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Traumatic Peripheral Nerve Lesions Medication

  • Author: Neil R Holland, MBBS, MBA, FAAN; Chief Editor: Nicholas Lorenzo, MD, MHA, CPE  more...
 
Updated: Dec 28, 2015
 

Medication Summary

As outlined in the text, a wide variety of analgesic medications may be effective in the treatment of neuralgic pain. These include both narcotic and nonnarcotic medications.

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Narcotic analgesics

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Fentanyl transdermal patch (Duragesic, Sublimaze)

 

Potent narcotic analgesic with much shorter half-life than morphine sulfate. DOC for conscious sedation analgesia. Ideal for analgesic action of short duration during anesthesia and immediate postoperative period.

Excellent choice for pain management and sedation with short duration (30-60 min) and easy to titrate.

Easily and quickly reversed by naloxone.

After initial dose, subsequent doses should not be titrated more frequently than q3h or q6h thereafter.

When using transdermal dosage form, pain in majority of patients controlled with 72-h dosing intervals; however, some patients require dosing intervals of 48 h.

Oxycodone (OxyContin)

 

Relieves moderately severe to severe pain.

Morphine sulfate (MS Contin, Duramorph, Astramorph)

 

DOC for analgesia because of reliable and predictable effects, safety profile, and ease of reversibility with naloxone.

Various IV doses used; commonly titrated until desired effect attained.

Methadone (Dolophine)

 

Used in management of severe pain; inhibits ascending pain pathways, diminishing perception of and response to pain.

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Oral analgesics

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Tramadol (Ultram)

 

Inhibits ascending pain pathways, altering perception of and response to pain; also inhibits reuptake of norepinephrine and serotonin.

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Tricyclic antidepressants

Class Summary

These agents are a complex group of drugs that have central and peripheral anticholinergic effects as well as sedative effects. They have central effects on pain transmission and block the active re-uptake of norepinephrine and serotonin.

Amitriptyline (Elavil)

 

By inhibiting re-uptake of serotonin and/or norepinephrine by presynaptic neuronal membrane, may increase synaptic concentration in CNS.

Useful as analgesic for certain chronic and neuropathic pain.

Nortriptyline (Pamelor, Aventyl HCl)

 

Has demonstrated effectiveness in treatment of chronic pain.

By inhibiting reuptake of serotonin and/or norepinephrine by presynaptic neuronal membrane, may increase synaptic concentration in CNS.

Pharmacodynamic effects, such as desensitization of adenyl cyclase and down-regulation of beta-adrenergic receptors and serotonin receptors, also appear to play role in its mechanisms of action.

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Anticonvulsants

Class Summary

These agents are used to manage severe muscle spasms and provide sedation in neuralgia. They have central effects on pain modulation.

Gabapentin (Neurontin)

 

Has properties common to other anticonvulsants and has antineuralgic effects. Exact mechanism of action not known. Structurally related to GABA but does not interact with GABA receptors.

Lamotrigine (Lamictal)

 

Triazine derivative used in neuralgia. Inhibits release of glutamate and inhibits voltage-sensitive sodium channels, leading to stabilization of neuronal membrane.

Follow manufacturer's recommendation for dose adjustments.

Pregabalin (Lyrica)

 

Structural derivative of GABA. Mechanism of action unknown. Binds with high affinity to alpha2-delta site (a calcium channel subunit). In vitro, reduces calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. FDA approved for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as adjunctive therapy in partial-onset seizures.

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Anesthetics

Class Summary

These agents stabilize the neuronal membrane so the neuron is less permeable to ions. This prevents the initiation and transmission of nerve impulses, thereby producing the local anesthetic action.

Lidocaine anesthetic (Anestacon, DermaFlex gel, Dilocaine)

 

Several recent studies have advocated topical administration of lidocaine as treatment of PHN.

Lidocaine gel (5%) in a placebo-controlled study showed significant relief in 23 patients studied. Lidocaine tape also decreased severity of pain.

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Contributor Information and Disclosures
Author

Neil R Holland, MBBS, MBA, FAAN Interim Chair Neurology, Geisinger Health System; Clinical Professor of Neurology, The Commonwealth Medical College

Neil R Holland, MBBS, MBA, FAAN is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Neil A Busis, MD Chief of Neurology and Director of Neurodagnostic Laboratory, UPMC Shadyside; Clinical Professor of Neurology and Director of Community Neurology, Department of Neurology, University of Pittsburgh Physicians

Neil A Busis, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Chief Editor

Nicholas Lorenzo, MD, MHA, CPE Founding Editor-in-Chief, eMedicine Neurology; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc

Nicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Association for Physician Leadership, American Academy of Neurology

Disclosure: Nothing to disclose.

Additional Contributors

Milind J Kothari, DO Professor, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Penn State Milton S Hershey Medical Center

Milind J Kothari, DO is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

References
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Large-amplitude compound muscle action potential (CMAP) response was recorded from the right biceps muscle after intraoperative direct bipolar stimulation of the proximal right musculocutaneous nerve at low stimulus intensities (3.9 mA). The time base shown is 10 milliseconds/div and the gain is 50 mcV/div.
Electrodiagnostic testing 1 day after the injury revealed the following: (Left) Right ulnar motor conduction study showed a normal distal amplitude with conduction block across the elbow segment (gain = 2 mV/div, time base = 2 milliseconds [ms]/div). (Second from left) Right ulnar sensory response was normal (gain = 20 mcV/div, time base = 2 ms/div). (Third from left) Right ulnar F-wave responses were absent. (Right) Needle electromyographic (EMG) examination of right abductor digiti minimi was quiet at rest but showed a single fast firing unit on attempted contraction (gain = 200 mcV/div, time base = 10 ms/div).
Electrodiagnostic testing 3 days after the injury revealed the following: (Left) Right distal ulnar motor response is of lower amplitude than on day 1, approximately 50% of baseline (gain = 2 mV/div, time base = 5 milliseconds [ms]/div) with persistent conduction block across the elbow. (Right) Right ulnar sensory response is still normal (gain = 20 mcV/div, time base =2 ms/div).
Electrodiagnostic testing 6 days after the injury revealed the following: (Left) Right distal ulnar motor response is less than 10% of baseline (gain = 2 mV/div, time base = 5 milliseconds [ms]/div) with persistent conduction block across the elbow. (Right) Right ulnar sensory response amplitude still is relatively preserved at 50% of baseline (gain = 20 mcV/div, time base = 1 ms/div).
Electrodiagnostic testing 10 days after the injury revealed the following: Right ulnar motor (middle) and sensory (right) responses are absent. Needle electromyography (EMG) of first dorsal interosseus shows sparse denervation potentials with 1 fast firing unit on attempted volitional activity.
Intraoperative nerve action potentials recorded from the lateral cord (point R) with successive stimulation (at points 1, 2, 3, 4, and 5) along the course of the musculocutaneous nerve (gain = 100 mcV/div, time base = 0.5 milliseconds [ms]/div). Normal responses are recorded from stimulation at points 1 and 2. A slight increase in latency and drop in amplitude are noted on stimulation at point 3 close to the nerve injury. Stimulation at points 4 and 5 (distal to the injury) fail to evoke a recordable response.
A 25-year-old man had a "flail" right arm after injury in a motorcycle accident (Case study 4). Left panel: Somatosensory evoked potentials (SEPs) recorded at the scalp from stimulation of the (healthy) middle trunk (gain = 0.2 mcV/div, time base = 10 milliseconds [ms]/div). Middle panel: SEPs recorded at the scalp from stimulation of the lower trunk—no reproducible responses present (gain = 0.2 mcV/div, time base = 10 ms/div). Right panel: "Super normal" nerve action potentials recorded at the lower trunk from stimulation of the medial cord (time base = 1.5 ms/div, gain = 20 mcV/div).
MRN of the brachial plexus. a: Abnormal signal in the brachial plexus elements on the affected (right) side. Compare to b: normal plexus on the unaffected (left) side.
MRN image through the cervical spine showing pseudomengocele (arrows) at the site of a cervical root avulsion in a patient with traumatic brachial plexopathy.
 
 
 
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