Ischemic Monomelic Neuropathy 

Updated: Jan 17, 2019
Author: Michael T Andary, MD, MS; Chief Editor: Dean H Hommer, MD 

Overview

Practice Essentials

Ischemic monomelic neuropathy (IMN) is an infrequent problem that usually occurs after acute arterial occlusion or low blood flow to an extremity. IMN is primarily a problem of the distal nerves in an extremity; it is best thought of as a term referring to multiple distal focal mononeuropathies involving the sensory and motor branches. (See Etiology.)

The condition usually involves axonal nerve injury and is not a demyelinating process. Reversible motor conduction block in the forearm has been reported early in the course of IMN, but this block does not occur later in the disease. The muscle, skin, bone, and other tissues are spared. There have been reported cases of ischemic changes such as pallor, coolness, and even gangrene. The nerves in the distal limb are most affected. (See Etiology and Presentation.)

IMN can occur after surgical procedures (for example, vascular surgery involving the thoracoabdominal aorta and its caudal arterial channels), as a result of the establishment of arteriovenous fistulas for hemodialysis access, or because of the development of arterial emboli or of thrombi. (See Etiology.)

Workup

The proper diagnosis of IMN as a vascular lesion can avoid incorrect classification of the injury as a plexus or a root lesion from trauma, as well as avoid incorrect positioning during surgery.

Depending on the clinical presentation, vascular studies that detect acute arterial occlusion may be useful, while in confusing clinical situations, imaging studies sometimes are necessary to rule out upper motor neuron problems (eg, stroke, spinal cord injury). Other imaging studies that can be helpful, depending on history, include arteriograms and venous or arterial Doppler studies.

Hours to days after the onset of IMN, an elevated creatine kinase level can be noted from muscle necrosis.

Occasionally, compartment pressure measurements are indicated immediately following ischemia if there is a concomitant compartment syndrome.

Electrodiagnosis establishes the pattern of peripheral nerve injury. If the findings are not consistent with IMN, additional diagnostic studies may be warranted.

Management

Surgery has little to offer in established IMN. In cases of acute thrombosis or compartment syndrome, surgical intervention may be beneficial.[1, 2]

Physical therapy

An aggressive and appropriate range-of-motion (ROM) program can prevent contractures in the involved limb. For gait activities, a double metal upright or solid plastic ankle-foot orthosis (AFO) may be indicated if there is poor control of ankle and foot movement.

Occupational therapy

An aggressive and appropriate ROM program, particularly for the hands, can prevent contractures. Working to improve activities of daily living (ADL) is important, and adaptive equipment may be beneficial in aiding independence.

Patient education

As with all medical conditions, explaining the problems associated with nerve injury can help patients to cope with issues related to the disorder and with rehabilitation. Patients should be instructed to care meticulously for their insensate skin areas in order to prevent skin breakdown. (See Treatment.)

Etiology

Upper extremity

The primary causes for IMN in the arm include any problem that causes a hypercoagulable state, as well as thoracic outlet obstruction (with angiographic confirmation), trauma or laceration of the brachial artery, intra-arterial injection, and cellulitis.[3] A shunt for an arteriovenous fistula also can be a culprit; most cases have been described in patients with diabetes, thus confounding the development of IMN superimposed on diabetic polyneuropathy.

Lower extremity

Risk factors include any problems that interrupt and cause acute arterial occlusion. These factors can include hypercoagulable states, methysergide (a vasoconstrictor used for migraine), cannulization of the femoral artery, aortic occlusion from arteriosclerotic vascular disease, abdominal aortic aneurysms, peripheral vascular disease, low cardiac output, an intra-aortic balloon pump (IABP),[4] or prolonged tourniquet time in surgery. The limb that has been cannulated for the IABP or for cardiopulmonary bypass is particularly susceptible to IMN.

A study by Biancari et al concluded that patients who, at the time of CABG, have diabetes, extracardiac arteriopathy, and a reduced glomerular filtration rate are at risk for developing late lower limb ischemia. The study involved more than 1300 patients who underwent coronary artery bypass grafting (CABG) between 1990 and 2006. The investigators found that during a mean follow-up period of 7.1 years, vascular procedures for lower limb ischemia were performed on 111 patients, with 25 major amputations taking place.[5] The specific incidence of IMN is not noted in this study.

In chronic IMN, the etiology is peripheral vascular disease. Upper and lower extremity IMN can be related to noniatrogenic and iatrogenic causes.

Epidemiology

Occurrence in the United States

The frequency of IMN's occurrence is unclear because IMN has never been studied prospectively, and recognition of the problem varies. Given these limitations, IMN appears to be a rare condition, but it may be underreported. The Mayo Clinic reported only 32 patients with IMN from 1962-1987. Honet and colleagues, in a study reviewing the initial use of the IABP in the early 1970s, reported a surprisingly high incidence of IMN.[6] Out of 39 patients who survived the initial use of the IABP, 6 of them were referred for leg problems that were diagnosed as IMN. Current use of the IABP is unlikely to have an incidence nearly this high.

IMN can also occur after the establishment of arteriovenous fistulas for hemodialysis access, but again, the frequency of such incidences is unclear and unusual.

Sex- and age-related demographics

Male-to-female ratios have not been clearly documented. The risk for arteriosclerosis is slightly higher in males; therefore, the incidence of IMN is slightly greater in males. Because they are at higher risk for arteriosclerosis, elderly individuals have a much higher risk for IMN.

Prognosis

Mortality is not associated with IMN; however, morbidity is significant. Depending on the severity of the injury, patients can be left with neurologic deficits that interfere with function and cause significant pain.

The prognosis depends on the amount of initial nerve damage. Functional improvement in the leg is expected because the nerve regenerates at 1 in/month (2.5 cm/mo). Weakness of the intrinsics is common in the leg, and weakness of ankle dorsiflexors and plantar flexors also is relatively common. Sensory loss in the foot and in the leg up to the midcalf is frequent as well. Pain in the areas of neurologic deficit is reported almost universally. This pain can be persistent or reversible, depending on the severity of the injury. Occasionally, there is weakness of knee extensors and flexors. Sensation in the foot and distal leg can remain permanently impaired. Contractures of the paralyzed or weakened joints are frequent. Residual pain may be the most troubling problem following nerve regeneration and rehabilitation.

The prognosis for the arm is similar to that for the leg. The nerve regenerates at 1 in/month (2.5 cm/mo). In the hand, weakness of the thenar and intrinsic muscles has been reported. This weakness coexists with sensory loss, which exists in all fingers and can extend proximally into the palm and hand. Contractures of weakened joints, especially those of the fingers, are possible.

The extent of disability from the above neurologic dysfunctions depends on the amount of nerve injury and may alter hand function or the ability to walk. For some patients, the pain associated with IMN is the most disabling aspect of the disease.

 

Presentation

History

The hospital is the most common place for presentation of ischemic monomelic neuropathy (IMN); this presentation can vary depending on the location of the IMN. Patients with upper extremity IMN usually complain of pain in the hand and arm, with weakness in the hand. This pain generally occurs after hours of arterial occlusion of the brachial or subclavian arteries or following surgery to establish an arteriovenous fistula for dialysis graft access.

IMN in the leg usually presents after hours of arterial occlusion, frequently following vascular surgery involving aortic occlusion (eg, abdominal aortic aneurysm repair, use of the IABP, revascularization surgery in the leg). Lower extremity IMN can also occur after prolonged tourniquet time in surgery or as a complication following arterial occlusion. If the patient is alert and not confused, he or she usually complains of pain in the foot and distal leg; the individual may also complain of weakness of toe movement and ankle dorsiflexion.

Immediately after major surgery, it is common for patients to be confused, medicated, and/or not fully cognizant of problems in their legs that occurred during the surgery or as a result of cardiac events. Since the patient is confused, he or she does not complain of symptoms. In the meantime, the treatment team focuses on other pressing medical issues and does not notice the IMN. This results in a delay in diagnosis that frequently lasts days or even weeks after the arterial occlusion has occurred.

Chronic IMN has been reported in patients with chronic critical leg ischemia. The patients studied had angiographic documentation of severe large vessel stenosis or occlusion. They also suffered from limb pain while at rest or had nonhealing foot ulcers for more than 4 weeks. Distal foot and leg symptoms were present, along with some toe weakness.[7, 8]

Physical Examination

Patients who have IMN in the arm usually have decreased sensation in all the fingers of the hand. Occasionally, the median or ulnar nerve territory is primarily affected. Allodynia or hyperesthesia in the distal radial, median, and ulnar nerve distribution is common. Frequently, weakness of the abductor pollicis brevis and the intrinsic muscles of the hand is exhibited. Occasionally, more proximal musculature can be affected (wrist flexors or wrist extensors), but this pattern is exceedingly rare.

Physical examination of the leg frequently shows decreased sensation in the foot and distal calf. Allodynia and hyperesthesia also may be present. Intrinsic wasting in the feet is usually present. Distal leg muscles also can be weak, including the extensor hallucis longus, anterior tibialis, peroneus longus, and gastrocnemius/soleus. In rare cases, the hamstrings, quadriceps, and hip abductors are affected. Gait may be abnormal in that the patient may have steppage gait associated with ankle dorsiflexion weakness (foot drop). Reflexes may be asymmetrical, especially at the ankle, with an absent Achilles reflex in the affected leg.

In cases of chronic disuse, contractures of the distal joints (fingers, toes, wrists, or ankles), with swelling, skin atrophy, and vasomotor changes, can be present. These conditions can coexist with complex regional pain syndrome (CRPS) type 2 (also known as reflex sympathetic dystrophy [RSD]).

Patients with chronic IMN most commonly have hypalgesia in their distal foot and toes and/or nonhealing skin ulcers.

 

DDx

 

Workup

Approach Considerations

The proper diagnosis of ischemic monomelic neuropathy (IMN) as a vascular lesion can avoid incorrect classification of the injury as a plexus or a root lesion from trauma, as well as avoid incorrect positioning during surgery.

Depending on the clinical presentation, vascular studies that detect acute arterial occlusion may be useful. Because IMN usually is not the presenting problem but is instead a complication that occurs after previous arterial occlusion, work up and/or treatments (eg, arteriogram, surgeries) already have been completed. In chronic IMN, results from vascular studies are abnormal and show arterial occlusion in 1 leg.

In confusing clinical situations, imaging studies sometimes are necessary to rule out upper motor neuron problems (eg, stroke, spinal cord injury). Other imaging studies that can be helpful, depending on history, include arteriograms and venous or arterial Doppler studies. These tests can help to include vascular occlusion in or to exclude it from the diagnosis. With an arteriovenous fistula in the upper extremity, a Doppler study to assess for vascular patency can be helpful.

Hours to days after the onset of IMN, an elevated creatine kinase level can be noted from muscle necrosis.

Occasionally, compartment pressure measurements are indicated immediately following the ischemia if there is a concomitant compartment syndrome.

A study by Shin and Park indicated that because IMN is a potential complication of arterial occlusion, neurologic and electrophysiologic assessment can be used to evaluate peripheral arterial occlusive disease (PAOD). In the study, which involved 38 patients with PAOD, primary outcomes took the form of neurologic symptom and impairment scores for the lower extremities, and secondary outcomes were represented by nerve conduction study results. Among the findings, the investigators determined that neurologic symptom and impairment scores tended to be worse in female patients with old age, hypertension, a low body weight, a low body mass index, a reduced ankle-brachial index, and a poorer Fontaine classification (for peripheral arterial disease).[9]

IMN does not require any direct procedures, although various procedures may be needed to treat associated conditions. Tissue biopsies rarely are taken after IMN and are not reported to be helpful in its diagnosis.

Electrodiagnosis

Electrodiagnosis establishes the pattern of peripheral nerve injury. If the findings are not consistent with IMN, additional diagnostic studies may be warranted.

Upper extremity evaluation

Abnormalities are seen in a distal-to-proximal pattern, and the distal nerve supply is affected much more than any other. Radial, median, and ulnar sensory nerve action potentials (SNAPs) usually are absent from the respective digits. More proximal SNAPs (medial antebrachial cutaneous, lateral antebrachial cutaneous) are likely to be present.

Motor nerve conduction from the median and ulnar nerves to the hand muscles is absent or has a low amplitude. Nerve conduction velocities, when present, are spared to a relative extent.

Needle electromyography shows evidence for axonal loss with positive sharp waves and fibrillation potentials in the hand muscles (median and ulnar innervation). If the lesion is severe, there may be no recruitment or evidence of decreased (neuropathic) recruitment. Evidence for reinnervation can be seen months to years after the nerve injury, including large motor unit action potentials (MUAPs) and/or polyphasic motor units. In complete injuries, there is scarring in the muscle, with decreased insertional activity. Needle electromyography is typically normal or less severe in proximal muscles (forearm and upper arm). This clear distal-to-proximal gradient is in contrast to a brachial plexopathy.

For the diagnosis of IMN to be clear, one arm needs to demonstrate significantly more injury than the other arm. In cases of severe diabetic neuropathy, in which both arms are affected equally, it is essentially impossible to make the diagnosis of an IMN that is superimposed on a severe polyneuropathy. For example, it can be difficult to differentiate a lower trunk plexopathy from an IMN in the hand. A lower trunk plexopathy generally shows severe abnormalities in the intrinsic muscles of the hand on electromyography, low compound motor action potentials (CMAPs) from the median and ulnar nerves, and an absent SNAP.

The major differentiation in the hand is that, in a lower trunk plexopathy, the radial SNAP and median SNAPs to the fingers probably are spared, while the medial antebrachial cutaneous SNAP is absent. In IMN, the median and radial SNAPs are absent, and the medial antebrachial cutaneous SNAP is spared. With a lower trunk plexopathy, needle electromyography abnormalities in the flexor carpi ulnaris, triceps, and extensor indices are expected; in IMN, the abnormalities of these proximal muscles are absent or minimal.

Lower extremity evaluation

SNAPs to the sural and superficial peroneal commonly are absent. CMAPs to the abductor hallucis and peroneal nerve to the extensor digitorum brevis are either absent or low in amplitude. Nerve conduction velocities are relatively spared, if they can be measured. In IMN, H-reflexes and CMAPs elicited from the tibial nerve at the gastrocnemius and from the peroneal nerve at the anterior tibialis are frequently normal or near normal.

Needle electromyography frequently shows marked abnormalities consistent with axon loss in foot intrinsic musculature and lesser findings in the anterior tibialis, gastrocnemius, and soleus. Abnormalities in the quadriceps, hamstrings, or gluteal muscles generally are not observed, although they have been reported.

As in the upper extremity, differentiation of the normal limb from the abnormal limb is helpful in diagnosing IMN. In severe peripheral polyneuropathies, primarily distal ones, findings can be very similar or identical to those of IMN. The diagnosis of IMN is contingent on a normal or near-normal contralateral limb. Occasionally, distal aortic occlusion with saddle emboli can cause bilateral IMN, or use of the IABP pump in both legs can contribute. In mild cases of IMN, electromyographic abnormalities (positive sharp waves and fibrillation potentials) have been seen only in the foot intrinsic muscles.

Differentiation of IMN from an L5-S1 or S2 radiculopathy or sciatic nerve neuropathy can be difficult. In IMN, the distal L5-S2 muscles have severe abnormalities, while the more proximal L5-S1 (gluteus medius, tensor fasciae lata) are likely to be normal or have minimal abnormalities. The tensor fasciae lata or gluteal muscles rarely are involved in IMN; in an L5-S2 radiculopathy, the tensor fasciae lata and/or gluteus medius should show similar abnormalities to the more distal L5-S2 muscles. This finding differentiates IMN from a plexopathy or radiculopathy.

In chronic IMN, the most common electrodiagnostic abnormality is a decreased CMAP in the tibial nerve to the abductor hallucis. Because the disease is chronic, both of a patient's legs can be affected, and the sural responses may be abnormal unilaterally or bilaterally. Quantitative sensory testing results have been reported to be abnormal in the distal foot.

Absent responses are a poor prognosis.

 

Treatment

Approach Considerations

Few predictable medical problems are associated with ischemic monomelic neuropathy (IMN). Evaluation by a physiatrist can help in the diagnosis, treatment, and rehabilitation of the condition.

Surgery has little to offer in established IMN. In cases of acute thrombosis or compartment syndrome, surgical intervention may be beneficial.[1, 2] There is at least one case of IMN caused by an arteriovenous fistula for dialysis that improved with surgery. The fistula was banded and neurologic function returned; the graft was saved for future use in dialysis.[10]

A case study by Coscione et al indicates that in patients with suspected IMN, good treatment results may be obtained through urgent management. In the case report, a male aged 75 years received a left prosthetic brachial-axillary access and 11 weeks later was found to have gross swelling and function loss in the left arm. The patient suffered from central venous stenosis, with swelling secondary to recurrent central venous occlusion. The authors suggested that this affected arterial flow through the graft and thus nerve perfusion, resulting in IMN. Following urgent ligation of the brachial-axillary access, however, the arm regained function. This suggests that early surgical intervention may in some cases improve outcome.[11]

Inpatient and outpatient care

Inpatient care for patients with IMN is 2-fold. Patients with IMN may have numerous comorbid medical and surgical problems that require monitoring and interventions. If the IMN significantly interferes with wrist/hand or ankle/foot function, physical and occupational therapy services are warranted under the direction of physiatry specialists.

Outpatient care is a continuation of rehabilitation goals and may include functional mobility training, preservation of range of motion (ROM), education with regard to limb care, and pain management. Psychological counseling to assist with adjustment to disability also may be warranted.

Physical and Occupational Therapy

Physical therapy

Rehabilitation measures to assist with recovery after IMN depend on the degree of nerve injury. An aggressive and appropriate ROM program can prevent contractures in the involved limb. Thermal agents should be used with caution, given concomitant sensory impairments. For gait activities, a double metal upright or solid plastic ankle-foot orthosis (AFO) may be indicated if there is poor control of ankle and foot movement.

In a study of two patients with IMN, Singh et al found that strength improved with rehabilitation therapy and that paresthesia vanished over time. IMN developed in the patients, both of whom had diabetes, after a left upper extremity brachiocephalic fistula was created, with the patients declining treatment with surgical litigation. Weakness was significantly reduced with rehabilitation therapy, while at 11-month follow-up, paresthesia was absent. The investigators suggested that the outcome of this study challenges the use of fistula ligation in such cases.[12]

Occupational therapy

An aggressive and appropriate ROM program, particularly for the hands, can prevent contractures. Working to improve activities of daily living (ADL) is important, and adaptive equipment may be beneficial in aiding independence.

 

Medication

Medication Summary

No medications are specific for ischemic monomelic neuropathy (IMN). Medications used to treat neuropathic pain may be helpful. Such pain may, in fact, be quite debilitating in IMN, although it is uncertain how frequently it presents. Medications for neuropathic pain include anticonvulsants (gabapentin, pregabalin), antidepressants (duloxetine, amitriptyline, paroxetine, sertraline, venlafaxine), and local anesthetics. Opioids (propoxyphene, methadone) may be helpful in the acute situation but probably do not benefit the chronic patient.

Anticonvulsants, Other

Class Summary

Use of certain antiepileptic drugs, such as the gamma-aminobutyric acid (GABA) analogue gabapentin (Neurontin), has proven helpful in some cases of neuropathic pain. These drugs have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The multifactorial mechanisms of analgesia could include improved sleep, altered perception of pain, and increase in the pain threshold.

Gabapentin (Neurontin)

Gabapentin has anticonvulsant properties and antineuralgic effects; however, its exact mechanism of action is unknown. This drug is structurally related to GABA but does not interact with GABA receptors. Titration to effect can take place over several days (300mg on day 1, 300mg twice on day 2, and 300mg 3 times on day 3).

Pregabalin (Lyrica)

Pregabalin is a structural derivative of GABA. Its mechanism of action is unknown. Pregabalin binds with high affinity to the alpha2-delta site (a calcium channel subunit). In vitro, it reduces the calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. Pregabalin has been approved by the US Food and Drug Administration (FDA) for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as an adjunctive therapy in partial-onset seizures.

Antidepressants, Other

Class Summary

These make up 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 they block the active reuptake of norepinephrine and serotonin.

Duloxetine (Cymbalta)

Duloxetine is indicated for diabetic peripheral neuropathic pain. It is a potent inhibitor of neuronal serotonin and norepinephrine reuptake.

Amitriptyline

Amitriptyline is an analgesic for certain chronic and neuropathic pain.

Paroxetine (Paxil, Pexeva)

Paroxetine is a potent selective inhibitor of neuronal serotonin reuptake. It also has a weak effect on norepinephrine and dopamine neuronal reuptake. Paroxetine may decrease neuropathic pain and help with sleep and mood disorders (depression or depressive symptoms).

Sertraline (Zoloft)

Sertraline selectively inhibits presynaptic serotonin reuptake. It may decrease neuropathic pain and help with sleep and other mood disorders (depression or depressive symptoms).

Venlafaxine (Effexor, Effexor XR)

Venlafaxine inhibits neuronal serotonin and norepinephrine reuptake. In addition, it causes beta-receptor down-regulation. The drug may decrease neuropathic pain and help with sleep and mood disorders (depression or depressive symptoms).

Opiate Analgesics

Class Summary

These agents may decrease neuropathic pain; they should be used to decrease pain, increase function, and improve quality of life. The adverse effects, which include, but are not limited to, cognitive difficulties, tolerance, addiction, and nausea, need to be taken very seriously. The use of contracts to assure the appropriate use of opiates and that link the use of opiate medication to good behavior are helpful.

If a patient's behavior deteriorates, consider decreasing or discontinuing the opiate medication, because it may be contributing to the problem. The use of opiates only at night to improve sleep may be the most effective use of these medications for the long-term treatment of neuropathic pain.

Methadone (Dolophine, Methadose)

Methadone is a long-acting opioid used in the management of severe pain. It inhibits ascending pain pathways, diminishing the perception of and response to pain.

 

Questions & Answers

Overview

What is ischemic monomelic neuropathy (INM)?

How is ischemic monomelic neuropathy (INM) diagnosed?

What is the role of surgery in the treatment of ischemic monomelic neuropathy (INM)?

What is the role of rehabilitation therapies in the treatment of ischemic monomelic neuropathy (INM)?

What is included in patient education about ischemic monomelic neuropathy (INM)?

What causes ischemic monomelic neuropathy (INM) in the upper extremities?

What causes ischemic monomelic neuropathy (INM) in the lower extremities?

What is the prevalence of ischemic monomelic neuropathy (INM)?

Which patient groups have the highest prevalence of ischemic monomelic neuropathy (INM)?

What is the prognosis of ischemic monomelic neuropathy (IMN)?

Presentation

Which clinical history findings are characteristic of ischemic monomelic neuropathy (INM) in the upper extremities?

Which clinical history findings are characteristic of ischemic monomelic neuropathy (INM) in the lower extremities?

Which clinical history findings are characteristic of chronic ischemic monomelic neuropathy (INM) in the lower extremities?

Which physical findings are characteristic of ischemic monomelic neuropathy (INM) in the upper extremities?

Which physical findings are characteristic of ischemic monomelic neuropathy (INM) in the lower extremities?

Which physical findings are characteristic of chronic ischemic monomelic neuropathy (INM)?

DDX

What are the differential diagnoses for Ischemic Monomelic Neuropathy?

Workup

What is the role of vascular studies in the workup of ischemic monomelic neuropathy (INM)?

What is the role of imaging studies in the workup of ischemic monomelic neuropathy (INM)?

Which findings on creatine kinase testing are characteristic of ischemic monomelic neuropathy (INM)?

What is the role of compartment pressure measurement in the workup of ischemic monomelic neuropathy (INM)?

How is peripheral arterial occlusive disease (PAOD) assessed in the workup of ischemic monomelic neuropathy (INM)?

What is the role of tissue biopsy in the workup of ischemic monomelic neuropathy (INM)?

What is the role of electrodiagnostic testing in the workup of ischemic monomelic neuropathy (INM)?

What is included in the electrodiagnostic evaluation of ischemic monomelic neuropathy (INM) in the upper extremities?

What is included in the electrodiagnostic evaluation of ischemic monomelic neuropathy (INM) in the lower extremities?

Treatment

How is ischemic monomelic neuropathy (INM) treated?

What is the role of inpatient care in the treatment of ischemic monomelic neuropathy (INM)?

What is included in the long-term monitoring of ischemic monomelic neuropathy (INM)?

What is the role of physical therapy (PT) in the treatment of ischemic monomelic neuropathy (INM)?

What is the role of occupational therapy (OT) in the treatment of ischemic monomelic neuropathy (INM)?

Medications

What is the role of medications in the treatment of ischemic monomelic neuropathy (INM)?

Which medications in the drug class Opiate Analgesics are used in the treatment of Ischemic Monomelic Neuropathy?

Which medications in the drug class Antidepressants, Other are used in the treatment of Ischemic Monomelic Neuropathy?

Which medications in the drug class Anticonvulsants, Other are used in the treatment of Ischemic Monomelic Neuropathy?