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Peripheral Neuropathy guidelines

most of neuropathy is really CIDP.

Article URL: http://merck.micromedex.com/index.asp?page=bpm_brief&article_id=BPM01NE12

Peripheral Neuropathy

by Frisso A Potts, MD, Best Practice of Medicine. April 2001.

Last modified November 14, 2001.

History

a complete current medical history, past medical history, occupational history, family history, and review of systems.

Try to determine whether presenting symptoms are motor, sensory, or both
Inquire about autonomic symptoms: e.g., fainting spells, orthostatic hypotension (lightheadedness when upright), abnormal sweating, gastrointestinal symptoms (early satiation, bloating, nausea), urinary symptoms (frequency, incontinence), and erectile dysfunction.
Ask the patient about the order in which the body parts became affected.
Inquire about the temporal course of signs and symptoms: i.e., are they acute, subacute, chronic, progressive, relapsing, or remitting?
Ask about a family history of nervous system or muscular diseases, or bone deformities, especially if an acquired generalized neuropathy is suspected.
Try to determine whether PN symptoms are related to an underlying infection or systemic illness.
Ask about potential occupational exposures to toxins [Table 6], and try to determine whether symptoms are related to occupational exposure(s).
Inquire about the use of any medications, both nonprescription and prescription.
Ask about dietary habits, vitamin intake, and use of alcohol.

Physical Examination

Perform a complete physical and neurological examination.
Assess the presence and distribution of weakness [Table 7] [Table 8] [Table 9].
Examine muscles for (bilateral) symmetry, bulk, tone, and fasciculations.
Determine the response, reproducibility, and symmetry of deep tendon reflexes.
Test pain, light touch, vibratory, and proprioceptive senses.
Palpate pertinent peripheral-nerve trunks to detect sites of compression or entrapment.

Testing > Office and Laboratory

Consider a basic battery of laboratory tests to rule out an underlying systemic disease, especially in the patient who presents with distal symmetrical sensorimotor neuropathy of uncertain cause [Table 10].
If after the initial clinical and laboratory evaluation the diagnosis is still unclear, request electrodiagnostic studies to confirm the presence of a neuropathy, to differentiate axonal from demyelinating conditions, and to differentiate myogenic from neurogenic causes of weakness [Table 11] [Table 12] [Table 13] [Table 14].

Testing > Radiologic

Consider MRI studies if nerve compression is suspected.
Order chest radiographs in an older patient with unexplained sensory PN and a long history of cigarette smoking.

Differential Diagnosis

Determine if the symptoms and signs are consistent with peripheral [Table 5] or central nervous-system disorders.
Determine the pattern of weakness and/or sensory loss.
Differentiate lower-motor-neuron (peripheral-nerve) disorders from neuromuscular junction or muscle disorders [Table 15].
If a single nerve is involved (mononeuropathy), suspected a peripheral-nerve entrapment syndrome.
Rule out systemic disease, toxic-metabolic processes, and psychiatric syndromes as the cause of weakness.

Diagnostic Criteria

First, determine whether the patient actually has peripheral neuropathy.
Second, determine the pattern of peripheral-nerve involvement [Table 7].
Third, determine the underlying cause. See the related Best Practice of Medicine articles on mononeuropathies and generalized neuropathies for further details.

Treatment

Acute Care/Hospitalization

Hospitalize patients presenting with symptoms indicative of Guillain-Barr� syndrome (GBS).
Hospitalize patients if there is clinical suspicion of tetrodon (puffer fish) poisoning, black widow spider bites, or rat poisoning.
Hospitalize patients with suspected chronic exposure to a toxin to avoid further exposure until the agent is identified.

Lifestyle Measures

Recommend a basically healthy lifestyle.

Medical Therapy

If identified and relevant, first treat the underlying disorder.
Direct symptomatic therapy toward pain control [Table 16]. See the related Best Practice of Medicine articles on mononeuropathies and generalized neuropathies for further details concerning treatment of specific disorders.

Invasive Procedures

Consider surgical treatment of entrapment mononeuropathies.

Complications

Neuropathic complications are specific to a particular condition. See the related Best Practice of Medicine articles on mononeuropathies and generalized neuropathies.

When to Consult or Refer

If the diagnosis is uncertain, refer the patient to a neurologist.
Refer patients with foot-related symptomatology to a podiatrist.

Prognosis

The prognosis depends on the diagnosis. See the neurology contents page for details on specific neuropathies.

Patient Education

General Information

Use appropriate measures to make movement easier and compensate for any type of sensory loss. See the related Best Practice of Medicine articles on mononeuropathies and generalized neuropathies for details.

Self-care Instructions

See General Advice.

Follow-up

Dependent on the specific condition. See the related Best Practice of Medicine articles on mononeuropathies and generalized neuropathies for details.

Prevention and Screening

Consider screening for PN in patients who are at increased risk.

Management Highlights

�	Determine patterns based on whether symptoms are acute or chronic, mononeuropathic or polyneuropathic, and motor or sensory. Use the time course to narrow the differential diagnosis, e.g., rapid onset suggests Guillain-Barr� syndrome, porphyric neuropathy, and some acute toxic neuropathies (e.g., insecticides or acrylamide). A stepwise or relapsing course can be found with inflammatory, hereditary, and vasculitic neuropathies, and with repeated exposure to toxins. A slow, progressive course is more typical of diabetic and alcoholic neuropathies, and of neuropathies due to chronic exposure to toxic substances (e.g., lead and some industrial solvents).
�	Recall that mononeuropathies are disorders of a single nerve that cause focal motor, sensory, or reflex changes and usually result from trauma or entrapment. Mononeuropathy multiplex is a focal involvement of two or more nerves that usually results from a generalized disorder such as diabetes or vasculitis. Generalized neuropathies involve multiple nerves and typically interrupt neural function predominantly in the distal extremities, and can be caused by diabetes, hereditary diseases, inflammatory/autoimmune disorders, toxic/metabolic/infectious etiologies (e.g., HIV, Lyme disease, alcoholism, or uremia) or be cancer related [Table 7]. Most peripheral neuropathies will have some sensory component; pure motor deficiencies suggest myopathy, motor-neuron disease, or a neuromuscular junction disease.
�	Look for autonomic dysfunction (e.g., erectile dysfunction or urinary, gastrointestinal, and orthostatic symptoms) as a clue to specific neuropathies such as diabetes, Guillain-Barr� syndrome, porphyria, HIV-related autonomic neuropathy, and some toxic neuropathies.
�	Base laboratory testing on history and exam findings [Table 10 ]. Consider testing for common causes with complete blood count, erythrocyte sedimentation rate, urinalysis, glycohemoglobin, glucose, BUN, creatinine, serum vitamin B12 level, serum protein electrophoresis, and TSH.
�	Order an MRI if nerve compression is suspected, particularly if a single nerve or root is involved or the pattern of weakness or sensory loss suggests a single location in the central nervous system.
�	Consider nerve conduction and electromyography studies to confirm the presence of neuropathy and differentiate among myogenic, axonal, and demyelinating conditions. Refer to a neurologist if the diagnosis remains uncertain.
�	In general, avoid potent narcotics in treating chronic neuropathic pain. Start with simple, non-narcotic analgesics such as nonsteroidal anti-inflammatory agents or tramadol hydrochloride up to 50 mg PO t.i.d. in treating mild neuropathic pain [Table 16].

Background

Overview

Primary care physician frequently managed the most common underlying diseases (i.e., diabetes mellitus, alcoholism). The term peripheral neuropathy refers to a variety of syndromes that result from lesions of the peripheral nerves [1]. The peripheral nervous system is comprised of the cranial nerves (except I and II) and the spinal nerves (sensory, motor, autonomic, and mixed). Fortunately, patterns of signs and symptoms facilitate diagnosis, as they generally reflect anatomical localization of the peripheral lesions. Mononeuropathies are disorders of a single nerve that usually result from trauma or entrapment. Any focal, motor, sensory, or reflex changes are restricted to the regions innervated by the specific nerve [1]. Mononeuropathy multiplex is a focal involvement of two or more nerves that usually results from a generalized disorder such as diabetes or vasculitis [1]. Generalized neuropathies involve multiple nerves and typically interrupt neural function predominantly in the distal extremities [Table 1].

Table 1. Mono- and Generalized Neuropathies Commonly Encountered in Clinical Practice

Mononeuropathies

Generalized neuropathies

Cranial neuropathies:

Trigeminal neuralgia
Bells palsy
Diabetic cranial neuropathies

Carpal tunnel syndrome (median nerve)
Cubital tunnel syndrome (ulnar nerve) Sciatic nerve damage following hip replacement
Diabetic mononeuropathy/mononeuropathy multiplex
Amyloidosis

Diabetic neuropathies:

Generalized sensorimotor polyneuropathy
Autonomic neuropathy
Polyradiculopathy

Hereditary neuropathies:

Charcot-Marie-Tooth disease
Amyloid polyneuropathy
Dejerine-Sottas disease
Refsums disease

Inflammatory/autoimmune neuropathies:

Guillain-Barr� syndrome (GBS)
Chronic inflammatory demyelinating polyneuropathy (CIDP)

Toxic/metabolic/infectious diseases:

Various toxin-induced neuropathies
Alcoholic neuropathy
HIV neuropathy
Lyme neuropathy
Uremia
Porphyria

Systemic/malignancy-related neuropathies:

Paraneoplastic
Dysproteinemia

Etiology/Pathophysiology

Normal nerve integrity and function rely on the proper functioning of four components of peripheral nerves: (1) the cell body, where protein manufacturing and the majority of metabolic processes occur; (2) the axon, whose plasma membrane conducts the nerve action potential, and in which axoplasmic transport carries structural and metabolic substances from the cell body to where they are needed, and toxins and metabolic by-products to the cell body for processing; (3) the myelin sheath, which facilitates the conduction of nerve impulses; and (4) connective tissue, which provides mechanical protection and blood supply. Interruption or impairment of any of these structures can lead to transient or permanent nerve injury. Various insults to peripheral nerves can lead to (1) neuronopathy, (2) axonal degeneration (

dying-back

neuropathy), (3) segmental demyelination, and/or (4) Wallerian degeneration

Figure 1. Main pathologic events of a distal axonal degeneration or axonopathy

The jagged lines indicate that either a toxin or a metabolic insult is acting at multiple sites along motor and sensory axons in the peripheral nervous system (PNS) and central nervous system (CNS). Axonal degeneration begins at the most distal part of the nerve fiber and progresses proximally by the late stage. Recovery occurs by axonal regeneration but is impeded by astroglial proliferation in the CNS.

From Schaumburg [4]

Figure 2. Main pathologic events of a sensory neuronopathy

A toxin, identified by the jagged lines, produces destruction of dorsal root ganglion neurons, which is accompanied by degeneration of their peripheral-central axonal processes. Recovery is poor, as no axonal regeneration can take place.

From Schaumburg [4]

Figure 3. Main pathologic events of primary segmental demyelination in immune-mediated inflammatory polyneuropathies

The attack by inflammatory cells causes multifocal demyelination along the entire length of nerve fibers but spares their axons. Recovery occurs by remyelination. The demyelinated segments become invested by several Schwann cells, resulting in a decrease in the internodal length of those areas.

From Schaumburg [4]

Table 2. Pathologic Events Affecting the Peripheral Nerves

Event

Description

Classification and Examples

Prognosis

Axonal degeneration^a

Distal breakdown of the myelin sheath and axon that progresses toward the nerve body^b

Axonal polyneuropathies

Most toxic/metabolic neuropathies

Recovery is delayed and often incomplete

Wallerian degeneration

Degeneration of axons and their myelin sheaths distal to the point of trauma

Any mechanical injury: e.g., focal nerve trauma

Ischemic nerve injury

Recovery depends on the extent of the Schwann cell-basal lamina tube/nerve sheath destruction, distance to injury site, patient age

Neuronopathy

Primary loss/destruction of nerve cell bodies accompanied by degeneration of their peripheral and central axons

Inherited disorders: e.g., spinal muscular atrophies, amyloidosis

Toxic: cadmium poisoning

Degenerative disorder of neuron cell body with no possibility of recovery

Segmental demyelination

Breakdown (acquired) or improper manufacture (congenital) of myelin sheaths with relative sparing of axons

Immune-mediated acquired demyelinating neuropathies: e.g.,
Guillain-Barr� syndrome

Hereditary disorders of Schwann cell-myelin metabolism: e.g., metachromatic leukodystrophy, Dejerine-Sottas disease

Compression or entrapment mononeuropathies

Recovery does not occur in congenital disorders

In acquired disorders, recovery is dependent on remyelination of demyelinated segments, which can take from days to several months

^a Most common pathologic peripheral-nerve reaction; often coexists with segmental demyelination.
^b Hence the term ?dying-back? neuropathy.
^c Clinically, may be difficult to distinguish from axonopathy.

Based on Bosch [2], Raynor [3].

Demographics/Epidemiology

The numbers of people affected by PN vary by specific type of neuropathy. However, age appears to have a significant influence on the distribution of neuropathies in the general population [Table 3]. This may relate to specific clinical, histologic, and physiologic age-related changes in the peripheral nervous system [Table 4].

Table 3. Distribution of Neuropathies by Age and in General Population
Subcategory^a	Age <49	Age >50	Overall population
Mononeuropathy
	35%	50%	30%
Generalized neuropathies
Toxic/metabolic	60%	55%	69%^a
Hereditary	5%	<1%	30%^a
Malignancy	2%	10%	5%
Idiopathic	8%	5%	5%
^a Categories coexist in up to one-third of cases.

Table 4. Age-Related Changes in the Peripheral Nervous System

Type

Changes

Clinical

Decreased vibratory sense
Decreased threshold response to tactile stimuli, but normal threshold response to pain
No change in position sense
Decreased muscle bulk and strength

Histologic

Reduction in number of nerve fibers
Preferential loss of large-diameter fibers
Reduction in muscle-fiber size
Decline in number of motor units (distal muscles)
Evidence of denervation and reinnervation with advancing age

Physiologic

Decline in motor- and sensory-nerve conduction velocity (MCV)
Decreased amplitude in sensory-nerve action potential (SNAP)
Increased amplitude and duration of voluntary motor units suggesting denervation and reinnervation

Diagnosis

History

Obtain a complete current medical history, past medical history, occupational history, family history, and review of systems.
Because peripheral neuropathy can be caused by a plethora of injuries, toxins, drugs, and diseases, determining the etiology of a PN can be difficult [5]. Nevertheless, a systematic review of onset, duration, and evolution of symptoms, as well as of associated disease, family history, and occupational factors, often yields important clues to the specific cause of the presenting complaints. Because the role of the history in identifying the underlying cause of PN (e.g., trauma, metabolic, infectious, inflammatory, ischemic, and paraneoplastic disorders) is well known to primary care physicians, the following information focuses on aspects on the history that are particularly pertinent to diagnosing PN per se.

Try to determine whether presenting symptoms are motor, sensory, or both [Table 5].
The nature of a patient's symptoms usually reveals the type of fiber (i.e., motor, sensory, autonomic) affected. Fiber dysfunction creates certain signs and symptoms that can be delineated by a lack of function (i.e.,

negative

) or by extra or abnormal function (i.e.,

positive

). Notably, sensory involvement is an important diagnostic key. Most peripheral neuropathies cause some degree of sensory pathology, even if it is only detected upon careful neurologic examination. Generalized neuropathies (e.g., Guillain-Barr� syndrome, chronic inflammatory demyelinating polyneuropathy, lead intoxication, and diabetic and alcoholic neuropathy) commonly present with sensory symptoms. Weakness without a sensory component suggests myopathy, motor-neuron disease, or a neuromuscular junction disease [6] [Table 5]. An important exception is multifocal motor neuropathy, which presents with weakness and a normal sensory examination [7].

Inquire about autonomic symptoms: e.g., fainting spells, orthostatic hypotension (lightheadedness when upright), abnormal sweating, gastrointestinal symptoms (early satiation, bloating, nausea), urinary symptoms (frequency, incontinence), and erectile dysfunction.
Autonomic symptoms can be important diagnostic clues, because certain causes of PN typically present with significant concurrent autonomic nervous system dysfunction [6]. Examples include diabetes mellitus, familial amyloidosis, Guillain-Barr� syndrome, porphyria, HIV-related autonomic neuropathy, some toxic neuropathies, and idiopathic pandysautonomia [6].

Ask specific questions about the nature/character of the sensory and/or motor involvement.
The nature or character of symptoms can reveal important information about which fibers (i.e., motor, sensory, autonomic) are involved [Table 5]. Inquire about the types of activities or movements the patient finds difficult. Interestingly, involvement of a particular muscle group (e.g., proximal upper extremity or distal lower extremity) tends to elicit similar reports of symptoms from most patients. For example, difficulties with combing hair or shaving are indicative of proximal upper-extremity muscle weakness, while difficulty in getting out of a chair or the bath are indicative of proximal lower-extremity muscle weakness.

Ask the patient about the order in which the body parts became affected.
The answers can help differentiate symmetric vs. asymmetric evolution [5]. Sensory disturbances, which originate in the feet and then ascend to the knees, or originate in the fingertips and then ascend to the forearms, demonstrate the so-called

dying-back

pattern, and are characteristic of acquired neuropathies [5]. If the history indicates an asymmetric evolution of symptoms, this may help identify cumulative multifocal deficits, which on physical examination sometimes appear to be symmetrical [5]. Because the way that a patient describes his or her symptoms may be inexact, specific questioning may be needed to obtain meaningful information. [8]. For example, patients often have trouble distinguishing between dyesthesia (unpleasant, abnormal sensations in response to ordinarily painless stimulus), paresthesias (unpleasant sensations arising spontaneously and apparently without stimulus), and allodynia (the perception of nonpainful stimuli as painful) [6]. Similarly, a complaint of

weakness

may indicate sensory perception rather than true motor dysfunction.

Inquire about the temporal course of signs and symptoms: i.e., are they acute, subacute, chronic, progressive, relapsing, or remitting?
Temporal characteristics of symptoms can help narrow the differential diagnosis. For example, Guillain-Barr� syndrome, porphyric neuropathy, and some acute toxic neuropathies (e.g., insecticides or acrylamide) have rapid presentations with a time to nadir (maximum deficits) of only days or weeks [2] [5]. A stepwise or relapsing course can be found with chronic inflammatory demyelinating polyradiculoneuropathy, Refsum

s disease, hereditary neuropathy with liability to pressure palsies, familial brachial plexus neuropathy, repeated exposure to toxins, and vasculitic neuropathies. A slow, progressive course is more typical of diabetic and alcoholic neuropathies, and of neuropathies due to chronic exposure to toxic substances (e.g., lead and some industrial solvents) [2].

Ask about a family history of nervous system or muscular diseases, or bone deformities, especially if an acquired generalized neuropathy is suspected.
Inherited generalized neuropathy is typically characterized by an insidious progression that goes unrecognized by the patient and family members alike. If there is no history of a diagnosed PN, a family history of slowly progressive weakness or bony deformities (e.g., pes cavus, clawed toes, scoliosis) may be the initial diagnostic clue. Systematically inquire about the medical history of the patient

s first- and second-degree blood relatives. If the patient is uncertain, obtain permission to contact relatives and/or take advantage of the opportunity to quickly examine any relatives who accompanied the patient. Many of the same clinical exercises used with the patient (i.e., walking on toes and heels, rising from a seated position, etc.) can be used with relatives, even if interviewed over the telephone. Notably, inherited neuropathy typically involves few positive sensory phenomena and family members may sometimes have demonstrable polyneuropathy when examined, even if asymptomatic [5]. Also, a symmetric distal symptom pattern is characteristic of familial neuropathies, while asymmetric presentation or proximal involvement are not [9] [Table 5].

Try to determine whether PN symptoms are related to an underlying infection or systemic illness.
In Western societies, diabetes is the most common source of both generalized neuropathy and mononeuropathy [5]. Other systemic endocrine diseases associated with PN include hypothyroidism, acromegaly, and adrenoleukodystrophy [9]. Common infectious etiologies include Borrelia burgdorferi (Lyme disease), HIV, herpes simplex, and herpes zoster. Certain malignancies - e.g., osteosclerotic myeloma and small-cell bronchogenic carcinoma - are also associated with PN.

Ask about potential occupational exposures to toxins [Table 6], and try to determine whether symptoms are related to occupational exposure(s).
The patient

s exposure history can often be unclear, either due to a similarity to other peripheral neuropathies or because the etiologic agent is no longer detectable (because of the lag time between exposure and examination) [10]. When considering a potential toxic PN, it is important to (1) determine if the clinical manifestations are consistent with neurotoxic disease and (2) to know the potential neurotoxicity of a particular compound. Notably, neurotoxin-induced PN rarely presents with focal or asymmetric symptoms; it usually presents as symmetrical distal axonopathy [10].

Next, ascertain if a dose-response relationship exists between exposure and the onset and severity of symptoms. Symptoms generally coincide with or shortly follow exposure, and rarely occur months to years afterwards [10]. Additionally, the degree of symptomatology is usually related to the length or degree of exposure. Ask about individual habits, such as the use of protective devices and clothing at work, sanitary habits (washing hands before eating), waxing and waning of symptoms (at work vs. other places), recent use of pesticides, and subsequent illnesses in neighbors, pets, and children [10].

Inquire about the use of any medications, both nonprescription and prescription.
Medications that frequently cause neuropathy include amiodarone, isoniazid, platinum antineoplastic drugs, pyridoxine, thalidomide, and vinca alkaloids [12]; those that occasionally cause PN include nitrofurantoin, vincristine, cisplatin, disulfiram, chloramphenicol, chloroquine, phenytoin, aurothioglucose, metronidazole, and gold salts [12] [Table 6]. Other often-overlooked but important culprits are herbal medicines. Chinese herbals in particular are sometimes rich in mercury and arsenic. Remarkably, unlike toxin-related PNs, drug-related PNs rarely are associated with a distinctive symptom pattern [12]. Hence, a thorough drug history is important whatever the pattern of PN.

Ask about dietary habits, vitamin intake, and use of alcohol.
Alcoholic neuropathy may be related to both nutritional deficiencies (chiefly, of thiamine [B₁] and other B-group vitamins) and the toxic effect of alcohol on nerves [12]. Patients typically present with a characteristic pattern of distal muscle wasting and weakness with prominent positive sensory symptoms (e.g., hypersensitivity and burning soles, calf tenderness). This pattern is also observed in thiamine, pantothenic acid, and niacin deficiencies. Like patients with other B-vitamin deficiencies, patients with pyridoxine (B₆) deficiency typically present with glossitis, cheilosis, weakness, and irritability. However, pyridoxine taken in megadoses (usually >2 g/day) can also cause a sensory neuropathy. Unlike other nutritionally related neuropathies, patients with vitamin B₁₂ deficiency classically present with sensory ataxia and a loss of vibration and joint position sense in the lower limbs. However, the distal sensory polyneuropathy may go unnoticed, because it is overshadowed by the CNS manifestations such as intellectual changes, myelopathy, and optic neuropathy.

Table 5. Signs and Symptoms of Peripheral-Nerve Disorders

System

Positive

Negative

Motor^a

Cramps
Fasciculations
Myokymia (quivering)
Restless legs
Tightness

Weakness
Fatigability
Hypotonia
Areflexia
Deformities (pes cavus, claw hand)

Sensory (large fiber)^b

Paresthesias
Tingling

Loss of vibration sense
Loss of joint position sense
Areflexia
Sensory ataxia (positive Romberg test)
Hypotonia

Sensory (small fiber)^c

Burning, jabbing pain (dysesthesias)

Loss of pain sense
Loss of temperature sense

Autonomic^d

Hyperhidrosis
Excess saliva

Orthostasis
Erectile dysfunction
Bowel and/or bladder dysfunction
Anhidrosis

^a All motor fibers are large fibers.
^b Mediate vibration, proprioception, touch.
^c Mediate pain, temperature sensations.
^d All autonomic fibers are small fibers.

Table 6. Drugs and Toxins Causing Peripheral Neuropathy

Drug

Special features

Antibiotics

Chloramphenicol

Distal, primarily sensory neuropathy, optic neuritis during prolonged high-dose use

Dapsone

Predominantly motor neuropathy

Dideoxycytidine, dideoxyinosine,
Dideoxythmidine

Painful sensory neuropathy

Ethambutol

Optic neuritis

Isoniazid

Distal axonal neuropathy, paresthesiae are prominent. Prevented by vitamin B₆

Metronidazole

Distal sensory neuropathy

Nitrofurantoin

Distal sensorimotor neuropathy; occurs in renal failure

Suramin

Distal sensorimotor and demyelinating neuropathy

Antineoplastics

Cisplatin

Sensory ataxia

Cytarabine

Sensorimotor neuropathy; rare

Misonidazole

Painful sensory neuropathy

Procarbazine

Distal paresthesias

Paclitaxel

Distal sensorimotor neuropathy

Vinca alkaloids: vincristine, vinblastine, vindesine, vinorelbine

Distal sensorimotor neuropathy

Antirheumatics

Chloroquine