Subclinical Peripheral Nerve Involvement Research Articles

Electrophysiological profile of serum vitamin B12 levels, correlation with serum methylmalonic acid levels, and determination of subclinical peripheral nerve involvement

Background/Aim: Vitamin B12 is essential for normal neural conduction in peripheral nerves. This study aimed to investigate the electrophysiological profile for varying degrees of serum B12 levels and to determine whether a correlation existed between electrophysiological profiles and serum methylmalonic acid (MMA) levels. Also, determination of subclinical peripheral nerve involvement with cold administration was planned in serum B12 levels. Methods: A total of 101 (63 females, 38 males) subjects with known serum vitamin B12 levels were selected randomly from the neurology outpatient clinic for this study. The subjects were divided into three groups based on the serum total Vitamin B12 levels: (1) B12 deficiency (<126 pg/mL), (2) low B12 (126-250 pg/mL), and (3) normal B12 (250–500 pg/mL). Serum MMA and nerve conduction studies (NCS) were assessed and compared between the three groups. After the cooling procedure was applied to the ulnar and sural nerves, NCS was repeated. Results: There were 13 subjects in the B12 deficiency group, 44 subjects in the low B12 group, and 44 subjects in the normal group. We found that ulnar sensory nerve action potential amplitudes were significantly decreased (P = 0.009), ulnar F latency (P = 0.003; P < 0.001)) was prolonged, and peroneal combined muscle action potential amplitudes decreased (P = 0.026) in the B12 deficiency when compared with the low and normal B12 groups. Sural nerve amplitude and conduction velocities were found to be significantly abnormal after the cold application in all groups (P < 0.001). The increase in sural nerve sensory nerve amplitude potentials (SNAP) amplitudes was higher in the B12 deficiency group than in the other groups. Mean serum MMA levels were high in all groups. A correlation of nerve conduction study (NCS) changes with serum vitamin B12 and MMA was not observed in the groups after cold application. Conclusion: Vitamin B12 deficiency may cause subclinical sensorial and motor axonal nerve conduction changes. Nerve conduction changes may not always reach pathological values based on electrophysiological studies but may be detected after cooling administration even in the normal serum B12 levels. A correlation between serum MMA and vitamin B12 levels was found. Therefore, serum levels of vitamin B12, which is important for nerve conduction, should be carefully evaluated in clinical practice.

Abstract 27: Neuropathy in primary hypothyroidism and response to thyroxine replacement

Background: Entrapment neuropathy and sensorimotor polyneuropathy has been described as a manifestation of hypothyroidism in many studies. Only few studies are available in Indian population to know the extent of neuropathies in hypothyroid patient and effect of thyroxine replacement on these abnormalities.Aims and Objectives: To study the extent and pattern of peripheral nerve involvement in hypothyroid (subclinical and overt) patients and the response to optimal thyroid hormone replacement in them.Methods: Consecutive patients with primary hypothyroidism were clinically and electrophysiologically evaluated for peripheral nerve dysfunction at baseline and after achieving euthyroid status.Results: A total of 61 patients, were studied (Mean age 39.2 yrs, Range 19 - 55 yrs, Mean TSH 22.32 ±15.6 IU/ml). Baseline clinical examination was abnormal in 13 (21.3%) and electrophysiology was abnormal in 21 (34.4%). Among these, 6 (29%) had demyelination, 8 (38%) axonal neuropathy and 07 (33%) entrapment neuropathy. After optimal thyroxine replacement, 14 (67%) showed complete recovery. While 8 (72.7%) out of 11 with sensory axonal neuropathy showed significant improvement, all 04 patients with motor neuropathy showed significant improvement. One patient with demyelinating neuropathy did not show any improvement. Out of 7 patients with CTS, 5 (71.4%) showed improvement after thyroxine replacementConclusion: Subclinical peripheral nerve involvement is frequent in primary hypothyroidism and most cases responds well to optimum thyroxine replacement.

Organophosphate induced delayed neuropathy after an acute cholinergic crisis in self-poisoning

Introduction Despite organophosphate pesticide is the most prevalent cause of acute poisoning in low- and middle-income countries, data on organophosphate induced delayed neuropathy (OPIDN) are limited. We aimed to characterize organophosphates’ long-term effects on the peripheral nervous system after an acute cholinergic crisis in adults. Methods We performed a prospective observational study in an academic hospital of north India in patients aged 13–40 years with acute organophosphate ingestion. After resolving the cholinergic crisis, the patients were followed for six months with neurologic assessments, including history, neurologic examination, and nerve conduction study (NCS). Results Twenty-three patients were recruited to the study. All but one had normal neurological examination and NCS at discharge from hospital a median duration of six days (interquartile range, 3–10) after self-poisoning. Eight (34.8%) developed OPIDN during the six-month follow-up. Three patients had symptomatic neuropathy, and NCS detected subclinical peripheral nerve involvement in five. All cases were associated with chlorpyrifos ingestion (8/17 total chlorpyrifos cases). Two OPIDN cases had foot drop and gait ataxia at three-month which persist at six-month. One patient had distal paresthesia at three months, which improved at a six-month follow-up. NCS in OPIDN cases invariably revealed axonal degeneration, injury to motor fibers more than sensory fibers, and frequent peroneal nerve involvement. None of the baseline characteristics, including the ingested amount, predicted clinical or subclinical OPIDN in chlorpyrifos self-poisoned patients on a univariant analysis. Conclusion Peripheral nerve involvement is not uncommon after recovery from a cholinergic crisis in chlorpyrifos self-poisoning and debilitating in some patients. Detection of subclinical injury on NCS may provide an early window to prevent severe symptomatic neuropathy.

Nerve ultrasound shows subclinical peripheral nerve involvement in neurofibromatosis type 2.

Neurofibromatosis type 2 (NF2) is mainly associated with central nervous system (CNS) tumors. Peripheral nerve involvement is described in symptomatic patients, but evidence of subclinical peripheral nerve involvement is scarce. We conducted a cross-sectional pilot study in 2 asymptomatic and 3 minimally symptomatic patients with NF2 to detect subclinical peripheral nerve involvement. Patients underwent clinical examination, nerve conduction studies (NCS), and high-resolution ultrasonography (HRUS). A total of 30 schwannomas were found, divided over 20 nerve segments (33.9% of all investigated nerve segments). All patients had at least 1 schwannoma. Schwannomas were identified with HRUS in 37% of clinically unaffected nerve segments and 50% of nerve segments with normal NCS findings. HRUS shows frequent subclinical peripheral nerve involvement in NF2. Clinicians should consider peripheral nerve involvement as a cause of weakness and sensory loss in the extremities in patients with this disease. Muscle Nerve 57: 312-316, 2018.

BMI, HOMA-IR, and Fasting Blood Glucose Are Significant Predictors of Peripheral Nerve Dysfunction in Adult Overweight and Obese Nondiabetic Nepalese Individuals: A Study from Central Nepal.

Objective. Nondiabetic obese individuals have subclinical involvement of peripheral nerves. We report the factors predicting peripheral nerve function in overweight and obese nondiabetic Nepalese individuals. Methodology. In this cross-sectional study, we included 50 adult overweight and obese nondiabetic volunteers without features of peripheral neuropathy and 50 healthy volunteers to determine the normative nerve conduction data. In cases of abnormal function, the study population was classified on the basis of the number of nerves involved, namely, “<2” or “≥2.” Multivariable logistic regression analysis was carried out to predict outcomes. Results. Fasting blood glucose (FBG) was the significant predictor of motor nerve dysfunction (P = 0.039, 95% confidence interval (CI) = 1.003–1.127). Homeostatic model assessment of insulin resistance (HOMA-IR) was the significant predictor (P = 0.019, 96% CI = 1.420–49.322) of sensory nerve dysfunction. Body mass index (BMI) was the significant predictor (P = 0.034, 95% CI = 1.018–1.577) in case of ≥2 mixed nerves' involvement. Conclusion. FBG, HOMA-IR, and BMI were significant predictors of peripheral nerve dysfunction in overweight and obese Nepalese individuals.

AB0718 Ultrasonographic assessment of subclinical median and ulnar nerve involvement in rheumatoid arthritis

BackgroundThe prevalence of subclinical neuropathy in Rheumatoid Arthritis (RA) is 65-85% (1). It has been shown that RA patients may have electrophysiological or histological abnormalities even in the absence of...

Peripheral nervous system involvement in patients with sickle cell disease

Peripheral nervous system involvement is rare in sickle cell disease (SCD). The aim of this study is to determine the peripheral nerve involvement electrophysiologically in SCD patients without clinically evident neurological signs, symptoms and to determine the relationship between the frequency of sickle cell crisis and peripheral neuropathy. Fifty-one patients with SCD and fifty-one healthy controls were enrolled to the study. Conventional electrophysiological studies of peripheral nerves were performed to all subjects. The data about the frequency of sickle cell crisis were obtained. Peripheral nervous system involvement was detected in ten (19.6%) patients. Five (9.8%) patients had sensorimotor axonal neuropathy, two (3.9%) sensory axonal neuropathy, one (2%) patient had ulnar sensory neuropathy and two (3.9%) had median sensory neuropathy. Sural nerve sensorial action potential was unobtainable in eight (15.7%) patients and prolonged F latencies were observed in three (5.9%). The frequency of neuropathy was higher in SCD patients when compared with the controls. The frequency of sickle cell crisis was not significantly correlated with peripheral neuropathy. Subclinical peripheral nerve involvement may be seen in SCD patients. Electrophysiological examinations are recommended in routine examination to diagnose early neuropathy in SCD patients without neurologic symptoms.

Neurological complications of swine influenza vaccination.

The emphasis upon the remarkably large number of cases of Guillain-Barre syndrome which resulted from the 1976 National Swine Influenza immunization program in the U.S.A. has obscured the fact that other neurological complications, involving the central nervous system also occurred. The anatomical distribution of lesions is almost identical with that seen following other types of vaccination: involvement of the brain, cerebellum, optic nerve, cranial nerves and spinal cord occurred with approximately the same frequency. 5 instances of the very rare subacute or chronic, progressive, post-vaccinal encephalopathy are described, a situation which is identical to the subacute and chronic forms of polyradiculoneuropathy. In a number of cases, in particular the myelopathies, a subclinical involvement of peripheral nerves was demonstrated by means of electrodiagnostic studies, illustrating the often overlooked fact that central nervous system involvement will mask peripheral nerve lesions. The etiological significance of the swine influenza vaccination was overlooked and completely erroneous diagnoses were established in a surprisingly large number of the 26 new cases reported here.

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.

Peripheral neuropathy in patients with hepatitis virus C infection in the Amazon region

Hepatitis virus C (HCV) infection is considered a health problem in the State of Acre localized in the Brazilian Amazon which has a prevalence rate of 5.9%. Peripheral neuropathy is a common extra-hepatic manifestation in patients with HCV. To determine the prevalence of peripheral neuropathies using clinical and neurophysiological parameters. A cross sectional study was performed in patients assisted by a specialized center of infectious diseases in the State of Acre. All patients completed a clinicoepidemiological questionnaire, physical examination and nerve conduction studies (NCS). We studied 78 patients with mean age 45.5 years (range from 10 to 76 years), two thirds were male, 51% had at least 8 years of formal education and 96% lived in the capital city of Acre State. Roughly 34% of patients complained about paresthesias mainly in upper limbs. The NCS diagnosed multiple mononeuropathy in 11 (14.1%; IC95% 7.6-23.2) patients and carpal tunnel syndrome in 4 (5.1%) patients. Subclinical involvement of peripheral nerves seems common in patients with HCV, with multiple mononeuropathy the main manifestation of nerve injury in this region as suggested by electrophysiological studies.

SUB‐CLINICAL PERIPHERAL NERVE INVOLVEMENT IN PSORIATIC ARTHRITIS

Immunological studies document the role of HLA in psoriasis and the correlation between neuropeptides, psoriasis, and related arthritis. Some anecdotal case reports, moreover, describe a noncasual association between peripheral neuropathy and psoriatic manifestations. To verify a possible subclinical peripheral nerve involvement in this disimmune pathology, we started a pilot study in twenty patients with psoriatic arthritis and in whom other common causes of peripheral neuropathies had been ruled out.We performed a complete clinical neurological examination and a neurophysiological examination (orthodromic sensory and motor nerve conduction velocity in median and tibial nerves; antidromic sensory nerve conduction velocity in sural nerve).In 40% of the patients there was a mild but definite “glove‐stocking” hypoesthesia, while hypopallesthesia was detected in only 20%. Electrophysiologic examinations were less informative borderline distal conduction velocities in 30% of patients.These preliminary data suggest a peripheral nerve involvement in this pathology, mainly affecting the small nerve fibres.

Subclinical peripheral nerve involvement in patients with rheumatoid arthritis.

Clinical involvement of the peripheral nervous system is uncommon in rheumatoid arthritis (RA); the most common disorders are multiple mononeuritis, sensorimotor neuropathy, and entrapment neuropathy. This study was undertaken to investigate the occurrence of electrophysiologically evident peripheral nerve involvement in RA patients without a clinical history of peripheral nerve involvement. Forty RA patients were examined neurologically and electrophysiologically, and sural nerve biopsies were performed in 4. No patient reported symptoms or signs of peripheral nerve involvement. Twenty-six patients (65%) exhibited electrophysiologic findings consistent with a sensorimotor neuropathy (in 2 of them a carpal tunnel syndrome was also present), while 3 patients showed isolated carpal tunnel syndrome. There was a moderate loss of myelinated fibers in 3 of the 4 nerve biopsy samples, and all showed an increased number of endo- and perineurial vessels and some signs of axonal degeneration. Patients with RA may have electrophysiologic and histologic findings of peripheral nerve damage, even in the absence of clinical evidence of peripheral nerve involvement.

Infective neuropathies

Infective neuropathies encompass neuropathies that are among the most common in the world. Retroviral infection, which includes infection with the human immunodeficiency virus, has now spread worldwide. This virus is responsible for a number of disabling peripheral neuropathies, either from the immune reaction that follows penetration of the virus into nervous system of the host, or by opportunistic infection secondary to the major cellular immunodeficit induced by gradual destruction of lymphocytes bearing the CD4 antigen on their surface. In the other class of retroviruses, human T lymphotrophic viruses (HTLV), which are responsible for the HTLV-I-associated myelopathy or tropical spastic paraparesis, peripheral nerve involvement and inflammatory myopathy are less common and milder than in HIV infection. Leprosy continues to pose problems concerning the understanding of the immune mechanisms that lead to the various patterns of nerve lesions encountered in this condition. Chagas' disease, which is due to infection with Trypanosoma cruzi, affects more than 15 million people in Latin America. It is accompanied by mostly subclinical peripheral nerve involvement and by cardiac manifestations from lesions of the autonomic nervous system and cardiac muscle.

Subclinical peripheral nerve involvement in AIDS: an electrophysiological and pathological study.

Thirty patients with AIDS without symptoms or signs of peripheral neuropathy were compared electrophysiologically with 23 age and sex matched healthy controls. The patients had a mean reduction in the amplitude of common peroneal compound muscle action potentials of 37% (95% CI 11-70%) and of sural sensory action potentials of 34% (CI 18-49%). Mean conduction velocity of both motor and sensory nerves was reduced by between 1 and 7 m/s, with a prolongation of F waves corrected for height of 5% in the arms and 13% in the legs. The distal motor latencies were unchanged. These changes did not correlate with the duration of AIDS, degree of immunosuppression (CD4 count), Body Mass Index, albumin or vitamin B12 level. Four patients had subclinical mononeuropathies. Sural nerve taken at necropsy from five asymptomatic AIDS patients had evidence of axonal degeneration without inflammation or demyelination. There was a mean reduction in myelinated fibre density of 30.5% (CI 10-51%) compared with eight age matched sudden death controls (p = 0.01). This loss principally affected the larger fibres. The pathological and electrophysiological changes indicate axonal degeneration and are similar to those seen in other chronic disorders and in normal ageing. It is concluded that this axonal degeneration is not specific to HIV.

Peripheral nerve involvement in Bell's palsy.

A group of patients with Bell's palsy were studied in order to disclose the presence of subclinical peripheral nerve involvement. 20 patients, 8 male and 12 female, with recent Bell's palsy as their unique disease were examined. In all cases other causes of polyneuropathy were ruled out. Patients were investigated with CSF examination, facial nerve latencies in the affected and in the sound sides, and maximal motor nerve conduction velocities, as well as motor terminal latencies from the right median and peroneal nerves. CSF laboratory examination was normal in all cases. Facial nerve latencies were abnormal in all patients in the affected side, and they differed significantly from those of control group in the clinically sound side. Half of the patients showed abnormal values in the maximal motor nerve conduction velocities and motor terminal latencies of the right median and peroneal nerves. These results agree with previous reports which have pointed out that other cranial nerves may be affected in Bell's palsy. However, we have found a higher frequency of peripheral nerve involvement in this entity. These findings, support the hypothesis that in some patients Bell's palsy is the component of a more widespread disease, affecting other cranial and peripheral nerves.

Sub-clinical involvement of peripheral nerves in Hodgkin's disease.

A wide variety of non-metastatic neurological syndromes occur in association with malignant lymphoma. 20 patients with Hodgkin’s disease and 20 matched healthy subjects underwent motor nerve conduction velocity testing of the right ulnar and left median nerves. The testing was carried out 3–5 days after confirmation of the diagnosis. The clinical neurological examination was normal in all the patients. In 6 patients, pathological motor nerve conduction velocity rates were found. The results indicate a high frequency of sub-clinical peripheral neuropathy in Hodgkin’s disease even during the very early stages of the disease.