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Neuropathic Pain Syndromes

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Sami Zamani

on 9 August 2013

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Transcript of Neuropathic Pain Syndromes

Medical Therapy of Neuropathic Pain Syndromes
Diabetic Neuropathy
Definition
Pathophysiology of disease
Pathophysiology of treatment

Treatment Options for
Diabetic Neuropathy
Antidepressants
Tricyclic (TCA), Duloxetine, Venlafaxine
Anticonvulsants
Pregabalin, Gabapentin
Capsaicin cream
Lidocaine patch
Opiods
Alpha lipoic acid
Aldolase reductase inhibitors

In summary
Needs More Research
Alpha lipoic acid
Antioxidant
Aldolase reductase inhibitors
Anticonvulsants- Gabapentin
Gabapentin
Found efficacious for pain AND sleep interference associated with diabetic neuropathy
MOA
Dosage
300-600mg TID
Titrate up to 900mg QID
Side effects
Somnolence, dizziness, ataxia
Anticonvulsants- Pregabalin
Pregabalin
Metanalysis- significant reduction in pain, rapid onset of sustained relief
Pain reduction correlated with dosage
MOA
Dosage
Side effects

Antidepressants- SNRI
Venlafaxine
Higher doses significant benefit of pain intensity and relief
75 vs 150-225mg vs placebo
Dosage
150-225mg daily
Side effects
Nausea
Somnolence

Antidepressants
Tricyclic (TCA)
Amitriptyline and desipramine
Equally effective and superior to fluoxetine or placebo
Benefit within 2 weeks
Effective in normal vs depressed mood
MOA
Dosage
Side effects
Antidepressants
Serotonin-Norepinephrine Reuptake Inhibitor (SNRI)
Duloxetine
Significant pain improvement than with placebo
Rapid onset of action
Sustained benefit
MOA
Dosage
Side effects

Peripheral Neuropathic pain
Diabetic neuropathy

Central Neuropathic pain
Post stroke pain

Autonomic Neuropathic pain
Complex regional pain syndrome I
Complex regional pain syndrome II

Sami Zamani, DO
IM PGY-2

Pathophysiology of
Diabetic Neuropathy
Capsaicin
0.075% QID
Intolerant side effects of burning pain
Lidocaine patch
Up to four patches (5%) for up to 18 hours/day
Opiods
Tramadol
Oxycodone CR
Combination therapy
Small trials nortriptyline and gabapentin
Gabapentin and morphine

The American Academy of Neurology (AAN)

In Summary
Max MB, Lynch SA, Muir J, et al. Effects of desipramine, amitriptyline, and fluoxetine on pain in diabetic neuropathy. N Engl J Med. 1992;326(19):1250.

Wide range of pharmacologic actions
Inhibition of norepinephrine (NE) and serotonin reuptake
Antagonism of cholinergic, histamine H1, and alpha adrenergic receptors

Analgesia mainly due to blocking reuptake of NE



No correlation between relief of pain, dosage, or plasma drug concentrations


Anticholinergic side effects
Dry mouth, somnolence
More common in amitriptyline than desipramine

TCAs contraindicated in patients with cardiac disease

Data from Max MB, Lynch SA, Muir J, et al, N Engl J Med 1992; 326:1250
Feldman, EL. Treatment of diabetic neuropathy. In: UpToDate, Dashe, JF (Ed), UpToDate, Waltham, MA, 2013

Raskin J, et al. A double-blind, randomized multicenter trial comparing duloxetine with placebo in the management of diabetic peripheral neuropathic pain. Pain Med. 2005;6(5):346.

Balanced affinity for both serotonin and NE reuptake inhibition

Serotonergic and noradrenergic neurons modulate the pain pathways

Effects on both neurotransmitter systems explains its effectiveness

Duloxetine
60mg once daily
No significant difference between 60mg daily and 60mg twice daily

Higher doses were less well tolerated

Lower initial dose for decreased tolerability and renal impairment

Most common side effects
Nausea
Somnolence
Dizziness
Decreased appetite
Constipation

Can be combined with anticonvulsant therapy

Freeman R, et al. Efficacy, safety, and tolerability of pregabalin treatment for painful diabetic peripheral neuropathy: findings from seven randomized, controlled trials across a range of doses. Diabetes Care. 2008;31(7):1448.

Binds to alpha2-delta subunit of voltage-gated calcium channels
Inhibiting excitatory neurotransmitter release

May affect descending noradrenergic and serotonergic pain transmission pathways from the brainstem to the spinal cord

Exerts antinociceptive and anticonvulsant activity.

No activity at GABA or benzodiazepine receptors

Most Common
Dizziness
Somnolence
Peripheral edema

Weight gain (>7% weight increase from baseline), did not affect the diabetes control.

Habit forming- Schedule V drug

American Diabetic Association (ADA)

Structurally related to GABA

Gabapentin binding sites correspond to voltage-gated calcium channels

Alpha-2delta-1 subunit

Modulate the release of excitatory neurotransmitters which participate in nociception and epileptogenesis

Backonja M, et al. Gabapentin for the symptomatic treatment of painful neuropathy in patients with diabetes mellitus: a randomized controlled trial. JAMA. 1998;280(21):1831.

Treatment
Treatment goal of pain reduction- not relief
Amitriptyline 75mg daily
Lamotrigine 200mg daily
MOA
Gabapentin 1200mg daily
Carbamazepines

Pathophysiology
Symptoms
Pain within smaller area than the sensory impairment
Ongoing vs paroxysmal
Burning, aching, pricking, lacerating, throbbing
Can occur in absence of weakness
Increased- Stress, cold
Relieved- Relaxation
Allodynia, dysaesthesia, hyperalgesia common

Definition
Post Stroke Pain
Most common forms of chronic post-stroke pain:
Shoulder pain
CPSP
Painful spasticity
Tension headache
Reduces quality of life, affects mood, sleep, and social functioning.
Incidence
Between 8-35%
Can occur up to 3 years after stroke

Central Post-Stroke Pain (CPSP)
Klit H, et al. Central post-stroke pain: clinical characteristics, pathophysiology, and management. Lancet Neurol. 2009 Sep;8(9):857-68.

Kumar B, et al. Central Postroke Pain: A Review of Pathophysiology And Treatment. Pain Medicine. 2009;108(5):1645

Exact pathophysiology is unknown

Proposed pathophysiology
Aberrant neural activity in

Postlesion imbalance between facilitatory and inhibitory pathways

Klit H, et al. Central post-stroke pain: clinical characteristics, pathophysiology, and management. Lancet Neurol. 2009 Sep;8(9):857-68.

Complex Regional
Pain Syndrome
50,000 new cases yearly in United States
More common in women
Most common initiating events:
Surgery
Fractures
Crush injuries
Sprains

Broad definition- Regional pain syndrome of unclear pathophysiology typically affecting
hand or foot
Excruciating pain
Definition
Pathophysiology
Definition
Symptoms
Pathophysiology
Treatment

Definition
Pathophysiology
Treatment
Complex Regional
Pain Syndrome
(CRPS)

Bruehl S. An Update on the Pathophysiology of Complex Regional Pain Syndrome. Anesthesiology 2010;113:713-25.

Definition Criteria
International Association for the Study of Pain (IASP) Diagnostic Criteria for CRPS-I and CRPS-II


CRPS-I (Reflex Sympathetic Dystrophy)

CRPS-II (Causalgia)

1. The presence of an initiating noxious event, or a cause of immobilization.

2. Continuing pain, allodynia, or hyperalgesia with which the pain is disproportionate to any inciting event.

3. Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of the pain.

4. This diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction.

Note: Criteria 2–4 must be satisfied.

CRPS-I
1. The presence of continuing pain, allodynia, or hyperalgesia after a nerve injury, not necessarily limited to the distribution of the injured nerve.

2. Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of the pain.

3. This diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction.

Note: All three criteria must be satisfied

CRPS-II
Treatment
Treatment is centered around 3 domains.

1. Rehabilitation

2. Psychological treatment

3. Pain management
Stanton-Hicks MD, et al. An Updated Interdisciplinary Clinical Pathway for CRPS: Report of an Expert Panel. Pain Practice 2002;2(1)

Stanton-Hicks MD, et al. An Updated Interdisciplinary Clinical Pathway for CRPS: Report of an Expert Panel. Pain Practice 2002;2(1)

Bruehl S. An Update on the Pathophysiology of Complex Regional Pain Syndrome. Anesthesiology 2010;113:713-25.

Is the mainstay of CRPS treatment

Pt should be seen by physical therapy, and treatment would involve
Gentle active ROM
Stress loading
Isotonic strengthening
General aerobic conditioning
Postural normalization
Rehabilitation
Focus of psychological treatment for CRPS is on improving QOL, developing pain coping skills, cognitive-behavioral psychotherapy

1) Emphasize that CRPS related pain sensations do not necessarily indicate tissue damage

2) Highlight the importance of re-activation of the affected extremity to prevent increased dysfunction and to facilitate improvement
Psychological Therapy
The key to success- reduce pain to allow physical therapy

Guideline developed by a consensus of experts in CRPS suggested beginning treatment for pain with:
TCA- Amitriptyline, Nortriptyline
Gabapentin
NSAIDs
Opiods

Pain Management
Pain Management
IV regional nerve block, and somatic nerve blocks have been found to minimize pain, thus allow for physical therapy

Tender point injections
Nerve stimulation
Spinal cord stimulation
Sympathectomy– controversial
Experimental- Ketamine infusion (pain relief, however no improvement in function)

Minimally Invasive Interventions
Glucocorticoids
Prednisone 30-80mg daily
Capsaicin cream
Treatment of painful diabetic neuropathy, applied topically QID
Calcitonin
Pain relief due to decreased bone resorption and a putative analgesic effect
Sympathetic blockers
Alpha-adrenergic blockers such as terazosin.

Rowbotham MC, et al. Venlafaxine extended release in the treatment of painful diabetic neuropathy: a double-blind, placebo-controlled study. Pain. 2004;110(3):697.
Pain Modulating System
http://encyclopedia.lubopitko-bg.com/Pain_Modulation.html
Tavakoli M, et al. Pathophysiology and Treatment of Painful Diabetic Neuropathy. Current Pain and Headache Reports 2008:12:192-197
Bril V, et al. Evidence-based guideline: Treatment of painful diabetic neuropathy: report of the American Academy of Neurology, the American Association of Neuromuscular and Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation. Neurology. 2011;76(20):1758.

Bril V, et al. Evidence-based guideline: Treatment of painful diabetic neuropathy: report of the American Academy of Neurology, the American Association of Neuromuscular and Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation. Neurology. 2011;76(20):1758.

Bril V, et al. Evidence-based guideline: Treatment of painful diabetic neuropathy: report of the American Academy of Neurology, the American Association of Neuromuscular and Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation. Neurology. 2011;76(20):1758.

Boulton AJ, et al. Diabetic neuropathies: a statement by the American Diabetes Association. Diabetes Care. 2005;28(4):956.

Klit H, et al. Central post-stroke pain: clinical characteristics, pathophysiology, and management. Lancet Neurol. 2009 Sep;8(9):857-68.

Frese A, et al. Pharmacologic treatment of Central Post-Stroke Pain. Clin J Pain. 2006;22(3):252-260
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