[Asymmetrical evolution of demyelinating process in peripheral neuropathy; analysis on Guillain-Barré syndrome and experimental lead neuropathy (author's transl)].
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Animals↗
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Macroglobulinemic neuropathy. Experimental macroglobulinemic neuropathy in mice.
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Animals↗
[Familial neuropathy with a tendency toward compression paralysis: problems in differential diagnosis from occupational neuropathies].
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Adult↗
Comment: 'silently arising clinical neuropathy' and extended indication of steroid therapy in leprosy neuropathy.
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Humans↗
The wide spectrum of clinical manifestations in Sjögren's syndrome-associated neuropathy.
We assessed the clinicopathological features of 92 patients with primary Sjögren's syndrome-associated neuropathy (76 women, 16 men, 54.7 years, age at onset). The majority of patients (93%) were diagnosed with Sjögren's syndrome after neuropathic symptoms appeared. We classified these patients into seven forms of neuropathy: sensory ataxic neuropathy (n = 36), painful sensory neuropathy without sensory ataxia (n = 18), multiple mononeuropathy (n = 11), multiple cranial neuropathy (n = 5), trigeminal neuropathy (n = 15), autonomic neuropathy (n = 3) and radiculoneuropathy (n = 4), based on the predominant neuropathic symptoms. Acute or subacute onset was seen more frequently in multiple mononeuropathy and multiple cranial neuropathy, whereas chronic progression was predominant in other forms of neuropathy. Sensory symptoms without substantial motor involvement were seen predominantly in sensory ataxic, painful sensory, trigeminal and autonomic neuropathy, although the affected sensory modalities and distribution pattern varied. In contrast, motor weakness and muscle atrophy were observed in multiple mononeuropathy, multiple cranial neuropathy and radiculoneuropathy. Autonomic symptoms were often seen in all forms of neuropathy. Abnormal pupils and orthostatic hypotension were particularly frequent in sensory ataxic, painful, trigeminal and autonomic neuropathy. Unelicited somatosensory evoked potentials and spinal cord posterior column abnormalities in MRI were observed in sensory ataxic, painful and autonomic neuropathy. Sural nerve biopsy specimens (n = 55) revealed variable degrees of axon loss. Predominantly large fibre loss was observed in sensory ataxic neuropathy, whereas predominantly small fibre loss occurred in painful sensory neuropathy. Angiitis and perivascular cell invasion were seen most frequently in multiple mononeuropathy, followed by sensory ataxic neuropathy. The autopsy findings of one patient with sensory ataxic neuropathy showed severe large sensory neuron loss paralleling to dorsal root and posterior column involvement of the spinal cord, and severe sympathetic neuron loss. Degrees of neuron loss in the dorsal and sympathetic ganglion corresponded to segmental distribution of sensory and sweating impairment. Multifocal T-cell invasion was seen in the dorsal root and sympathetic ganglion, perineurial space and vessel walls in the nerve trunks. Differential therapeutic responses for corticosteroids and IVIg were seen among the neuropathic forms. These clinicopathological observations suggest that sensory ataxic, painful and perhaps trigeminal neuropathy are related to ganglioneuronopathic process, whereas multiple mononeuropathy and multiple cranial neuropathy would be more closely associated with vasculitic process.
Activities of Daily Living↗
The pattern of leprosy-related neuropathy in the AMFES patients in Ethiopia: definitions, incidence, risk factors and outcome.
The ALERT MDT Field Evaluation Study (AMFES) began in 1988 and followed patients prospectively for up to 10 years after release from treatment (RFT). This paper presents the findings from this cohort with regard to neuropathy and nerve damage. Five hundred and ninety-four new cases of leprosy are included in the study, 300 multibacillary (MB) and 294 paucibacillary (PB) cases. Fifty-five percent of patients had some degree of impairment at diagnosis and a further 73 (12%) developed new nerve function impairment (NFI) after starting multiple drug therapy (MDT). The overall incidence rate for neuropathy was 39 episodes per 100 PYAR in the first year after diagnosis, gradually declining to 12 episodes per 100 PYAR in the sixth year. In those patients without impairment at diagnosis, the incidence rate of neuropathy was 25 episodes per 100 PYAR for MB cases and 11 per 100 PYAR for PB cases in the first year; in 33% of MB cases whose first episode of neuropathy occurred after diagnosis, that first episode took place after the first year, or after the normal period of treatment with MDT. Seventy-three patients with neuropathy developing after diagnosis are reported more fully: 34 (47%) had only one nerve involved and of these 25 (73%) had a single, acute episode of neuropathy. Nine (27%) had further episodes. Thirty-nine (53%) had more than one nerve involved and of these 16 (41%) had a single, acute episode, while 23 (59%) had further episodes. The terms 'chronic' and 'recurrent' neuropathy are defined and used to describe the pattern of neuropathy in those with repeated attacks. In patients with no impairment at the start of the study, treatment with steroids resulted in full recovery in 88% of nerves with acute neuropathy but only 51% of those with chronic or recurrent neuropathy. The median time to full recovery from acute neuropathy was approximately 6 months, but in a few cases recovery occurred gradually over 2-3 years. Severe neuropathy was less likely to be followed by a complete recovery than mild or moderate neuropathy. Forty-two percent of nerves with acute neuropathy that were not treated with steroids also fully recovered. In the group of patients who were thought to have old, permanent impairments at diagnosis, full recovery of nerve function occurred in 87/374 (23%) of the nerves involved. The overall outcome is illustrated by examining the average EHF score for groups of patients. Patients with no new neuropathy after diagnosis show a gradual improvement in their EHF score, while those with any episodes of neuropathy after diagnosis show a gradual deterioration after completion of MDT. Possible explanations for these findings are discussed. Risk factors for neuropathy, for chronic and recurrent neuropathy, and for a poor outcome 5 years after release from treatment, are examined. Impairment at diagnosis was the main risk factor for a poor outcome, accompanied by the occurrence of chronic/recurrent neuropathy or a reversal reaction.
Adult↗
Frequency, characteristics, and reversibility of peripheral neuropathy during treatment of advanced multiple myeloma with bortezomib.
PURPOSE: To determine the frequency, characteristics, and reversibility of peripheral neuropathy from bortezomib treatment of advanced multiple myeloma. PATIENTS AND METHODS: Peripheral neuropathy was assessed in two phase II studies in 256 patients with relapsed and/or refractory myeloma treated with bortezomib 1.0 or 1.3 mg/m2 intravenous bolus on days 1, 4, 8, and 11, every 21 days, for up to eight cycles. Peripheral neuropathy was evaluated at baseline, during the study, and after the study by patient-reported symptoms using the Functional Assessment of Cancer Therapy Scale/Gynecologic Oncology Group-Neurotoxicity (FACT/GOG-Ntx) questionnaire and neurologic examination. During the study, peripheral neuropathy was also evaluated by investigator assessment. A subset of patients underwent nerve conduction studies (n = 13). RESULTS: Before treatment, 194 (81%) of 239 patients had peripheral neuropathy by FACT/GOG-Ntx questionnaire, and 203 (83%) of 244 patients had peripheral neuropathy by neurologic examination. Treatment-emergent neuropathy was reported in 35% of patients, including 37% (84 of 228 patients) receiving bortezomib 1.3 mg/m2 and 21% (six of 28 patients) receiving bortezomib 1.0 mg/m2. Grade 1 or 2, 3, and 4 neuropathy occurred in 22%, 13%, and 0.4% of patients, respectively. The incidence of grade > or = 3 neuropathy was higher among patients with baseline neuropathy by FACT/GOG-Ntx questionnaire compared with patients without baseline neuropathy (14% v 4%, respectively). In all 256 patients, neuropathy led to dose reduction in 12% and discontinuation in 5%. Of 35 patients with neuropathy > or = grade 3 and/or requiring discontinuation, resolution to baseline or improvement occurred in 71%. CONCLUSION: Bortezomib-associated peripheral neuropathy seemed reversible in the majority of patients after dose reduction or discontinuation. Although severe neuropathy was more frequent in the presence of baseline neuropathy, the overall occurrence was independent of baseline neuropathy or type of prior therapy.
Adult↗
Evaluation of a new indicator test for sudomotor function (Neuropad) in the diagnosis of peripheral neuropathy in type 2 diabetic patients.
UNLABELLED: Sudomotor neuropathy is associated with reduction of plantar sweating and contributes to the pathogenesis of diabetic foot ulcers. The aim of the present study was to evaluate the new indicator test for sudomotor function (Neuropad) in the diagnosis of peripheral neuropathy among type 2 diabetic patients. This study included 104 type 2 diabetic patients (51 men) with a mean age of 64.2+/-5.6 years and a mean diabetes duration of 12.8+/-3.7 years. Peripheral neuropathy was diagnosed by means of the Diabetic Neuropathy Index (DNI). Sudomotor neuropathy was assessed by means of colour change in the indicator test. Peripheral neuropathy was diagnosed in 71 patients (68.3 %). Sudomotor neuropathy was diagnosed in 67 patients (94.4 %) with peripheral neuropathy and in 10 patients (30.3 %) without peripheral neuropathy (p=0.0001). Compared with DNI, sensitivity of the indicator test for diagnosing peripheral neuropathy was 94.4 % and specificity was 69.7 %. Overall prevalence of neuropathy was higher using the indicator test (77 patients, 74.0 %) than using the DNI (71 patients, 68.3 %). Time until complete colour change of the indicator test was 23.8+/-6.7 min in patients with peripheral neuropathy and 7.7+/-1.2 min in patients without peripheral neuropathy (p=0.001). Among patients with peripheral neuropathy, time until complete colour change of the indicator test was 14.2+/-1.9 min in those with a DNI value between 2.5 and 4.5, while it was 32.8+/-2.6 min in those with a DNI value between 5 and 8 (p=0.003). CONCLUSIONS: Use of the new indicator test has a very high sensitivity in detection of diabetic peripheral neuropathy. Sudomotor dysfunction can be demonstrated in a considerable part of patients with normal clinical examination. Time until complete colour change of the indicator test is associated with severity of peripheral neuropathy.
Diabetes Mellitus, Type 2↗
Peripheral neuropathy in liver cirrhosis.
BACKGROUND AND AIMS: Neuropathy in association with chronic liver disease, including cirrhosis, is recognized; however, there are differences in the incidence and type of neuropathy reported. The causal relationship of liver disease to neuropathy has been questioned. This study was designed to evaluate the incidence and character of peripheral neuropathy in patients with liver cirrhosis. The effect of alcohol consumption, severity of liver disease and encephalopathy on the incidence and severity of neuropathy were also studied. METHODS: Patients having an identifiable cause of peripheral neuropathy, except alcohol, were excluded from the study. Patients with evidence of vitamin B12 deficiency or diabetes were also excluded from the study. In this study, 33 patients with liver cirrhosis were evaluated clinically and electrophysiologically to detect any evidence of peripheral neuropathy. Nerve conduction studies were performed in the upper and lower limbs using surface electrodes. These patients also underwent a detailed clinical examination. RESULTS: Clinical signs of peripheral neuropathy were found in seven (21%) patients. Nerve conduction studies were abnormal in 24 (73%) patients. The pattern of involvement was predominantly of an axonal sensory motor polyneuropathy. Neuropathy was found both in patients with alcohol-related and non-alcohol-related cirrhosis. The presence of encephalopathy did not have a significant bearing on the incidence and severity of neuropathy. The neuropathy was also not significantly related to the severity of liver disease. CONCLUSIONS: The present study reveals that a significant number of patients with liver cirrhosis show evidence of peripheral neuropathy, which is present regardless of the etiology of cirrhosis, and is subclinical in a majority of these patients. The cause of neuropathy was probably the liver disease itself, as the incidence and severity of neuropathy in the alcohol-related cirrhosis, although higher, was not significantly different from the neuropathy in patients with non-alcohol-related cirrhosis.
Chi-Square Distribution↗
Contribution of nerve biopsy findings to the diagnosis of disabling neuropathy in the elderly. A retrospective review of 100 consecutive patients.
Peripheral neuropathy is an important factor of disability in the elderly. In order to learn more on the usefulness of intensive evaluation of patients over 65 years of age with subacute or chronic disabling peripheral neuropathy, we reviewed the clinical and nerve biopsy findings of the last 100 patients of this age group who suffered from a peripheral neuropathy severe enough to justify performance of a nerve biopsy for a diagnostic or prognostic purpose. Normal nerve biopsy findings led to the diagnosis of lower motor neuron disease in three patients and pointed to lesions of the spinal roots in six other patients. Necrotizing arteritis was demonstrated in the biopsy specimens of 23 patients, and non-necrotizing vasculitis in five. In five additional patients the diagnosis of vasculitic neuropathy was kept in spite of non-contributive biopsy findings. In two diabetic patients who had a multifocal neuropathy the biopsy also revealed the presence of vasculitis. Thus 35% of the patients included in this series had one form or another of vasculitic neuropathy. Fourteen patients had a chronic inflammatory demyelinating polyneuropathy. In 11 patients the neuropathy was associated with monoclonal gammopathy, which was benign in nine and associated with malignant plasma cell dyscrasia in two. Among the six patients with diabetes mellitus, two patients who presented with a multifocal neuropathy were found to have vasculitis in the nerve specimen; in the others the biopsy was performed because of uncommonly severe pains or motor involvement due to an extremely severe diabetic neuropathy. Six patients suffered from a long-lasting disability secondary to a drug-induced neuropathy. The remaining 15% had neuropathies of different origin, including amyloidosis, lepromatous leprosy, carcinomatous neuropathy and alcoholic neuropathy. Six patients had a mild, non-progressive or slowly progressive axonopathy of unknown origin, ageing of the peripheral nervous system may have played a role in its development. Our findings show that vasculitis is an important and treatable cause of disabling neuropathy in the elderly and that the proportion of patients with severe neuropathy of unknown origin is small.
Aged↗
Ulnar neuropathy. Incidence, outcome, and risk factors in sedated or anesthetized patients.
BACKGROUND: Ulnar neuropathy is well-recognized as a potential complication of procedures performed on anesthetized patients. However, reported outcomes and risk factors for this problem are based on small series and anecdotes. METHODS: We retrospectively reviewed the perioperative courses of 1,129,692 consecutive patients who underwent diagnostic and noncardiac surgical procedures with concurrent anesthetic management at the Mayo Clinic from 1957 through 1991 (inclusive). The medical diagnoses of patients who had these procedures were scanned for 26 diagnoses associated with neuropathy. Persistent neuropathy of an ulnar nerve was defined as a sensory or motor deficit of greater than 3 months' duration. Risk factors anecdotally associated with persistent neuropathy were analyzed by comparing patients with an ulnar neuropathy with control subjects in a 1:3 case-control study. RESULTS: Persistent ulnar neuropathies were identified in 414 patients, a rate of 1 per 2,729 patients. Of these, 38 (9%) patients had bilateral neuropathies. Approximately equal numbers of the neuropathies included sensory loss only or mixed sensory and motor loss. Initial symptoms form most neuropathies were noted more than 24 h after the procedure. Factors associated with persistent ulnar neuropathy included male gender and a duration of hospitalization of more than 14 days (P < 0.01). Neuropathy was more likely to develop in very thin and obese patients than in patients with average body habitus. Neither the type of anesthetic technique nor the patient position was found to be associated with this neuropathy. Of the 382 patients who survived the 1st postoperative yr, 53% regained complete motor function and sensation and were asymptomatic. Of those with neuropathies persisting for more than 1 yr, most had moderate or greater disability from pain or weakness. CONCLUSIONS: These data suggest that perioperative ulnar neuropathies are associated with factors other than general anesthesia and intraoperative positioning. Men at the extremes of body habitus who have prolonged hospitalizations are particularly susceptible to development of ulnar neuropathies.
Adult↗
A profile of childhood neuropathies at a university hospital in Oman.
OBJECTIVE: To analyze all cases of childhood neuropathies (under 14 years of age) and report on their profile, pattern, clinical features and management. METHODS: Children with acute flaccid paralysis, longstanding weakness of extremities, neuroregression and children receiving anti cancer drugs with symptoms suggestive of neuropathy were evaluated for evidence of peripheral neuropathy. The evaluation of children with acute flaccid paralysis was a prospective study from January 1992 through to December 2000. The rest of the patients were studied retrospectively from the hospital medical records, pediatric neurology outpatient clinic and the neurophysiology laboratory, Sultan Qaboos University Hospital, Al-Khod, Oman RESULTS: Eighty-two (39 Male: 43 Female) children were found to have peripheral neuropathy. Acute Guillain-Barré [corrected] syndrome was the most common with 37 children (45.1%), followed by genetic neuropathies [hereditary motor and sensory neuropathy with 17 (20.7%), hereditary sensory and autonomic neuropathy with 2 (2.4%), hereditary spastic paraplegia associated neuropathy with 9 (11%) and metachromatic leucodystrophy with 9 (11%)]. Chronic inflammatory demyelinating neuropathy was seen in 5 (6.1%) and vincristine induced neuropathy in 3 (3.5%) children. CONCLUSION: Acute Guillain-Barré [corrected] syndrome is the most common neuropathy amongst the acquired neuropathies. The treatable neuropathies constituted 54.7% (45 children) and the preventable genetic neuropathies accounted for the remaining 45.3% (37 children)
Adolescent↗
Diabetic neuropathy in elderly patients. What can be done?
The prevalence of diabetes mellitus increases markedly with age. Furthermore, advancing age is a strong risk factor for diabetic neuropathy, independent of the duration of diabetes mellitus and glycaemic control. Several biological changes occurring during the aging process may account for the facilitating effect of age on diabetic neuropathy. These include an increase in the production of advanced glycosylation end-products (AGEs), a defect in the polyol pathway, nerve vascular alterations and impaired resistance to oxidative stress. The clinical diagnosis of diabetic neuropathy is often difficult in elderly patients. The relationship between symptoms and neuropathy and that between neuropathy and diabetes mellitus are more difficult to ascertain in elderly patients due to age-related changes in the peripheral and autonomic nervous system and associated diseases frequently encountered in this population. Diagnosis of diabetic neuropathy is based on nerve conduction studies, vibratory perception threshold determination and assessment of autonomic function. For most of these tests, reference values are markedly influenced by age and their interpretation should use carefully age-adjusted reference intervals. Identification of peripheral diabetic neuropathy indicates a high risk of foot complications, such as ulcers and gangrene, often resulting in amputation, whereas cardiovascular autonomic neuropathy is associated with an increased risk of postural hypotension and coronary events. All these risks increase markedly with aging. Therapeutic trials in elderly patients with diabetic neuropathy are lacking. Treatment of diabetic neuropathy consists of achievement of better glycaemic control and treatment of symptoms related to neuropathy. Specific treatments capable of preventing or curing neuropathy are under investigation. The interesting results obtained with aldose reductase inhibitors in animal studies contrast with disappointing results in patients with diabetes mellitus. Other metabolic approaches, like antioxidants and gamma-linolenic acid, seem promising. Clinical complications of diabetic neuropathy in the elderly are often severe. Early detection is required, since at the present time a preventive approach is the most effective way to avoid or postpone debilitating complications. More research is needed to make effective curative treatments of diabetic neuropathy available.
Age Factors↗
Occurrence, predictors, and clinical significance of autonomic neuropathy in NIDDM. Ten-year follow-up from the diagnosis.
Little is known about the occurrence and predictive factors of autonomic neuropathy and its relationship to cardiovascular mortality in NIDDM patients, and no long-term follow-up studies including nondiabetic control subjects are available. A total of 133 patients with newly diagnosed NIDDM (70 men) and 144 control subjects (62 men) were examined at baseline and after 5 and 10 years of follow-up. Deep-breathing tests (baseline, 5-year, and 10-year) and active orthostatic tests (5- and 10-year) were performed. Criteria for autonomic neuropathy were parasympathetic (expiration-to-inspiration ratio </- 1.10), sympathetic (systolic blood pressure decrease >/- 30 mmHg in the orthostatic test), and combined autonomic neuropathy (parasympathetic with sympathetic neuropathy). The frequency of parasympathetic neuropathy (NIDDM patients versus control subjects) was 4.9 vs. 2.2% (P = 0.224) at baseline, 19.6 vs. 8.5% (P = 0.017) at 5 years, and 65.0 vs. 28.0% (P < 0.001) at 10 years of follow-up. The frequency of sympathetic neuropathy was 6.8 vs. 5.6% (P = 0.709) at 5 years and 24.4 vs. 9.0% (P = 0.003) at 10 years of follow- up. These figures for combined autonomic neuropathy were 2.1 vs. 1.8% (P = 0.869) at 5 years and 15.2 vs. 4.2% (P = 0.007) at 10 years of follow-up. NIDDM patients with parasympathetic neuropathy at the 10-year examination showed worse glycemic control and higher insulin values than those without parasympathetic neuropathy. Furthermore, in our subjects, women were more prone to have parasympathetic neuropathy than men. Parasympathetic neuropathy at baseline was more frequent in those who died from a cardiovascular cause than those who did not (13 vs. 3%, P = 0.045). Similarly, sympathetic autonomic nervous dysfunction at the 5-year examination predicted the 10-year cardiovascular mortality. In conclusion, the frequency of autonomic neuropathy in NIDDM patients increases sharply with time. The development of autonomic neuropathy is connected with poor glycemic control. Interestingly, a high insulin level seems to have a predictive role in the development of parasympathetic autonomic neuropathy irrespective of obesity and glycemia.
Autonomic Nervous System Diseases↗
Neuropathies associated with excessive exposure to lead.
Exposure to lead is a ubiquitous problem of the modern era. The majority of cases of all forms of lead intoxication, especially lead neuropathy, result from industrial exposure. In the Western world meticulous monitoring in industry has reduced the risk of overt lead neuropathy. The classic form of lead neuropathy consists of weakness that primarily involves the wrist and finger extensors but which later spreads to other muscles. There is only minimal sensory involvement. Less commonly, there is a more typical toxic neuropathy with distally accentuated sensory and motor involvement. The motor neuropathy is more likely to develop following relatively short-term exposure to high lead concentrations and evolves in a subacute fashion. Prognosis for recovery is good as long as exposure is terminated promptly. The distal sensory and motor neuropathy develops after many years of exposure, evolves more slowly, and recovery is less certain. There is a generally weak relationship between the development of lead neuropathy and blood lead levels, at least for the subacute motor neuropathy, leading to speculation that the metabolic basis for the neuropathy is interference with porphyrin metabolism. Lead intoxication in humans causes axonal degeneration, but in some other species it causes a primarily demyelinating neuropathy. It should be possible to prevent lead neuropathy by good industrial hygiene. Close monitoring should identify excessive lead exposure before it causes overt neuropathy. If evidence of excessive exposure is found or if overt neuropathy develops, exposure must be terminated immediately. The role of chelation therapy in the treatment of lead neuropathy is controversial.
Animals↗
Pudendal neuropathy and the importance of EMG evaluation of fecal incontinence.
A prospective study was undertaken to evaluate pudendal neuropathy in fecal incontinence. Fifty-two patients (38 women and 14 men) with fecal incontinence underwent manometric and electromyographic evaluation (measurement of pudendal nerve terminal motor latency [PNTML] and sphincter muscle mapping). The average age of all patients was 54 +/- 17 years. Fifty-two percent (27/52) were found to have a pudendal neuropathy (PNTML > 2.1 milliseconds). Seventeen of these 27 patients (63 percent) had a bilateral pudendal neuropathy. Patients with a pudendal neuropathy were older than those without a neuropathy (63.7 years vs. 51.9 years; P = 0.01). Women were significantly more likely than men to have a pudendal neuropathy (P = 0.03). Nine patients had an anatomic sphincter defect identified, and six of these (67 percent) had a neuropathy; 4/6 (67 percent) had a bilateral pudendal neuropathy. In the 43 patients who did not have an anatomic sphincter defect, there was no difference in resting pressure (69 mmHg vs. 60 mmHg; P = 0.4) or maximum voluntary contraction (95 mmHg vs. 86 mmHg; P = 0.5) when patients without a neuropathy were compared with those with a neuropathy. Patients with a pudendal neuropathy had a shorter sphincter length than those without a neuropathy (3.0 cm vs. 3.9 cm; P = 0.01). Bilateral pudendal neuropathy tended to occur more frequently in women (P = 0.08) and was not associated with poorer resting pressure, maximum voluntary contraction, or shorter sphincter length. We conclude that pudendal neuropathy is a common cause of fecal incontinence, particularly in older women, and frequently occurs in association with a sphincter defect. Manometric evaluation alone is not helpful in identifying the neuropathic patient. PNTMLs should be routinely measured in the evaluation of fecal incontinence.
Adult↗
Utility of decompressive surgery in the prophylaxis and treatment of cisplatin neuropathy in adult rats.
Cisplatin produces a dose-dependent and dose-limiting peripheral neuropathy in patients. This study tested the hypothesis that this clinical neuropathy results from the chronic compression of peripheral nerves rendered susceptible to injury because of cisplatin-induced microtubular dysfunction. A quantitative model of cisplatin neurotoxicity was developed by administering cisplatin to rats and measuring the neuropathy by hindlimb walking track assay. The study aims were: (1) to characterize neuropathy induced by cisplatin in the adult rat; (2) to evaluate the role of decompressive surgery in the prevention of cisplatin neuropathy; and (3) to determine whether decompressive surgery was an effective treatment for established neuropathy. The assay demonstrated an increased print length in animals after 8 weeks of cisplatin (p < 0.01). This neuropathy progressed for 6 weeks after cisplatin was stopped, and reversed slowly over 3 months. These abnormalities were prevented by early tarsal tunnel decompression. Decompressive surgery was also beneficial, if performed early in the course of the neuropathy; abnormalities reversed in 5 weeks and remained normal for the remainder of the study. Control animals had progressive abnormalities which slowly resolved over a period of 18 weeks after discontinuing cisplatin. However, decompressive surgery performed after the neuropathy was established did not alter the neuropathic walking-track pattern. These studies provide insight into the etiology and possible therapeutic approaches to cisplatin neuropathy. Although further studies are required, they suggest that, in selected patients, decompressive surgery may have a role in the prevention or early treatment of cisplatin-induced neuropathy. Patients with underlying clinical or subclinical compressive neuropathies could be at high risk for the development of cisplatin neuropathy, and quantitative monitoring of neuropathies may be useful.
Animals↗
Paraneoplastic peripheral neuropathy associated with anti-Hu antibodies. A clinical and electrophysiological study of 20 patients.
Although paraneoplastic subacute sensory neuronopathy is the most frequent presentation of peripheral neuropathy in patients with anti-Hu antibodies, other neuropathies have been reported. In order to investigate the clinical and electrophysiological manifestations of neuropathies associated with anti-Hu antibodies, we conducted a retrospective study of 20 patients. For the electrophysiological study, each nerve was classified as normal, demyelinating, axonal/neuronal or axonal/demyelinating. Peripheral neuropathy was the presenting symptom in 95% of patients. CNS and autonomic neuropathy were present in 40% and 30% of patients, respectively. The course of the neuropathy was acute, mimicking Guillain-Barré syndrome in one patient (5%), and subacute (55%) or progressive (40%) in the others. Clinically, the neuropathy was sensory (70%), sensorimotor (25%) or motor (5%). At onset, symptoms were symmetrical (65%), asymmetrical (25%) or multifocal (10%). Pain was a predominant manifestation (80%). Amyotrophia and fasciculations were rare. The median Rankin's score was 2, three patients having an indolent form. Electrophysiology showed the axonal/neuronal pattern to be the most frequent (46.9% of studied nerves); an axonal/demyelinating or demyelinating pattern being seen in 18.3% and 4.9% of nerves, respectively. The axonal/neuronal pattern was more frequent in sensory nerves and the mixed axonal/demyelinating pattern more frequent in motor nerves (P < 0.01). A higher proportion of abnormal nerves correlated with a progressive course (P < 0.05) or a Rankin's score between 3 and 5 (P < 0.01). In patients with sensory neuropathy, 88.5% of sensory nerves were abnormal, mostly with an axonal/neuronal pattern. In addition, 47% of motor nerves were abnormal so that only four out of 14 patients with a clinically pure sensory neuropathy (28.6%) had an electrophysiological pattern typical of sensory neuronopathy. In patients with a sensorimotor neuropathy, 96.6% of sensory and 71% of motor nerves were abnormal. The only statistical difference between sensory and sensorimotor neuropathies was that patients with sensorimotor neuropathy had more frequent motor nerve involvement (P < 0.05) without differences concerning the distribution of the abnormal patterns. Needle neuromyography showed only limited evidence of motor neurone degeneration in both sensory and sensorimotor neuropathy. The present work shows that the typical clinical and electrophysiological pattern of subacute sensory neuronopathy is rarely encountered in patients with anti-Hu antibody and that motor nerve involvement is frequently seen, even in the absence of a motor deficit. In addition to their potential pathophysiological involvement in the mechanism of the paraneoplastic neuropathy, these findings have practical consequences for the diagnosis of the disorder.
Aged↗