eMedicine Specialties > Neurology > Neuromuscular Diseases
Traumatic Peripheral Nerve Lesions: Treatment & Medication
Updated: Oct 11, 2006
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
Decisions regarding surgical intervention must take into account both the mechanism of injury and completeness of the nerve injury.
- Incomplete injuries
- Incompletely injured nerves remain in (at least partial) continuity; therefore, they are likely to recover spontaneously. In general, patients with incomplete nerve injuries should be treated conservatively. Lesions are judged to be partial when some residual motor or sensory function is noted in the distribution of the injured nerve segment.
- Needle EMG examination can be used to confirm that a nerve injury is partial by demonstrating the presence of some recruited voluntary motor unit potentials or signs of reinnervation even in clinically paralyzed muscles. However, note that in some cases of mixed or multiple nerve injuries in which some branches or fascicles are injured incompletely, some are likely to recover while others are not (see Case study 3 in Medical/Legal Pitfalls). These cases are best managed as complete lesions.
- Complete injuries
- Complete nerve lesions caused by lacerations or penetrating injuries should be referred for early surgical exploration and direct end-to-end repair.
- Management of other complete nerve injuries depends on whether the pathophysiology of injury is thought to be neurapraxic, axonotmetic, or neurotmetic. This underscores the importance of an appropriately and carefully timed electrodiagnostic study in the evaluation of all these cases.
- Complete nerve injuries that are predominantly neurapraxic can be expected to recover favorably over the course of weeks to months. When such cases do not recover as expected, patients should undergo follow-up electrodiagnostic testing, which may show the presence of significant secondary axonal loss suggesting that the initial testing was done too early, before the electrophysiologic abnormalities had fully evolved (see Case study 2 in Medical/Legal Pitfalls). However, if the follow-up study shows persistent conduction block across the injury site, then the patient should be evaluated carefully for an ongoing compressive lesion (eg, hematoma) by appropriate imaging studies.
- Complete lesions with electrophysiologic evidence of axonal loss may be axonotmetic or neurotmetic. Axonotmetic injuries are more likely to recover spontaneously. Neurotmetic injuries often require surgical repair for adequate recovery. The only way to differentiate these injury types noninvasively is to monitor the patient for signs of recovery. However, the chances of successful surgical repair begin to decline by 6 months after the injury. By 18-24 months, the denervated muscles usually are replaced by fatty connective tissue, making functional recovery impossible. In most cases, close clinical observation is warranted for 3-6 months after this type of nerve injury. If no clinical or electrophysiologic evidence of recovery is noted during this period, these patients should be referred for surgical exploration.
- Symptomatic management of patients with nerve injury
- Many patients develop neuropathic pain in addition to motor and sensory deficits from nerve injury. The author uses an escalating drug regimen for symptomatic control of neuropathic pain.
- Some patients with very mild pain can be treated effectively with long-acting nonsteroidal anti-inflammatory drugs (NSAIDs).
- Topical lidocaine patches are very useful or patients with small areas of cutaneous pain, eg, pain in the lateral foot after a sural nerve biopsy or other injury.
- Patients with moderately severe pain usually respond to low-dose tricyclic agents such as nortriptyline or antiepileptic drugs such as gabapentin (Neurontin) and lamotrigine (Lamictal).
- Patients with severe neuropathic pain, unresponsive to these agents, may require narcotic analgesia. The author usually begins with tramadol (Ultram). If and when this becomes ineffective, oxycodone (OxyContin) is used with increasing doses. The author uses fentanyl patches for patients who are allergic to codeine, morphine sulfate (MS Contin) and methadone for patients with severe pain.
- Spinal cord stimulators may be useful for patients with segmental neuropathic pain.
- Patients with weakness and deformity after nerve injury should receive physical and occupational therapy. Function may be improved significantly by the use of the appropriate assistive devices such as cock-up wrist splints (for radial nerve injuries) and AFO splints (for foot drop with peroneal or sciatic nerve injuries).
- Many patients develop neuropathic pain in addition to motor and sensory deficits from nerve injury. The author uses an escalating drug regimen for symptomatic control of neuropathic pain.
Surgical Care
- Indication for surgical exploration and (nerve graft) repair
- Complete nerve lesions caused by lacerations or penetrating injuries should be referred for early surgical exploration and direct end-to-end repair.
- Other significant nerve injuries with no clinical or electrophysiologic evidence of recovery after 3-6 months of clinical observation are also indications for surgical exploration.
- Intraoperative nerve conduction testing and surgical repair
- At the time of surgical exploration, the injured nerve may be obviously severed, in which case the injured segment should be resected and an end-to-end anastomosis (usually with an intervening nerve graft) performed. If the injured nerve segment appears to remain in continuity, intraoperative nerve conduction studies can differentiate axonotmetic from neurotmetic injury.
- Sterile bipolar hook electrodes are used to stimulate and record nerve action potentials (NAPs) from surgically exposed nerve segments. Low stimulus intensities and durations should be used to avoid further iatrogenic nerve injury. Responses are recorded directly from nerves, so the patients can be paralyzed pharmacologically. Lifting the electrodes and nerve out of the operative field during testing is important to avoid current spread through blood and other fluids.
- The presence of an evoked NAP across the injured segment indicates that the lesion is axonotmetic and recovering spontaneously. Surgical intervention should be limited to external neurolysis in these cases; however, note that normal (or "super normal") NAPs can also be recorded from the brachial plexus sensory fibers in cases of root avulsion (see Image 7).
- The absence of a recordable NAP across the injured nerve segment more than 2-3 months after injury suggests that the injury is neurotmetic, necessitating nerve graft repair. In this instance, a normal nerve segment should always be tested as a positive control to confirm the integrity of the stimulating and recording apparatus. Furthermore, if a tourniquet was used during surgery, it should be released for at least 30 minutes prior to testing, as ischemia may attenuate normal NAP responses.
- Intraoperative somatosensory-evoked potential testing and surgical repair
- Brachial plexus injuries may be intraspinal (eg, root avulsions). In these cases, a NAP cannot be conducted across the injured segment to test continuity without performing very extensive surgery (eg, multilevel laminectomies). Intraoperative SEP testing may be very helpful in this regard.
- A handheld bipolar stimulator is used to electrically activate the most proximally exposed region of the plexus with recordings made from surface electrodes placed over the contralateral scalp. The absence of cortical SEP responses suggests more proximal nerve root avulsion. However, cortical SEP responses can also be absent in the presence of high doses of volatile anesthetic agents, so testing a normal plexus element as a positive control is always important (see Case study 4 in Medical/Legal Pitfalls). Nerve root avulsions can only be repaired by neurotization from adjacent nerves, such as the spinal accessory nerve, or by cross-chest nerve root transfer.
- For further information, please see Brachial Plexus Injuries, Traumatic and Facial Nerve Repair.
Consultations
Physicians typically involved in the care of patients with nerve injuries may include the following:
- Peripheral nerve surgeon with experience in nerve exploration and graft repair
- Neurologist with experience in nerve injuries and electrodiagnostic testing
- Pain management physician
- Physical and occupational therapists
Medication
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.
Narcotic analgesics
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.
Adult
25 mcg/h (10 cm2), 50 mcg/h (20 cm2), 75 mcg/h (75 cm2), 100 mcg/h (100 cm2) administered transdermally
Pediatric
Not established
Phenothiazines may antagonize analgesic effects; TCAs may potentiate adverse effects
Documented hypersensitivity; hypotension or potentially compromised airway in which establishing rapid airway control would be difficult
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in hypotension, respiratory depression, constipation, nausea, emesis, and urinary retention; idiosyncratic reaction, known as chest wall rigidity syndrome, may require neuromuscular blockade in order to increase ventilation
Oxycodone (OxyContin)
Relieves moderately severe to severe pain.
Adult
5 mg PO q6h prn pain
Pediatric
6-12 years: 1.25 mg PO q6h prn pain
>12 years: 2.5 mg PO q6h prn pain
Phenothiazines may decrease analgesic effects; CNS depressants or TCAs may increase toxicity
Documented hypersensitivity
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Duration of action may increase in elderly
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.
Adult
15-30 mg PO/IV q8-12h prn pain
Pediatric
0.3-0.6 mg/kg/dose PO/IV q12h prn
Phenothiazines may antagonize analgesic effects; TCAs, MAOIs, and other CNS depressants may potentiate adverse effects
Documented hypersensitivity; hypotension; potentially compromised airway in which establishing rapid airway control would be difficult
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
Methadone (Dolophine)
Used in management of severe pain; inhibits ascending pain pathways, diminishing perception of and response to pain.
Adult
2.5-10 mg PO q3-8h prn pain
Pediatric
0.7 mg/kg/24 h PO divided q4-6h prn pain
Phenytoin, rifampin, and pentazocine may decrease blood levels; phenothiazines, TCAs, MAOIs, and CNS depressants may increase toxicity
Documented hypersensitivity; bronchial asthma; increased intracranial pressure
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in severe liver disease; due to its relatively long half-life, titrate dose slowly
Oral analgesics
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.
Adult
50-100 mg PO q4-6h, not to exceed 400 mg/d
Pediatric
Not established
Decreases carbamazepine effects significantly; cimetidine increases toxicity; antidepressants increase risk of serotonin syndrome
Documented hypersensitivity; opioid-dependence; MAOIs within last 14 days; use of SSRIs, TCAs, opioids; acute alcohol intoxication
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Can cause dizziness, nausea, constipation, sweating, pruritus, and additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in liver disease, myxedema, hypothyroidism, hypoadrenalism, pregnancy, breastfeeding, seizure; development of tolerance or dependency with extended use
Tricyclic antidepressants
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.
Adult
Early in course: 25 mg/d PO hs
After neuropathy develops: 30-100 mg PO hs
Pediatric
Children: 0.1 mg/kg PO hs; increase, as tolerated, over 2-3 wk to 0.5-2 mg/d hs
Adolescents: 25-50 mg/d PO; increase gradually to 100 mg/d in divided doses
Phenobarbital may decrease effects; CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram
Documented hypersensitivity; MAOIs in past 14 d; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention
Pregnancy
D - Unsafe in pregnancy
Precautions
Caution in cardiac conduction disturbances, history of hyperthyroidism, renal or hepatic impairment; avoid using in elderly
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.
Adult
25 mg tid/qid PO; not to exceed 150 mg/d
Pediatric
<25 kg: Not established
25-35 kg: 10-20 mg/d PO
35-54 kg: 25-35 mg/d PO
>54 kg: Administer as in adults
Cimetidine may increase levels; may increase prothrombin time in patients whose coagulation parameters are stabilized with warfarin
Documented hypersensitivity; narrow-angle glaucoma; MAOIs within past 14 d
Pregnancy
D - Unsafe in pregnancy
Precautions
Caution in cardiac conduction disturbances, history of hyperthyroidism, renal or hepatic impairment; due to pronounced effects in cardiovascular system, best to avoid in elderly
Anticonvulsants
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.
Adult
100 mg PO tid and titrate to 900 mg qid if tolerated
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Antacids may reduce bioavailability significantly (administer at least 2 h following antacids); may increase norethindrone levels significantly
Documented hypersensitivity
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in severe renal disease
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.
Adult
Adjunctive therapy with enzyme-inducing anticonvulsant
Weeks 1-2: 50 mg/d PO
Weeks 3-4: 100 mg/d PO in 2 divided doses
Maintenance: 300-500 mg/d PO (in 2 divided doses); may increase by 100 mg/d q1-2wk
Adjunctive therapy with anticonvulsant regimen containing valproate
Weeks 1-2: 25 mg PO qod
Weeks 3-4: 25 mg/d PO
Maintenance: 100-200 mg/d PO qd or divided bid; may increase by 25-50 mg/d q1-2wk
Conversion from single enzyme-inducing anticonvulsant to lamotrigine monotherapy
Weeks 1-2: 50 mg/d PO
Weeks 3-4: 100 mg/d PO in 2 divided doses
Maintenance: 300-500 mg/d (in 2 divided doses) PO; may increase by 100 mg/d q1-2wk; enzyme-inducing anticonvulsant gradually withdrawn over 4-wk interval in 20% decrements/wk
Pediatric
2-12 years
Monotherapy
Weeks 1-2: 0.6 mg/kg/d PO in 2 divided doses, rounded down to nearest 5 mg
Weeks 3-4: 1.2 mg/kg/d PO in 2 divided doses, rounded down to nearest 5 mg
Maintenance: 5-15 mg/kg/d PO; not to exceed 400 mg/d PO divided bid; to achieve maintenance dose, increase doses q1-2wk as follows: Calculate 1.2 mg/kg/d and round down to nearest 5 mg; add this amount to previously administered daily dose
Concomitant therapy with valproic acid
Weeks 1-2: 0.15 mg/kg/d PO qd or divided bid, rounded down to nearest 5 mg; if initial calculated daily dose is 2.5-5 mg, take 5 mg on alternate days for first 2 wk
Weeks 3-4: 0.3 mg/kg/d PO qd or divided bid, rounded down to nearest 5 mg
Maintenance: 1-5 mg/kg/d PO qd or divided bid, not to exceed 200 mg/d; to achieve maintenance dose, increase doses q1-2wk as follows: Calculate 0.3 mg/kg/d, round down to nearest 5 mg, and add amount to previously administered qd dose
>12 years
Monotherapy
Weeks 1-2: 50 mg/d PO
Weeks 3-4: 100 mg/d PO divided bid
Maintenance: 300-500 mg/d PO divided bid; to achieve maintenance, increase doses by 100 mg/d q1-2wk
Concomitant therapy with valproic acid
Weeks 1-2: 25 mg PO qod
Weeks 3-4: 25 mg PO qd
Maintenance: 100-400 mg/d PO qd or divided bid; to achieve maintenance dose, may increase by 25-50 mg/d q1-2wk
Acetaminophen increases renal clearance, decreasing effects; similarly, phenobarbital and phenytoin increase lamotrigine metabolism, causing decrease in levels; valproic acid increases half-life
Documented hypersensitivity
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in impaired renal or hepatic function
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.
Adult
50 mg PO tid initially; if needed, may increase to 100 mg tid within 1 wk
Pediatric
Not established
May cause additive effects on cognitive and gross motor functioning when coadministered with drugs that cause dizziness or somnolence
Documented hypersensitivity
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Discontinue gradually (over a minimum of 1 wk) to minimize increased seizure frequency in patients with seizure disorders; may cause insomnia, nausea, headache, or diarrhea with abrupt withdrawal; common adverse effects include dizziness, somnolence, blurred vision, weight gain, and peripheral edema; may elevate creatinine kinase level, decrease platelet count, and increase PR interval; doses >300 mg/d associated with higher rate of adverse effects and treatment discontinuation; decrease dose with renal impairment (ie, CrCl <60 mL/min)
Anesthetics
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 (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.
Adult
Apply to affected area(s) prn
Pediatric
Administer as in adults
None reported
Documented hypersensitivity; Adams-Stokes syndrome; Wolff-Parkinson-White syndrome
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
For external or mucous membrane use only; do not use in eyes
More on Traumatic Peripheral Nerve Lesions |
| Overview: Traumatic Peripheral Nerve Lesions |
| Differential Diagnoses & Workup: Traumatic Peripheral Nerve Lesions |
 Treatment & Medication: Traumatic Peripheral Nerve Lesions |
| Follow-up: Traumatic Peripheral Nerve Lesions |
| Multimedia: Traumatic Peripheral Nerve Lesions |
| References |
| « Previous Page | Next Page » |
References
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Kline DG, Hudson AR. Nerve Injuries: Operative Results for Major Nerve Injuries. Philadelphia, Pa: WB;1995.
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Landi A, Copeland SA, Parry CB, Jones SJ. The role of somatosensory evoked potentials and nerve conduction studies in the surgical management of brachial plexus injuries. J Bone Joint Surg [Br]. Nov 1980;62-B(4):492-6. [Medline].
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Tiel RL, Happel LT Jr, Kline DG. Nerve action potential recording method and equipment. Neurosurgery. Jul 1996;39(1):103-8; discussion 108-9. [Medline].
Wilbourn AJ. Assessment of the brachial plexus and the phrenic nerve. In: Johnson EW, Pease WS, eds. Practical Electromyography. Baltimore: Williams & Wilkins;1997:273-310.
Further Reading
Keywords
peripheral nerve injuries, complete nerve injury, incomplete nerve injury, segmental demyelination, neurapraxia, axonal injury, wallerian degeneration, axonal regeneration, focal remyelination, myelin sheath, evaluation of peripheral nerve injury, management of peripheral nerve injury, treatment of peripheral nerve injury
