical evidence for neuropathic pain through MT2 receptor-mediated modulation of descending antinociceptive pathways.[27][28] However, a recent RCT found no significant difference between melatonin (mean dose 11.9 mg/day) and placebo for neuropathic pain intensity.[17] Despite this, melatonin’s favorable safety profile, effects on sleep (commonly disrupted in CPSP), and NLRP3 inflammasome inhibition support its inclusion.

Resveratrol has robust preclinical evidence for neuroprotection in ischemic stroke, with a meta-analysis showing significant reductions in infarct size, edema, and neurofunctional impairment.[36]

Important caveats: CPSP is notoriously treatment-resistant, and even first-line pharmacotherapies show only modest effect sizes.[1] Nutraceuticals should be viewed as adjunctive therapy to enhance pharmacological treatment, not as monotherapy. The multimodal approach targeting neuroinflammation, oxidative stress, and central sensitization is mechanistically sound but requires clinical validation in CPSP specifically.

Would you like me to create a comprehensive summary document combining all six condition-specific protocols, or develop monitoring flowsheets and drug-nutraceutical interaction tables for clinical implementation?

References

1. Management of Central Poststroke Pain: Systematic Review and Meta-Analysis. Tamasauskas A, Silva-Passadouro B, Fallon N, et al. The Journal of Pain. 2025;26:104666. doi:10.1016/j.jpain.2024.104666.
2. Guidelines for Adult Stroke Rehabilitation and Recovery: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Winstein CJ, Stein J, Arena R, et al. Stroke. 2016;47(6):e98-e169. doi:10.1161/STR.0000000000000098.
3. Pharmacotherapy to Manage Central Post-Stroke Pain. Choi HR, Aktas A, Bottros MM. CNS Drugs. 2021;35(2):151-160. doi:10.1007/s40263-021-00791-3.
4. MED1/BDNF/TrkB Pathway Is Involved in Thalamic Hemorrhage-Induced Pain and Depression by Regulating Microglia. Infantino R, Schiano C, Luongo L, et al. Neurobiology of Disease. 2022;164:105611. doi:10.1016/j.nbd.2022.105611.
5. The Role of the Immune System in the Generation of Neuropathic Pain. Calvo M, Dawes JM, Bennett DL. The Lancet. Neurology. 2012;11(7):629-42. doi:10.1016/S1474-4422(12)70134-5.
6. P2X4R Contributes to Central Disinhibition via TNF-α/TNFR1/GABAaR Pathway in Post-Stroke Pain Rats. Lu J, Guo X, Yan M, et al. The Journal of Pain. 2021;22(8):968-980. doi:10.1016/j.jpain.2021.02.013.
7. A Novel Endoplasmic Reticulum-Targeted Metal-Organic Framework-Confined Ruthenium (Ru) Nanozyme Regulation of Oxidative Stress for Central Post-Stroke Pain. Bai Q, Han Y, Khan S, et al. Advanced Healthcare Materials. 2024;13(2):e2302526. doi:10.1002/adhm.202302526.
8. Neuroinflammation: Friend and Foe for Ischemic Stroke. Jayaraj RL, Azimullah S, Beiram R, Jalal FY, Rosenberg GA. Journal of Neuroinflammation. 2019;16(1):142. doi:10.1186/s12974-019-1516-2.
9. Research Progress on the Mechanisms of Central Post-Stroke Pain: A Review. Cheng Y, Wu B, Huang J, Chen Y. Cellular and Molecular Neurobiology. 2023;43(7):3083-3098. doi:10.1007/s10571-023-01360-6.
10. Meta-Analysis of Palmitoylethanolamide in Pain Management: Addressing Literature Gaps and Enhancing Understanding. Viña I, López-Moreno M. Nutrition Reviews. 2025;83(7):e1604-e1618. doi:10.1093/nutrit/nuae203.
11. Ultramicronized N-Palmitoylethanolamine Associated With Analgesics: Effects Against Persistent Pain. Nobili S, Micheli L, Lucarini E, et al. Pharmacology & Therapeutics. 2024;258:108649. doi:10.1016/j.pharmthera.2024.108649.
12. Palmitoylethanolamide in the Treatment of Chronic Pain Caused by Different Etiopathogenesis. Gatti A, Lazzari M, Gianfelice V, et al. Pain Medicine (Malden, Mass.). 2012;13(9):1121-30. doi:10.1111/j.1526-4637.2012.01432.x.
13. Palmitoylethanolamide, a Special Food for Medical Purposes, in the Treatment of Chronic Pain: A Pooled Data Meta-Analysis. Paladini A, Fusco M, Cenacchi T, et al. Pain Physician. 2016;19(2):11-24.
14. Efficacy and Safety of Magnesium for the Management of Chronic Pain in Adults: A Systematic Review. Park R, Ho AM, Pickering G, et al. Anesthesia and Analgesia. 2020;131(3):764-775. doi:10.1213/ANE.0000000000004673.
15. Management of Headache (2023). Jane Abanes PhD DNP MSN/Ed PMHCNS PMHNP-BC RN, Natasha M. Antonovich PharmD BCPS, Andrew C. Buelt DO, et al. Department of Veterans Affairs.
16. A Double-Blinded Randomised Controlled Study of the Value of Sequential Intravenous and Oral Magnesium Therapy in Patients With Chronic Low Back Pain With a Neuropathic Component. Yousef AA, Al-deeb AE. Anaesthesia. 2013;68(3):260-6. doi:10.1111/anae.12107.
17. Melatonin for Neuropathic Pain: A Double-Blind, Placebo-Controlled, Randomized, Crossover Trial. Gilron I, Elkerdawy H, Tu D, et al. Pain. 2025;:00006396-990000000-00905. doi:10.1097/j.pain.0000000000003651.
18. Melatonin Treatment Has Consistent but Transient Beneficial Effects on Sleep Measures and Pain in Patients With Severe Chronic Pain: The DREAM-CP Randomised Controlled Trial. Onyeakazi UM, Columb MO, Rosalind A, Kanakarajan S, Galley HF. British Journal of Anaesthesia. 2024;132(4):725-734. doi:10.1016/j.bja.2024.01.012.
19. Analgesic Efficacy of Melatonin: A Meta-Analysis of Randomized, Double-Blind, Placebo-Controlled Trials. Oh SN, Myung SK, Jho HJ. Journal of Clinical Medicine. 2020;9(5):E1553. doi:10.3390/jcm9051553.
20. The Non-Surgical Management of Hip & Knee Osteoarthritis (OA) (2020). Matthew Bair MD MS, John Cody MD, Jess Edison MD, et al. Department of Veterans Affairs.
21. Palmitoylethanolamide in the Treatment of Pain and Its Clinical Application Prospects. Wang Y, Duan X, Li Z, Pan Y, Deng J. Drug Design, Development and Therapy. 2025;19:6897-6923. doi:10.2147/DDDT.S540327.
22. Reduction of Ischemic Brain Injury by Administration of Palmitoylethanolamide After Transient Middle Cerebral Artery Occlusion in Rats. Ahmad A, Genovese T, Impellizzeri D, et al. Brain Research. 2012;1477:45-58. doi:10.1016/j.brainres.2012.08.006.
23. Magnesium in Pain Research: State of the Art. Srebro D, Vuckovic S, Milovanovic A, et al. Current Medicinal Chemistry. 2017;24(4):424-434. doi:10.2174/0929867323666161213101744.
24. The Safety and Efficacy of a Single Dose (500 Mg or 1 G) of Intravenous Magnesium Sulfate in Neuropathic Pain Poorly Responsive to Strong Opioid Analgesics in Patients With Cancer. Crosby V, Wilcock A, Corcoran R. Journal of Pain and Symptom Management. 2000;19(1):35-9. doi:10.1016/s0885-3924(99)00135-9.
25. Magnesium as a Neuroprotective Agent: A Review of Its Use in the Fetus, Term Infant With Neonatal Encephalopathy, and the Adult Stroke Patient. Lingam I, Robertson NJ. Developmental Neuroscience. 2018;40(1):1-12. doi:10.1159/000484891.
26. Melatonin Improves Mitochondrial Dysfunction and Attenuates Neuropathic Pain by Regulating SIRT1 in Dorsal Root Ganglions. Zeng Y, Fang Q, Chen J, et al. Neuroscience. 2023;534:29-40. doi:10.1016/j.neuroscience.2023.10.005.
27. Targeting Melatonin MT2 Receptors: A Novel Pharmacological Avenue for Inflammatory and Neuropathic Pain. Posa L, De Gregorio D, Gobbi G, Comai S. Current Medicinal Chemistry. 2018;25(32):3866-3882. doi:10.2174/0929867324666170209104926.
28. Selective Melatonin MT2 Receptor Ligands Relieve Neuropathic Pain Through Modulation of Brainstem Descending Antinociceptive Pathways. Lopez-Canul M, Palazzo E, Dominguez-Lopez S, et al. Pain. 2015;156(2):305-317. doi:10.1097/01.j.pain.0000460311.71572.5f.
29. The Role of Neuro-Supportive Substances of Natural Origin in Neurological Conditions-a Literature-Based Formulators’ Perspective. van Brummelen R, van Brummelen AC. Frontiers in Neurology. 2025;16:1647092. doi:10.3389/fneur.2025.1647092.
30. Flavonoids and Ischemic Stroke-Induced Neuroinflammation: Focus on the Glial Cells. Lu W, Chen Z, Wen J. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie. 2024;170:115847. doi:10.1016/j.biopha.2023.115847.
31. The Natural (Poly)phenols as Modulators of Microglia Polarization via TLR4/NF-κB Pathway Exert Anti-Inflammatory Activity in Ischemic Stroke. Li R, Zhou Y, Zhang S, et al. European Journal of Pharmacology. 2022;914:174660. doi:10.1016/j.ejphar.2021.174660.
32. Phytochemicals as Regulators of Microglia/Macrophages Activation in Cerebral Ischemia. Subedi L, Gaire BP. Pharmacological Research. 2021;165:105419. doi:10.1016/j.phrs.2021.105419.
33. Bioactive Compounds for Neuropathic Pain: An Update on Preclinical Studies and Future Perspectives. Shen CL, Castro L, Fang CY, et al. The Journal of Nutritional Biochemistry. 2022;104:108979. doi:10.1016/j.jnutbio.2022.108979.
34. Long-Chain Omega-3 Fatty Acids Supplementation Accelerates Nerve Regeneration and Prevents Neuropathic Pain Behavior in Mice. Silva RV, Oliveira JT, Santos BLR, et al. Frontiers in Pharmacology. 2017;8:723. doi:10.3389/fphar.2017.00723.
35. Beneficial Effects of Fish Oil Enriched in Omega-3 Fatty Acids on the Development and Maintenance of Neuropathic Pain. Unda SR, Villegas EA, Toledo ME, Asis Onell G, Laino CH. The Journal of Pharmacy and Pharmacology. 2020;72(3):437-447. doi:10.1111/jphp.13213.
36. Effect and Mechanisms of Resveratrol in Animal Models of Ischemic Stroke: A Systematic Review and Bayesian Meta-Analysis. López-Morales MA, Castelló-Ruiz M, Burguete MC, et al. Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism. 2023;43(12):2013-2028. doi:10.1177/0271678X231206236.
37. Post-Stroke Administration of Omega-3 Polyunsaturated Fatty Acids Promotes Neurovascular Restoration After Ischemic Stroke in Mice: Efficacy Declines With Aging. Jiang X, Suenaga J, Pu H, et al. Neurobiology of Disease. 2019;126:62-75. doi:10.1016/j.nbd.2018.09.012.
38. Efficacy and Safety of Different Antidepressants and Anticonvulsants in Central Poststroke Pain: A Network Meta-Analysis and Systematic Review. Chen KY, Li RY. PloS One. 2022;17(10):e0276012. doi:10.1371/journal.pone.0276012.

Emphasis on Education

Accurate Clinic promotes patient education as the foundation of it’s medical care. In Dr. Ehlenberger’s integrative approach to patient care, including conventional and complementary and alternative medical (CAM) treatments, he may encourage or provide advice about the use of supplements. However, the specifics of choice of supplement, dosing and duration of treatment should be individualized through discussion with Dr. Ehlenberger. The following information and reference articles are presented to provide the reader with some of the latest research to facilitate evidence-based, informed decisions regarding the use of conventional as well as CAM treatments.

For medical-legal reasons, access to these links is limited to patients enrolled in an Accurate Clinic medical program.

Should you wish more information regarding any of the subjects listed – or not listed –  here, please contact Dr. Ehlenberger. He has literally thousands of published articles to share on hundreds of topics associated with pain management, weight loss, nutrition, addiction recovery and emergency medicine. It would take years for you to read them, as it did him.

For more information, please contact Accurate Clinic.

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