General Child Neurology
May. 31, 2021
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Antibiotic-induced neuropathy is a rare complication of several antimicrobial agents. In this article, the author discusses antibiotics that have been associated with peripheral neuropathy, focusing on those in general use and with the most established associations, and detailing the possible underlying pathophysiologic mechanisms leading to neuropathy. In most cases, the antibiotics result in a predominantly sensory axonopathy with a “dying back” of distal segments, and patients improve after the drug is discontinued.
Although the Egyptians may have been the first to appreciate the antibiotic properties of some living matter when they applied moldy bread to wounds, and Sir Alexander Fleming discovered penicillin in 1928 and showed that it was active against Staphylococcus in culture, it wasn’t until Rene Dubos isolated tyrothricin from the soil microbe Bacillus brevis in 1939 that an antibiotic was isolated and used successfully to treat human disease.
The term antibiotic derives from the Greek, meaning “against life.” Strictly speaking, an antibiotic is a substance that is produced by one microorganism that is able to inhibit the growth or kill other microorganisms. More generally, the term is used to refer to any naturally produced, semi-synthetic, or synthetic compound that acts against microorganisms, and includes antibacterials, antifungals, antiprotozoals, and anthelminthics. Antivirals can be loosely considered antibiotics, and the only members of that class associated with significant peripheral neuropathy are the nucleoside analogs, used against HIV-1, which characteristically cause a distal symmetric dysesthetic sensory neuropathy, and podophyllin resin, which is used to treat warts caused by human papilloma virus and is associated with a sensory and autonomic neuropathy; neither of these will be addressed here.
Several antibiotics are associated with peripheral neuropathy. With some notable exceptions, these toxic effects are rare compared to the relatively high incidence of neuropathy associated with antiretroviral drugs and antineoplastic agents. Despite widespread antibiotic use, most of the associations are based on relatively few case reports, and on fewer detailed animal studies to support an underlying pathogenic mechanism. The essential basis of a connection relies at a minimum on a temporal association with drug intake, followed by symptomatic stabilization, improvement or resolution after stopping the drug. Table 1 lists those antimicrobials that have been associated with peripheral neuropathy. This review will cover antimicrobials that are in more general use and those with well-established associations. Antimicrobials (which have been associated solely with damage to cranial nerves or their end organs), such as the aminoglycosides (which are oto- and vestibulotoxic) and vancomycin (which is vestibulotoxic) are not covered. Suramin, which is not approved in the United States but which is used elsewhere as an antiprotozoal agent, and is under investigation as an antineoplastic drug, is covered.
Symptoms are generally sensory more than motor, and are similar to those typical of other toxic neuropathies or other causes of distal symmetric polyneuropathy, and include distal paresthesias, often with burning, dysesthetic, and stocking-glove sensory loss. Both small and large fiber modalities may be involved, the latter reflected in distally diminished or absent tendon reflexes. Motor nerve involvement, if present at all, is typically less pronounced and occurs later, and is reflected in distal atrophy and weakness. Dapsone and nitrofurantoin, however, have prominent and early motor involvement (41; 31; 84). Onset may be insidious, subacute, or acute, and symptoms typically progress if the antibiotic is continued. In most cases, symptoms improve or resolve after the drug is discontinued. This, as well as the temporal correlation of symptom onset and the use of the medication, serves to strengthen the causal association. In some cases, as with isoniazid, recovery can be slow and incomplete, especially after prolonged use.
The neuropathy is generally reversible if the antibiotic is discontinued early, although in some case recovery is slow and incomplete.
Most of these agents cause a length-dependent sensory or sensorimotor polyneuropathy, with a “dying back” axonal pattern. Although data are sparse, for some agents this appears related to disturbances of axoplasmic flow that preferentially affect more distal axon segments (83).
Chloramphenicol. Chloramphenicol is a broad-spectrum antibiotic that inhibits protein synthesis by interfering with the 50S ribosomal subunit. It is sometimes used to treat bacterial meningitis caused by Haemophilus influenzae or Neisseria meningitides, but its use is generally limited by rare (approximately 1 in 50,000) but often fatal aplastic anemia.
Cases of neuropathy are rare, perhaps due to the typical short course of treatment, but with prolonged and high-dose therapy it can cause a mild but painful distal symmetric sensory neuropathy. Optic neuritis is more common, although in one report most patients with optic neuropathy also had evidence of peripheral neuropathy (56). Optic neuropathy has been reported with chronic chloramphenicol use in patients treated for cystic fibrosis (25). With short-term use recovery is typically full, although with prolonged use it may be incomplete (25).
Data on the pathophysiologic mechanism of nerve injury are scant. One animal study, using electron microscopy, suggested that Schwann cells and myelin rather than axons were the focus of injury; Schwann cells were hypertrophied, and myelin sheaths were swollen and fragmented, but changes in the axons were milder, showing an increase of neurofilaments and local accumulation of mitochondria (38).
Chloroquine. Chloroquine is an antiparasitic agent that prevents nucleic acid synthesis by intercalating into DNA. It is used in the treatment of malaria caused by resistant Plasmodia species, and it is also used in autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis and Sjögren syndrome.
Chloroquine rarely causes a mild, sensory greater than motor distal peripheral neuropathy that appears due to both axonal damage and to demyelination (77; 82; 70). There is a single case report of paresthesias caused by the related antiparasitic mefloquine (54). The onset of neuropathy typically occurs after one or more years of use. Cerebrospinal fluid protein may be elevated, which may confuse the diagnosis with chronic inflammatory demyelinating polyneuropathy (82; 19). The major neuromuscular complication is a vacuolar myopathy (17). There are also isolated reports of chloroquine causing retinopathy and hearing loss. Marked improvement is seen on discontinuation of the drug (Leger et al 1986; 17). Neuromuscular toxicity from short-term use of hydroxychloroquine or this agent against COVID19 is speculative at present.
Nerve biopsies have shown segmental demyelination and remyelination along with lamellar cytoplasmic inclusions in Schwann cells and perineurial cells but not in axons, all suggesting that chloroquine neuropathy is primarily due to myelin/Schwann cell damage, and not to axonal injury (Leger et al 1986; 77).
Dapsone. Dapsone is an antiparasitic and antifungal agent that acts by inhibiting the production of folinic acid, which is required for purine and pyrimidine synthesis. Its main use is in the treatment of leprosy (Mycobacterium leprae), but it is also used for malaria (Plasmodia) and Pneumocystis carinii prophylaxis, for toxoplasmosis (Toxoplasms gondii), and to treat the rare skin condition dermatitis herpetiformis.
A rare but well-characterized, primarily motor axonal neuropathy may develop (31; 59). New cases continue to be reported (52). Patients develop progressive muscle weakness and wasting in distal muscles of the extremities, especially in the hands. It typically occurs many years after drug use, and with doses greater than 300 mg/day (81). Patients typically show complete clinical recovery, but this may be slow because it requires axonal regeneration and sprouting, and some show coasting, or clinical progression, after the drug is discontinued (37; 59). Drug-resistant leprosy strains emerged in India but only about 2% to 3% of strains are dapsone resistant (43).
The pathophysiologic mechanism of nerve injury is unknown. Abnormally slow drug metabolism by liver N-acetyltransferase has been documented in many cases, suggesting that there is a genetic predisposition to developing neuropathy due to persistent excessively high dapsone levels (37; 59; 81). Most cases of neuropathy reported are for leprosy treatment; however, one patient with pemphigus treated with dapsone is reported to have developed motor neuropathy (58). Cases of neuropathy following treatment of other dermatological problems are also known (46).
Ethambutol. Ethambutol is an antitubercular antibiotic developed in 1962 and has an unknown mechanism of action. Its use is largely confined to treating life threatening or drug resistant Mycobacterium tuberculosis, in a multidrug regimen.
A mild, predominantly sensory peripheral neuropathy is seen in as many as 4% of patients (73). It most often occurs after prolonged doses greater than 20 mg/kg/day. Optic neuropathy is more common, occurring in as many as 10% of patients treated for pulmonary tuberculosis (16). The extent of optic neuropathy can be quantified by measuring retinal nerve fiber layer thickness using optical coherence tomography (09). The risk of toxic optic neuropathy is increased in patients carrying mutation in the optic atrophy 1 (OPA1) gene, possibly through a mitochondrial toxicity mechanism (30). The peripheral neuropathy typically improves after cessation of the drug, but several reports suggest that the optic neuropathy is sometimes irreversible (73; 08; 48). Accelerated ethambutol toxic peripheral neuropathy is reported in a patient with a mitofusin 2 (MTFN2) mutation, the most common cause of axonal Charcot-Marie-Tooth disease (CMT2A). The patient developed accelerated weakness, vocal cord paralysis, and optic atrophy after receiving ethambutol (20). Interestingly, this mutation also affects mitochondrial function, namely mitochondrial fusion. After drug cessation the neuropathy stabilized and vision partially improved. Optic neuropathy is considerably more common. A well-characterized case was reported after exposure to a supratherapeutic dose (22).
The pathophysiologic mechanism of nerve damage in humans is not clear. Primary axonal injury is suggested by electrophysiologic studies, although segmental demyelination and remyelination has been reported (73). In rats given 150 mg/kg/day of ethambutol for 9 months, teased fiber analysis of lower extremity nerves showed extensive axonal degeneration and regeneration, suggesting that axonal degeneration may be primary (45).
Fluoroquinolones. Fluoroquinolones are broad-spectrum antibiotics that prevent DNA recoiling after replication by inhibiting DNA gyrase. They are used extensively for a wide range of bacterial infections, and are especially useful for gram-negative meningitis.
The evidence that fluoroquinolones might cause a peripheral neuropathy is tenuous, especially given their extensive use, but is increasingly accepted. Transient paresthesias and numbness, which resolve within a few weeks of drug discontinuation, have been reported. Other cases of multisystem and multisymptom disabling toxicity have been reported and termed mitochondrial neurogastrointestinal encephalomyopathy (27). Fluoroquinolones were first reported to cause peripheral neuropathy in a 1992 case report of a patient treated for 5 months with pefloxacin for osteomyelitis; a sensorimotor axonal polyneuropathy developed (03). Another case report describes an instance of demyelinating polyneuropathy in a patient after taking trovafloxacin (50). A study using pefloxacin to treat urinary tract infections found a single instance of transient peripheral neuropathy in 1 of 27 patients (10). However, many other studies using fluoroquinolones have not reported neuropathy as a side effect (64). A Swedish paper describes 37 patients who reported sensory disturbances to an adverse drug reaction advisory committee after having taken fluoroquinolones; over 80% described paresthesias and half described numbness; in the majority of cases, symptoms occurred within one week of starting treatment and resolved within 2 weeks after stopping the drug (33). One survey of Internet websites found that 36 of 45 of patients had severe neuropathic symptoms and in the majority of cases symptoms lasted longer than one year (14). The possible pathophysiology is unknown. Most studies, however, have limited more objective examination or electrophysiologic data. Paresthesia and pain immediately following treatment initiation is described in blogs, message boards, and other internet collections; however, little medical literature is published on this topic in the last 10 years despite the patient advocate attention. Tendinopathy is a well reported treatment complication that may have overlapping symptoms.
Despite the relatively sparse evidence of a link between fluoroquinolones and neuropathy, on August 15, 2013 the U.S. FDA announced the requirement of all makers of oral and intravenous fluoroquinolones to add the risk of the serious side effect of peripheral neuropathy (02). The decision was based on reports from the FDA’s Adverse Event Reporting System (AERS) database that serves the important function of post-marketing safety surveillance. However, the data are based on self-reports from healthcare providers, patients, and patient agents, including legal representatives; the information is not often corroborated (02). Analysis of the AERS data also found that development of Guillain-Barré syndrome and fluoroquinolones exposure, using an Empirical Bayes Geometric Mean disproportionality measure, was twice as likely (01). This support led to numerous lawsuits, including active class actions against fluoroquinolone makers, alleging that the companies withheld the risk of neuropathy. Physician reports in medicolegal journals highlight the contentious and typically anecdotal evidence (21). Etminan and colleagues attempted to better quantify this entity using a pharmacoepidemiologic approach (18). Using health claims data and identifying men coded to have neuropathy and excluding other identifiable causes of neuropathy, mainly diabetes and heredity, the authors compared exposure to fluoroquinolones against a larger control group. An increased incidence of neuropathy was found in the treated group leading to the conclusion that there is an increased risk of neuropathy with oral fluoroquinolone use; a higher incidence was found with current drug use. There appears to be a clear link to drug initiation and neuropathic symptoms that often persist; however, the true incidence and neurologic impact remains to be determined (69). A United Kingdom group performed a very large case-control study mining data from a primary care database in the United Kingdom (49). The cohort of over 1.3 million adults was issued prescriptions for a fluoroquinolone (34.3%) or amoxicillin-clavulanate (65.7%) antibiotic. Patients coded to have neuropathy were matched with controls treated with the same antibiotics but were not coded to have neuropathy. Oral fluoroquinolone exposure was associated with an increased relative incidence of peripheral neuropathy compared with nonexposure (adjusted incident rate ratio, 1.47; 95% CI, 1.13-1.92); amoxicillin-clavulanate exposure had no increased risk. They noted a 10-day treatment of over 150,000 patients was needed to produce one additional neuropathy case. Fluoroquinolone prophylaxis was studied in 598 children with acute lymphoblastic leukemia that also received vincristine. There was no significant difference in chemotherapy neuropathy rates between those exposed to fluoroquinolones and those who were not (35). Care should be taken with drug use in this class of patients that already know they have symptomatic neuropathy.
Isoniazid. Isoniazid has been used to prevent tuberculosis (Mycobacterium tuberculosis) since the early 1950s. It works by an unknown but specific mechanism.
Although hepatitis is the most dangerous adverse effect of isoniazid, peripheral neuropathy is the most common; it occurs in 1% to 3% of patients receiving conventional doses of 3 to 5 mg/kg per day (07). Isoniazid causes a predominantly sensory, predominantly large-fiber symmetric axonal peripheral neuropathy (13). Initially, patients describe distal tingling paresthesias and numbness in the feet. Occasionally, numbness can have a burning quality that can be severe. If untreated, symptoms may ascend to the knees and spread to the hands, and weakness can develop. Symptoms typically occur after several months of treatment (26). Recovery is rapid if the problem is detected early but may be slow and incomplete if the cause remains unrecognized. As with other neurotoxins, isoniazid neuropathy is more likely to occur in those with an underlying neuropathy, renal insufficiency. HIV-infected patients are at increased neuropathy risk prior to initiation of treatment if they were treated for tuberculosis; in a study, many were pyridoxine deficient (78). Additionally, isoniazid is acetylated in the liver by N-acetyltransferase, and those who carry mutations in N-acetyltransferase leading to slow acetylation are at increased risk for neuropathy (26).
Isoniazid is an antagonist of pyridoxine (vitamin B6), a coenzyme essential for protein, carbohydrate and fatty acid metabolism; it causes a functional pyridoxine deficiency, which is regarded as the underlying cause of the peripheral neuropathy. Daily pyridoxine supplementation (10 to 100 mg/day) protects against the development of neuropathy. In rats given toxic doses of isoniazid, teased nerve fiber studies are consistent with a “dying back” distal axonopathy, with sparing of cell bodies (13). Other medications that likely produce neuropathy by similar pyridoxine mechanisms include phenytoin and phenelzine. Sensory and motor neuropathy has also been reported in a patient on high-dose isoniazid (5 mg/kg/day) without pyridoxine supplements; she partially improved after pyridoxine supplement despite isoniazid continuation (04).
Linezolid. Linezolid, first approved in 2000, is a synthetic oxazolidinone antibiotic used against methicillin-resistant and vancomycin-resistant gram-positive microorganisms and increasingly against multidrug-resistant tuberculosis (63). It binds to the 50S ribosomal subunit and prevents the formation of the initiation complex required to translate mRNA into protein. Linezolid was recently reclassified as a Group A drug by the World Health Organization (WHO) for treatment of multi-drug resistant tuberculosis (65).
Linezolid can cause a predominantly sensory axonal neuropathy and neuronopathy when used for months and at a high dose (57; 86; 80). Vibration and proprioception senses are severely affected (86). Chronic use is associated with a painful, predominantly sensory polyneuropathy, optic neuropathy, and deafness (57; 11; 32). Only minor adverse effects were seen in phase III trials; however, several more serious adverse effects were reported after commercial release, including cases of lactic acidosis, peripheral and optic neuropathy, and serotonin syndrome (51). Abnormalities of nerve conduction studies and diminished epidermal nerve fiber density are reported (57; 11). The optic neuropathy is usually reversible after discontinuing the drug (47; 62), but it can be irreversible (05). A case noting reversibility is also reported (79). The peripheral sensory loss is often permanent (67; 86; 80), or it may partially reverse (11). The antibiotic is increasingly used against treatment-resistant tuberculosis. A meta-analysis of available data from multiple registries found neuropathy and anemia to be the most common toxicities; overall neuropathy occurred in 31% on chronic therapy (85). A 15-year-old boy from Tajikistan had 5 years of type I diabetes but no symptomatic neuropathy (72). He contracted multidrug resistant tuberculosis and was treated with a cocktail containing linezolid 600 mg daily. After 8 months he developed symptomatic and electrodiagnostic neuropathy. He improved after drug cessation and was asymptomatic after 21 months. The underlying role of the diabetes was raised.
The mechanism of nerve injury is unknown but may be impairment of mitochondrial protein synthesis (60). There is no recognized treatment other than symptomatic measures and discontinuation of the drug or decreasing the dose (36). Prolonged linezolid treatment induced a mild, predominantly small sensory fiber neuropathy in mice (06). Linezolid exposure caused mitochondrial dysfunction primarily in cultured sensory neurons and less prominently in Schwann cells. Sensory axonopathy could be partially prevented by co-administration of the Na(+)/Ca(2+) exchanger blocker KB-R7943.
Metronidazole. Metronidazole is a broad-spectrum antibiotic that binds to DNA and blocks replication. It is effective against protozoa (eg, Trichomonas, Giardia, Entamoeba), bacteria (Clostridium difficile, Helicobacter pylori), parasites (Trichomonas vaginalis), and microsporidia. It is also used chronically in the treatment of inflammatory bowel disease.
Metronidazole carries a low but well-documented risk of sensory neuropathy, especially after months to years of use and with cumulative doses exceeding 30g (87). A distal pansensory neuropathy characterized by pain, burning paresthesias, and dysesthesias in the feet and hands is typical. Improvement may take months once the drug is stopped.
Little is known about the etiology and pathogenesis of metronidazole neurotoxicity. A sural biopsy study revealed that myelinated fibers appear preferentially affected, although on electron microscopy unmyelinated axons also showed degeneration (74). The pathogenesis of metronidazole peripheral nerve injury is largely inferred from studies of misonidazole, a related compound that is used as a chemotherapeutic adjunct to sensitize hypoxic cells to the effects of ionizing radiation. As with metronidazole, misonidazole neurotoxicity consists of a predominantly sensory polyneuropathy, with pain and distal burning dysesthesias. Animal studies show distal axonal degeneration, especially sensory terminals and in intramuscular fibers, and studies in cultured neuronal cell suggest that the mechanism may be disruption and degradation of the neurofilament lattice (29; 71). Other postulated mechanisms include impaired membrane transport and inhibition of protein synthesis (44). Skin biopsy of epidermal nerve fiber density is another means to document the toxic effect of prolonged exposure. Serial skin biopsies demonstrated emergence of painful sensory neuropathy in a 53-year-old man treated with metronidazole at a cumulative dose of 146 g over 88 days (75). A metanalysis based on available published reports intended to guide clinical practice concluded that incidence was rare if dose was below 42 g total and less than four weeks duration (28). However, cases starting very soon after drug initiation are reported (53). A Canadian group conducted a population-based nested case control study of adults admitted for various neurologic conditions including neuropathy whom also received a metronidazole or clindamycin prescription within 100 days of admission—1212 cases were identified (15). A conditional logistic regression model was used to estimate relative risk. A relative increased risk of 1.34 was found after adjusting for other factors. Rates of central and peripheral nerve toxicity were similar.
Nitrofurantoin. Nitrofurantoin is a broad-spectrum antibiotic approved in 1953 that disrupts bacterial cell wall formation and may inhibit RNA and DNA synthesis. It is occasionally used to treat urinary tract infections. It has no systemic antibacterial effect because its activity depends on its being concentrated in the urine; it is, therefore, ineffective in renal failure.
Nitrofurantoin causes a symmetric, motor greater than sensory axonal neuropathy, characterized by distal weakness, paresthesias, and numbness. It may arise acutely and within weeks to months of starting the drug, and may be unrelated to dose (84). Renal insufficiency or failure appears to predispose to neuropathy, possibly due to concomitant excessive tissue concentrations (42). Recovery may be slow, partial and unrelated to cumulative dose (84).
An early histologic study showed axonal degeneration and chromolysis in anterior horn cells (41). A second histologic study using both light microscopy and electron micrography was consistent with severe axonal degeneration (84). It has been postulated that neurotoxicity may be due to a dose-dependent depletion of glutathione (68). In addition, cases of small fiber sensory and painful neuropathy are recognized. Morphological changes, such as clustered terminal nerve swellings, in skin biopsy samples demonstrated support of 2 cases of clinical nitrofurantoin-induced neuropathy despite normal sensory and motor nerve conduction studies (76).
Suramin. Suramin is a polysulfonated naphthylurea that is not approved in the United Stated, but which is used as an antiprotozoal antibiotic to prophylaxis against sleeping sickness (Trypanosoma sp). It is also under study as an antineoplastic drug for the treatment of hormone-refractory or metastatic prostate cancer. The primary factor limiting its use is toxic neuropathy.
Up to 50% of patients develop a mild symmetric distal sensorimotor axonal polyneuropathy (12). The risk appears much greater if serum concentrations are greater than 350 mg/ml, and appear unrelated to cumulative dose or duration of treatment (66; 23). Patients typically report burning paresthesias, which usually involve the distal extremities but occasionally also involve the face; distal weakness may follow, and occasionally this may be more proximal than distal. A minority of patients develop a subacute and progressive demyelinating polyneuropathy similar to Guillain-Barré syndrome (12; 66). There are some reports of severe symptoms, with bulbar weakness, respiratory weakness, and even dysautonomia (39; 23). In those with demyelination, cerebrospinal fluid protein is elevated; patients have improved with plasmapheresis (12).
Human electrophysiologic studies show both axonal and demyelinating neuropathy (12; 66). Sural nerve specimens have has shown lymphocytic infiltrates (12). In rats, one sees a length- and dose-dependent axonal sensorimotor polyneuropathy with an accumulation of lysosomal ceramide inclusions (23; 61). Postulated pathophysiologic mechanisms include disruption of glycolipid metabolism leading to apoptosis, disruption of calcium signaling via antagonism of purinergic receptors, and inhibition of mitogenic growth receptors (23; 24; 55).
Overall, the detailed cell-biological and biochemical basis for the antibiotic-induced neuropathies is poorly understood. However, the susceptibility of peripheral nerves to toxic injury may be related to the relatively leaky blood-peripheral nerve barrier; drugs can, thus, more readily reach peripheral nerve, dorsal root and autonomic ganglia, compared to spinal cord or other central nervous system neurons (34; 83).
No general predisposition to the neurotoxic effects of antibiotics is known. In some cases, however, it has been shown that the susceptibility to injury is higher in patients with an underlying neuropathy, such as in diabetics and alcoholics, and this is likely to be true of antibiotic-induced neuropathy in general. Slow acetylators are at increased risk for peripheral neuropathy due to isoniazid and dapsone. No male to female discrepancy has been noted.
Prevention consists of avoiding these antibiotics, if possible, in patients who have an existing peripheral neuropathy, and in screening patients considered for isoniazid and dapsone to determine whether they are slow acetylators. Isoniazid neuropathy can be prevented by concomitant use of pyridoxine (vitamin B6), 10 to 100 mg/day, to avoid functional pyridoxine deficiency. However, excessive pyridoxine exposure can independently cause sensory neuropathy. Nitrofurantoin should be used cautiously if at all in those with renal insufficiency. Extreme vigilance for the onset of peripheral neuropathy must be maintained, and the drugs should be stopped as soon as symptoms occur.
Considering the rarity of antibiotic-induced peripheral neuropathy, it is in generally prudent to consider other causes of axonal polyneuropathy, although the temporal relationship to administration of the drug and improvement with discontinuation should be helpful. In patients taking chloroquine and suramin, other causes of demyelinating polyneuropathy should be considered.
Electrodiagnostic studies that demonstrate axonal neuropathy may be useful. Spinal fluid analysis is generally normal, but protein may be elevated in some cases (eg, chloroquine, suramin). Nerve biopsy may show evidence of an acute or subacute axonopathy, but is not typically specific or diagnostic; however, lysosomal inclusions can be found in many cases of suramin neuropathy.
Supportive measures are discussed in Peripheral neuropathies: supportive measures and rehabilitation.
In most cases, timely discontinuation of the antibiotic is sufficient. In severe suramin neuropathy, plasmapheresis may be beneficial (12). Future treatments using neurotrophins may blunt the neurotoxic effects (83).
Louis H Weimer MD
Dr. Weimer of Columbia University has received consulting fees from Roche.See Profile
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