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At least 829 records · Page 46Linked to original sources
PubMed1999

Pudendal neuropathy and severity of incontinence but not presence of an anal sphincter defect may determine the response to biofeedback therapy in fecal incontinence.

PURPOSE: It has been suggested that the severity of fecal incontinence, the presence of pudendal neuropathy, or an external anal sphincter defect does not preclude clinical improvement with biofeedback therapy. A discrepancy, however, is frequently found between subjective improvement and objective results after biofeedback therapy. Our aim was to assess whether severity of fecal incontinence, presence of pudendal neuropathy, or an external anal sphincter defect could influence the results of manometric parameters after biofeedback therapy in patients with fecal incontinence. METHODS: Biofeedback therapy was used to treat 27 patients with fecal incontinence (25 women; mean age, 53; range, 29-74 years), according to a strict protocol. Manometry, pudendal nerve terminal motor latency, and anal ultrasound were performed in all patients before biofeedback therapy. Manometric evaluation of external anal sphincter function was performed after the biofeedback sessions. RESULTS: Eight of 27 patients had a good clinical response to biofeedback, but with no significant difference in their mean amplitude and duration of squeeze pressure before and after biofeedback. There was no relationship between the clinical results of biofeedback therapy and the initial severity of fecal incontinence, pudendal neuropathy, or external sphincter defect. Patients with severe incontinence (incontinence to solids) and pudendal neuropathy failed to improve the amplitude and duration of their maximum voluntary contraction after biofeedback therapy. Patients with mild fecal incontinence (incontinence to flatus, liquids, or both) (P<0.04), without pudendal neuropathy (P<0.02), or with (P<0.05) and without (P<0.05) external sphincter defect improved their external anal sphincter function after biofeedback therapy. CONCLUSION: In patients with fecal incontinence, the severity of symptoms and pudendal neuropathy should be considered as two factors of poor prognosis of favorable manometric results after biofeedback therapy. Improvement, on the other hand, may be expected after biofeedback therapy despite an external anal sphincter defect.

Anal Canal↗
PubMed2004

Techniques for the neurological examination of taxane-induced neuropathy.

Taxanes are considered to be the key drugs in the treatment of breast cancer. Although physicians who treat patients with breast cancer have rarely seen patients with neuropathy as an adverse effect of treatment before the advent of taxanes, patients with breast cancer who are treated with taxanes frequently exhibit peripheral neuropathy. As peripheral neuropathy often causes deterioration of the quality of life of patients, it is very important to precisely assess the extent of peripheral neuropathy at an early stage. Clinical oncologists should be familiar with the techniques of neurological examination. In this article we describe the basic techniques for the neurological examination of patients with taxane-induced peripheral neuropathy. In the hope of facilitating the precise evaluation of taxane-induced peripheral neuropathy, the items of neurological examinations in this article are described with reference to the physician neuroexamination form (PNEF) designed by BioNumerik Pharmaceuticals Inc.

Antineoplastic Agents, Phytogenic↗
PubMed1995

Organophosphate polyneuropathy and neuropathy target esterase: studies with methamidophos and its resolved optical isomers.

Methamidophos (O,S-dimethyl phosphorothioamidate) causes polyneuropathy in man and hens. However, experiments in the hen show that lower doses of methamidophos either protect from or promote the neuropathy caused by certain organophosphates. The initiation of neuropathy as well as protection from neuropathy are thought to be related to neuropathy target esterase (NTE), whereas promotion is likely to be due to interactions with another unknown target. Methamidophos is a racemate and we report studies with its resolved optical isomers, aimed at elucidating which isomer is responsible for the described effects. The time-course of acetylcholinesterase (AChE) and NTE activity in nervous tissues of hens after inhibition by single doses of either isomer showed that after D-(+) methamidophos (25 mg/kg PO) peak inhibition of both enzymes was achieved within 24 h (80-90%). However, after L-(-) methamidophos (15 mg/kg PO), peak inhibition (80-90%) was obtained within 24 h for AChE, whereas similar NTE inhibition (120 mg/kg PO) was observed only 4 days after dosing. The minimal neuropathic doses of D-(+) and L-(-) methamidophos were 60 and 120 mg/kg PO, respectively, and correlated with > 80% NTE inhibition in nervous tissues. OPIDP initiation by either isomer was slightly promoted by phenylmethanesulfonyl fluoride (120 mg/kg SC). D-(+) Methamidophos (25 mg/kg PO) partially protected from dibutyl dichlorovinyl-phosphate (DBDCVP) neuropathy (up to 0.8 mg/kg SC). This effect correlated with about 70% NTE inhibition. L-(-) Methamidophos (15 or 60 mg/kg PO) did not protect from DBDCVP neuropathy (0.2-0.8 mg/kg SC).

Animals↗
PubMed1998

Repeated low doses of O-(2-chloro-2,3,3 trifluorocyclobutyl) O-ethyl S-propyl phosphorothioate (KBR-2822) do not cause neuropathy in hens.

Certain esterase inhibitors such as O-(2-chloro-2,3,3-trifluorocyclobutyl) O-ethyl S-propyl phosphorothioate (KBR-2822) and phenylmethanesulfonyl fluoride (PMSF) cause exacerbation (promotion) of toxic and traumatic axonopathies. Although these chemicals are capable of inhibiting neuropathy target esterase (NTE), which is the target for organophosphate induced delayed neuropathy, the target for promotion is unlikely to be NTE. Experiments were aimed to ascertain if neuropathy is caused by repeated dosing with a promoter not causing NTE inhibition and in the absence of deliberate injury to axons. Hens were treated with KBR-2822 (0.2 or 0.4 mg/kg per day) by gavage for 90 days and observed for clinical signs up to 21-23 days after treatment when histopathological examination was carried out. NTE and acetylcholinesterase (AChE) were measured at intervals and mean percentages of inhibition at steady state of inhibition/resynthesis (on day 20) were as follows: mean inhibition NTE was < or = 8% in the 0.2 mg/kg group and between 15 and 18% in the 0.4 mg/kg group in brain, spinal cord and peripheral nerve; mean AChE inhibition in brain was 31 and 57% in the two experimental groups, respectively. Controls treated with paraoxon (not neuropathic or a promoter and given at 0.05 mg/kg per day by gavage) showed 45% mean AChE inhibition and no NTE inhibition. Neither clinical nor morphological signs of neuropathy were observed in any group. To ascertain whether subclinical lesions were produced by the repeated treatment with KBR-2822, hens were given KBR-2822 (0.2 mg/kg per day) for 21 days by gavage followed by PMSF (120 mg/kg s.c. 24 h after the last dose of KBR-2822). A control group of hens was treated with the neuropathic DFP (0.03 mg/kg s.c. daily for 21 days causing 40-50% NTE inhibition) followed by PMSF (120 mg/kg s.c.). After PMSF, the KBR-2822 treated hens did not develop neuropathy whereas DFP treated hens did. Lack of neuropathy after repeated treatment with KBR-2822 indicates that a continuous promoting 'pressure' on hen axons is harmless in the absence of a concurrent biochemical or neurotoxic injury.

Acetylcholinesterase↗
PubMedDate not supplied

Neuronal autoantibody titers in the course of small-cell lung carcinoma and platinum-associated neuropathy.

The aims of this study were to investigate, in patients with newly diagnosed small-cell lung carcinoma (SCLC), whether or not there may be a relationship between the presence, type or titer of circulating neuronal autoantibodies and (i) the extent of SCLC dissemination at presentation, (ii) the development of peripheral neuropathy during platinum chemotherapy, (iii) survival time. We studied stored serum from 58 patients with uncomplicated SCLC who had participated in two trials conducted by the North Central Cancer Treatment Group (NCCTG); 29 had extensive disease and 29 had limited disease. No patient had neuropathy or other neurological or paraneoplastic problems at the time of enrollment but each group included 14 or 15 patients respectively who developed peripheral neuropathy in the course of chemotherapy. We tested five consecutive serum specimens from each patient in blinded fashion by (i) an indirect immunofluorescence assay optimized to detect neuron-restricted nuclear and cytoplasmic antibodies (triple substrate of mouse cerebellum, gut and kidney), and (ii) immunoprecipitation assays to detect neuronal Ca2+-channel-binding antibodies (N-type and P/Q-type). Sera that were positive by immunofluorescence were analyzed further by Western blotting. Neuronal autoantibodies were significantly more frequent in patients who had limited SCLC at presentation (12/29 or 41% positive) than in those with extensive SCLC (5/29 or 17% positive, P = 0.02). Neuronal autoantibodies of nuclear or cytoplasmic specificity were found in 50% of the seropositive patients with limited SCLC (21% of the total group), but in no patient with extensive SCLC (P = 0.01). The frequency of neuronal autoantibodies did not differ significantly among patients who did and did not develop peripheral neuropathy. Titers fell progressively during chemotherapy and did not rise again when peripheral neuropathy became clinically evident. This argues against a synergism between drug toxicity and neuronal autoimmunity as the mechanism of platinum-associated peripheral neuropathy. Seropositivity for neuronal autoantibodies did not affect the survival of patients with either limited or extensive SCLC. It is conceivable that the immunosuppression attendant on combined cisplatin/etoposide therapy cancels a pre-existing protective antitumor immune response (presumably cytotoxic-T-cell-mediated) for which the nuclear and cytoplasmic paraneoplastic IgG autoantibodies serve as a surrogate marker. Testing of this hypothesis would require the survival of seropositive and seronegative patients to be compared in a larger trial, using a therapeutic modality that does not compromise immunocompetence.

Antineoplastic Agents↗
PubMed2002

Peripheral neuropathy in systemic lupus erythematosus: pathomorphological features and distribution pattern of matrix metalloproteinases.

Matrix metalloproteinases (MMPs) are endoproteases that have been implicated in the pathogenesis of inflammatory and vasculitic neuropathies. In systemic lupus erythematosus (SLE), a peripheral neuropathy is frequently seen that is thought to be caused by ischemic nerve damage due to vasculopathy and/or vasculitis of the nutritional vessels. However, the exact pathomechanisms causing SLE neuropathy are largely unknown. Elevated MMP levels have been reported in the serum of SLE patients. Supposing that altered expression of MMPs may contribute to vessel wall damage in SLE neuropathy, we investigated the expression of MMP-1, -2, -3, -9, -10 and -13, and their tissue inhibitors (TIMP-1 and -2) in sural nerves from 12 SLE patients in comparison to normal controls. All MMPs could be detected within blood vessel walls from SLE nerves, whereas in controls MMP-3 and MMP-9 was not found. TIMP-1 and TIMP-2, on the other hand, were not informative. Generally, small and large nutritional vessels in the epineurium were immunoreactive for MMPs and TIMPs. Mononuclear cells, which expressed MMP-1, - 3, -10, -13, and TIMP-1 were also observed in most of the SLE nerves, mostly around epineurial blood vessels, but only occasionally in controls. This indicates that expression of MMPs in mononuclear cells may be related to leukocyte trafficking through the vessel walls. However, the density of TIMP-positive and MMP-positive inflammatory cells did not correlate with morphometric parameters regarding the severity of the neuropathy. Our findings suggest that especially the up-regulation of MMP-3 and MMP-9 within the vessel walls may be responsible for the vascular damage seen in SLE and the resulting chronic combined axonal and demyelinating type of neuropathy frequently found in SLE.

Adult↗
PubMed2004

Immune mediated neuropathies--an update on therapeutic strategies.

This paper reviews recent treatment strategies of immune mediated neuropathies, in particular it includes data regarding Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy (MMN), neuropathy with IgM monoclonal gammopathy and other dysglobulinemic neuropathies. In the treatment of Guillain- Barré syndrome, there is no significant difference between IVIg, plasma exchange or plasma exchange followed by IVIg. However, for reasons of convenience and safety, IVIg is used as standard treatment in most centers. There is so far insufficient evidence for the use of corticosteroids in the therapy of GBS. In treating CIDP corticosteroids, intravenous immunoglobulin and plasma exchange seem to be equally effective. However, the high costs and relative lack of availability of IVIg, the only short-term benefit and the invasive nature of the plasma exchange procedure, and on the other hand serious long-term side effects of corticosteroids are the most important disadvantages of these treatments and have to be taken into consideration before a decision about therapy can be made. In multifocal motor neuropathy the intravenous immunoglobulin therapy is the only treatment that has been shown to be effective in controlled trials. However, inadequate response in a proportion of patients, high cost and variable availability of IVIg show the need for the search of adjunctive immunosuppressive therapies. Neuropathies with IgM monoclonal gammopathy may improve after treatment with chemotherapeutic agents, though the long-term effects are not known. In addition, such treatment modalities may be associated with serious side effect and even severe toxicity. Recent data support the use of a new promising drug: Rituximab, a monoclonal antibody directed against the B cell surface membrane marker CD 20.

Adrenal Cortex Hormones↗
PubMed2006

Peripheral neuropathy in Behçet disease: an electroneurophysiological study.

The aim of this study was to determine the peripheral nerve involvement electrophysiologically in Behçet patients without clinically evident neurological signs and symptoms. Sixty-three patients who fulfilled the International Study Group Classification Criteria for Behçet's disease (BD) and 49 healthy control subjects were enrolled to the study. Conventional electrophysiological studies of peripheral nerves including F latencies were performed to all subjects. Thirty-one male and 32 female Behçet patients with a mean age of 33.6+/-11.1 years and (22 male and 27 female healthy control subjects with a mean age of 35.8+/-9.9 years were included to the study. All but four of the patients were active. In the BD group, electrophysiologically diagnosed neuropathy was detected in nine (14.28%) patients. One (1.58%) patient had sensorimotor polyneuropathy, one patient (1.58%) had sural and ulnar sensorimotor neuropathy, three (4.75%) patients had median and one patient (1.58%) had ulnar sensorimotor neuropathy. Sural nerve sensorial action potential was unobtainable in two (3.17%) patients and prolonged F latencies were observed in two (3.17%) patients. In the control group only one subject (2.4%) had low sural sensorial conduction velocity. The frequency of neuropathy was higher in the patients with BD when compared with the control subjects. Sensory nerves were affected more prominently than motor nerves. There was no relationship between the clinical and laboratory characteristics of the patients and the electrophysiologic findings. No significant difference was observed between the clinical parameters of the patients with and without electrophysiologically detected neuropathy, except the levels of disease duration (8.8+/-5.1 vs 5.28+/-4.3 years, respectively, p<0.05). In conclusion, Behçet patients may have subclinical peripheral nerve involvement. Conventional electrophysiologic nerve conduction studies including F responses are recommended in routine examination to diagnose early neuropathy in Behçet patients without evident neurologic symptoms.

Adolescent↗
PubMed2003

Medication-induced peripheral neuropathy.

Although not very common, medication-induced neuropathy is a treatable condition and, therefore, is important to identify. Medications continue to grow in number and expand in usage; consequently, toxic neuropathy continues to be relevant to neurologists. Many agents have toxicities that are tolerated because the treatments are necessary, such as therapies for HIV and malignancy. Additional agents to prevent or ameliorate the toxic neuropathy are being sought and trials are ongoing. Certain patients, however, may be at high risk for peripheral nerve toxicity due to genetic factors or another underlying neuropathy. Newer drug-delivery methods, such as viral transfection, may produce less toxicity in the future. The underlying pathomechanisms remain incompletely elucidated; however, apoptosis is emerging as an important final pathway in some forms of toxic neuropathy. Although most cases demonstrate acute or subacute onset after exposure, recent experiences with statin drugs raise the possibility of occult toxic causes of chronic idiopathic neuropathy.

Animals↗
PubMed2001

Paraproteinemic Neuropathy.

Few prospective, randomized, placebo-controlled trials have been performed to guide clinicians in the management of neuropathies seen in the setting of monoclonal gammopathies (paraproteins). Recommendations must be made on the basis of clinical experience and information gleaned from various uncontrolled and open-label trials. In every instance, decisions concerning therapy must be based on the clinical setting in which the paraprotein occurs. Treatment of paraproteinemic neuropathies associated with multiple myeloma, amyloidosis, and Waldenström's macroglobulinemia should be directed at the treatment of the underlying disease. These neuropathies often remain recalcitrant to therapy. If the paraprotein results from cryoglobulinemia due to hepatitis C virus infection, interferon-alpha (with or without ribavirin) provides optimal subjective and objective relief from symptoms. For neuropathy associated with osteosclerotic myeloma (POEMS syndrome) and solitary bone lesions, radiation therapy is the most effective and least toxic initial therapy. In those patients with monoclonal gammopathies of undetermined significance (MGUS), consideration of the clinical syndrome may be very helpful in selecting appropriate treatment. Patients who fulfill diagnostic criteria for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are best treated in a manner similar to that used for idiopathic CIDP (ie, with intravenous immunoglobulin, plasma exchange, and corticosteroids). Class I evidence documents plasma exchange to be effective in peripheral neuropathies associated with MGUS of the IgG and IgA, but not IgM, types. The most difficult cases to treat are those with peripheral neuropathies associated with IgM monoclonal gammopathies, with or without reactivity to myelin-associated glycoprotein (MAG). A number of published case series propose therapeutic regimens for these conditions, yet optimal treatment remains to be established. In many cases, mildly symptomatic patients should not be subjected to the morbidity associated with current treatment regimens. In those patients requiring treatment, this author initially tries plasma exchange, followed by a course of chlorambucil if the symptoms and signs are predominantly sensory. For cases with rapid progression or significant disability, a regimen of monthly pulses with prednisone and cyclophosphamide is recommended. If improvement does not ensue, a trial of a newer agent, such as rituximab, is recommended. Supportive treatment with physical therapy, orthotics, and ambulatory aids enhances patient independence at a relatively low cost.

Journal Article↗
PubMed1982

Trigeminal neuropathy in progressive systemic sclerosis.

Trigeminal neuropathy was identified in 16 (4 percent) of 442 consecutive patients with progressive systemic sclerosis (PSS) who were first evaluated during the period between 1972 and 1980. These cases, together with 25 others that are adequately documented in the literature, were reviewed and compared with the 426 cases of PSS (96 percent) without trigeminal neuropathy. Trigeminal neuropathy occurred most frequently in young women with PSS in overlap with other disorders, particularly the mixed connective tissue disease syndrome with clinical evidence of myositis. Serum antibodies to ribonucleoprotein were identified in nine (45 percent) of 20 PSS patients with trigeminal neuropathy as compared to 25 (8 percent) of 329 PSS patients without trigeminal neuropathy. Leukopenia, hypothyroidism, and Sjögren's syndrome were also found to be associated with trigeminal neuropathy.

Adult↗
PubMed1989

Abnormalities of sympathetic vasomotor tone in distal axonal neuropathy.

Microneurographic studies have shown that sympathetic vasomotor nerve activity is observed less frequently in patients with peripheral neuropathy than in controls, but when detected its pattern and the baroreflex latencies appear to be normal. Vasomotor nerve function was examined in chloralose-urethane anaesthetised dogs by comparing the discharge of renal sympathetic nerves in control animals and animals with acrylamide neuropathy. There was a normal pattern of pulse related inhibition of sympathetic nerve activity as well as normal amplitude spontaneous compound nerve action potentials in the animals with neuropathy. When vasomotor tone was altered abruptly by raising pressure in a bilateral isolated carotid sinus preparation, the baroreflex latencies were normal in the affected animals. However, when carotid sinus pressure was kept constant, pulse-related sympathetic inhibition, normally mediated by vagal cardiopulmonary baroreceptors, was absent in animals with neuropathy. It is likely that the vagal nerve fibres to cardiopulmonary baroreceptors as well as the receptors themselves are damaged while shorter carotid sinus nerve fibres are relatively spared in axonal neuropathies. As long as these shorter nerves are intact patients with axonal neuropathy should have relatively normal baroreflexes and normal sympathetic vasomotor tone when measured microneurographically.

Acrylamide↗
PubMed1994

Radiation optic neuropathy after megavoltage external-beam irradiation: analysis of time-dose factors.

PURPOSE: To investigate the risk of radiation-induced optic neuropathy according to total radiotherapy dose and fraction size, based on both retrospective and prospectively collected data. METHODS AND MATERIALS: Between October 1964 and May 1989, 215 optic nerves in 131 patients received fractionated external-beam irradiation during the treatment of primary extracranial head and neck tumors. All patients had a minimum of 3 years of ophthalmologic follow-up (range, 3 to 21 years). The clinical end point was visual acuity of 20/100 or worse as a result of optic nerve injury. RESULTS: Anterior ischemic optic neuropathy developed in five nerves (at mean and median times of 32 and 30 months, respectively, and a range of 2-4 years). Retrobulbar optic neuropathy developed in 12 nerves (at mean and median times of 47 and 28 months, respectively, and a range of 1-14 years). No injuries were observed in 106 optic nerves that received a total dose of < 59 Gy. Among nerves that received doses of > or = 60 Gy, the dose per fraction was more important than the total dose in producing optic neuropathy. The 15-year actuarial risk of optic neuropathy after doses of > or = 60 Gy was 11% when treatment was administered in fraction sizes of < 1.9 Gy, compared with 47% when given in fraction sizes of > or = 1.9 Gy. The data also suggest an increased risk of optic nerve injury with increasing age. CONCLUSION: As there is no effective treatment of radiation-induced optic neuropathy, efforts should be directed at its prevention by minimizing the total dose, paying attention to the dose per fraction to the nerve, and using reduced-field techniques where appropriate to limit the volume of tissues that receive high-dose irradiation.

Adolescent↗
PubMed1989

Intraoperative cortical somatosensory evoked potentials for detection of sciatic neuropathy during total hip arthroplasty.

Approximately 3% of patients undergoing hip arthroplasty develop postoperative sciatic neuropathy. The factors associated with changes in somatosensory evoked potentials (SSEP) and sciatic neuropathy were examined in patients undergoing hip arthroplasty, to evaluate whether the use of intraoperative SSEP could help reduce the incidence of postoperative sciatic neuropathy. Eighty-eight patients were assigned to either monitored or unmonitored groups. SSEP were recorded following peroneal nerve stimulation, using contralateral stimulation to detect systemic influences on SSEP. Amplitude reduction of less than 50% of control and/or latency increase of greater than 10% of control was considered significant, and surgical intervention was attempted to restore SSEP. Previous surgery and a lateral incision approach tended to be associated with sciatic neuropathy (p less than 0.053). The incidence of sciatic neuropathy in the monitored group (4.3%) was not different from the unmonitored group (2.4%). Isolated reduction in amplitude or prolongation in latency of the SSEP was not predictive of postoperative neurologic function of the sciatic nerve. Six patients, two of whom developed sciatic neuropathy, demonstrated complete flattening of the SSEP. Both of these patients had flattened SSEP for two or more surgical events (p less than 0.01) and flattened SSEP were present at the end of the surgical procedure. There were no false-negative SSEP changes. Simultaneous amplitude and latency changes appear to be predictive of sciatic nerve function following hip arthroplasty.

Evoked Potentials, Somatosensory↗
PubMed2005

Linezolid-induced optic neuropathy.

PURPOSE: To report a case of optic neuropathy associated with prolonged use of a new antibiotic, linezolid. DESIGN: Interventional case report. METHODS: Optic and peripheral neuropathy occurred in a 27-year-old woman who was undergoing prolonged linezolid therapy for osteomyelitis. The use of corticosteroid exacerbated visual loss. Discontinuation of the linezolid therapy resulted in marked improvement of optic neuropathy. RESULTS: Linezolid-induced optic neuropathy was diagnosed in this case, because prolonged linezolid therapy was performed at a higher dose than usual and because the patient recovered after linezolid therapy was discontinued. CONCLUSIONS: With prolonged linezolid therapy, ophthalmologists should be aware that bilateral optic neuropathy can occur and that corticosteroids are not indicated for this neuropathy.

Acetamides↗
PubMed2005

Hereditary optic neuropathies: from the mitochondria to the optic nerve.

PURPOSE: To review our current knowledge of inherited optic neuropathies. DESIGN: Perspective. METHODS: Literature review. RESULTS: The hereditary optic neuropathies consist of a group of disorders in which optic nerve dysfunction figures solely or prominently and direct inheritance is clinically or genetically proven. The most common of these disorders are autosomal dominant optic atrophy (Kjers' disease) and maternally-inherited Leber's hereditary optic neuropathy. Other inherited neurologic and systemic syndromic diseases will frequently manifest optic neuropathy. A selective vulnerability of the optic nerve to perturbations in mitochondrial function may underlie a final common pathway among these disorders. CONCLUSIONS: The ophthalmologist should be familiar with the clinical characteristics and diagnosis of the hereditary optic neuropathies. Recent advances in our understanding of the underlying pathophysiology of the inherited optic neuropathies may provide insight into their treatment and the treatment of acquired optic nerve disorders.

Humans↗
PubMed2006

Chemotherapy-induced neuropathy.

Increasingly, surgeons are becoming aware of the successful treatment of symptomatic peripheral neuropathy by surgical decompression of peripheral nerves. Armed with the knowledge that patients can have underlying neuropathy with overlying anatomic compressions, surgeons have affected improvement in diabetes-induced neuropathy, neuropathy of unknown etiology, and chemotherapy-induced neuropathy. This article details the most well-known culprits in chemotherapy-induced neuropathy and discusses the putative mechanisms of action, medical management, and surgical data.

Animals↗
PubMed2005

Symptomatic and neurophysiological responses of paclitaxel- or cisplatin-induced neuropathy to oral acetyl-L-carnitine.

Acetyl-L-carnitine (ALC) improves non-oncological neuropathies. We tested oral ALC (1 g tid) for 8 weeks in 25 patients with neuropathy grade 3 (common toxicity criteria--CTC) during paclitaxel or cisplatin therapy, or grade 2 persisting for at least three months after discontinuing the drugs. An independent neurologist assessed patients before and after ALC. All patients except one reported symptomatic relief, and only two described grade 1 nausea. The sensory neuropathy grade improved in 15 of 25 (60%), and motor neuropathy in 11 of 14 patients (79%). Total neuropathy score (TNS) that included neurophysiological measures improved in 23 (92%). Amelioration of sensory amplitude and conduction velocity (sural and peroneal nerves) was measured in 22 and 21 patients, respectively. Symptomatic improvement persisted in 12 of 13 evaluable patients at median 13 months after ALC. In view of its effect in improving established paclitaxel- and cisplatin-neuropathy, we recommend ALC testing in preventing progression or revert symptoms during neurotoxic chemotherapy.

Acetylcarnitine↗