Increase In Distal Latency Research Articles

Evaluation of Esophageal Motility in Obese Patients before and after Bariatric Surgery: Role of Multichannel Intraluminal Impedance and High-resolution Manometry

Abstract Background: A high prevalence of esophageal motor disorders has been reported in obese patients. Roux-en-Y gastric bypass (RYGB) can trigger symptoms of dysphagia by worsening preexisting esophageal motor disorders. Investigation of esophageal motility with multichannel intraluminal impedance (MII) and high-resolution manometry (HRM) is available. Objective: The aim is to compare the results of MII and HRM of nonobese patients with those of obese patients before and after RYGB to identify possible preoperative predictive factors of postoperative dysphagia. Materials and Methods: Twenty-eight obese patients were evaluated with a questionnaire of symptoms, endoscopy, HRM, and MII in different postures (supine and sitting) before and 6 months after laparoscopic RYGB. They were compared with eleven nonobese subjects. Chicago classification parameters were used to characterize esophageal motility disorders. Results: Obese patients evolved with more symptoms of dysphagia after surgery (7.10% preoperatively and 32.10% postoperatively). None had gastrojejunal anastomosis stenosis. After bariatric surgery, there was an increase in distal latency (HRM) and also a decrease in esophageal alimentary bolus progression (MII). Twenty-one percent of obese patients already had some dysmotility before the surgery and 92% of them evolved to dysphagia after the operation. Conclusions: Previous esophageal motility disorder is a good predictive factor of postoperative dysphagia. HRM and MII should be performed in some situations, such as bariatric surgery for older adults and before narrowing the gastrojejunal anastomosis as a treatment for weight recidivism.

ASSESSMENT OF THE AUTONOMIC AND PERIPHERAL NERVE FUNCTION IN PATIENTS WITH THALASSAEMIC SYNDROME IN A TERTIARY CARE HOSPITAL - A CROSS SECTIONAL STUDY

INTRODUCTION: β-thalassaemia is an inherited disorder of haemoglobin characterized by an absence or reduced synthesis of the β-globin chain. The net result is an excess of α-chains, which precipitate and destroy the red cell precursors, leading to anaemia, skeletal changes, splenomegaly and numerous other complications. Treatment is by regular blood transfusion coupled with iron chelation therapy to prevent iron accumulation and organ damage. AIM: To assess the autonomic and peripheral nerve function in patients with thalassaemic syndrome. MATERIALAND METHODS: Patients attending the Thalassaemia Clinic of Medical College Hospital, Kolkata. Indoor patients from Medicine st th ward and Institute of Haematology and Transfusion Medicine wards of Medical College Hospital, Kolkata from 1 May 2008 to 30 April 2009. After inclusion patients were divided into following groups: Group1 (THAL1): Patients requiring regular blood transfusion and are either receiving inadequate iron chelation or no iron chelation at all. Group2 (THAL2): Patients who require regular blood transfusion and are receiving adequate iron chelation. Group3 (THAL3): Patients who do not require regular blood transfusion RESULT: The median value of distal latency of right common peroneal nerve is slightly increased in all 3 groups. The normal value should be < 4.55ms, thus increase in distal latency is seen in all 3 groups. The median values of distal latency of left common peroneal nerve as well as distal latency of common peroneal nerve as a whole is within normal limits. Distal latency of common peroneal nerve (p value=0.012). Proximal latency of left common peroneal nerve(p value=0.013). Proximal latency of common peroneal (p value=0.001) CONCLUSION: There is demyelinating type of neuropathy of right common peroneal nerve of all the groups. This indicates presence of motor peripheral neuropathy in patients of thalassaemia. All other latencies and amplitudes of both motor and sensory nerves are within normal limits. There were statistically increased motor latencies in patients receiving iron chelation therapy with adequate chelation when compared to the other groups, although the overall latency was within acceptable limits of the laboratory standards. This may be due to subclinical affection of the motor nerves in the form of demyelination. Therefore, the role of toxic effects of iron chelator on peripheral nerves needs to be studied further.

Neurophysiological biomarkers of peripheral nervous system affection in patients with stable chronic obstructive pulmonary disease (COPD)

BackgroundChronic obstructive pulmonary disease (COPD) is accompanied by substantial systemic dysregulations that comprise systemic inflammation and neurohormonal activation in addition to many neurological involvements, such as cerebrovascular diseases, polyneuropathies, motor neuron diseases, and cognitive impairment has been described in COPD patients. The aim of the current work was to detect the subclinical affection of the peripheral nervous system in patients with stable COPD.ResultsForty COPD patients and 30 subjects as healthy control were enrolled. All included subjects were submitted to complete medical history, clinical evaluations, investigations in the form of; arterial blood gases, spirometry, in addition to nerve conduction study. The patients with COPD were classified according to GOLD criteria for severity in grade I in 7.5% grade II in 62.5%, grade III in 20%, and grade IV in 10%. The results show a statistically significant increase in distal latency and a statistically significant decrease of amplitude and conduction velocity in patients with COPD when compared to the examined nerves of control group. The demyelinating nerve affection was the most common.ConclusionIn COPD patients the peripheral nervous system could be affected subclinically once the severity of COPD increased and the patient should be neurophysiologically observed for early recognition of peripheral nervous system affection.

A guillain-barre syndrome revealing cutaneous leishmaniasis in an immunocompetent adolescent

Guillain-Barre Syndrome (GBS) is an acute autoimmune polyradiculoneuropathy, that often follows an antecedent infection. Leishmaniasis is a zoonosis due to a flagellate protozoan of the Leishmania genus and transmitted by the sandfly. Here we report a 15 years old teenager who presented with an ascending installation of the motor deficit in three weeks associated with dysphonia and swallowing disorders. The physical examination showed a flaccid proximo-distal quadriparesis, akinesthesia, apallesthesia and cutaneous lesions on the forehead, wrist and calf that appeared two months earlier. The HIV serology was negative and cerebro-spinal fluid examination was normal. The electroneuromyography showed a reduction in motor and sensitive amplitudes with an increase in distal latencies and F waves in the upper limbs and segmental and focal conduction blocks. Parasitological examination of the dermal juice around the edges of the skin lesions revealed amastigote forms of leishmaniasis. The evolution was favorable with only symptomatic treatment.

P53-T Evaluation of atypical chronic autoimmune inflammatory polyneuropathies - clinical and neurophysiological comparison

Background Chronic autoimmune inflammatory polyneuropathies (CAIP) is a group of rare and potentially treatable conditions that are often underdiagnosed due to non-compatibility with recognized diagnostic criteria that might be partially related to incomplete neurophysiological investigation or lack of follow-up. Methods Case series study of 4 CAIP patients with atypical clinical and/or neurophysiological features. Results Case 1. 10 year history of distal weakness in upper extremities (UE), NCS – diffuse conduction slowing with conduction block (CB) and marked sensory involvement. Improvement with IVIG. Case 2. Slow progression of asymmetrical weakness in distal UE and right lower extremity (LE), NCS – axonal loss with CB in all extremities. No response to glucocorticoids, improvement on IVIG. Case 3. Progressive weakness in distal UE with marked sensory involvement and diffuse severe fasciculations, 1st ENMG – no CB, slight axonal loss with demyelination not below 75% of lower normal, slight sensory impairment, with diffuse fasciculations. Follow up ENMG – 1 definitive CB, 2 probable CB (1 in Erb point), with significant demyelination and sensory impairment in UE. Slight improvement with glucocorticoids. Case 4. Progressive asymmetrical tetraparesis LE > UE, with sensory signs proximally in LE and distally in UE and LE. NCS – axonal loss with conduction slowing not below 75% normal range, no CB, no increase in distal latencies, significant sensory nerve involvement. No improvement on IVIG, marked response to glucocorticoids. Conclusions NCS should be comprehensive, including proximal stimulations. Follow-up ENMG studies and immunomodulatory treatment should be considered in all patients with suspected CAIP.

Peripheral neuropathy in chronic obstructive pulmonary disease

IntroductionPeripheral neuropathy in chronic obstructive pulmonary disease (COPD) has received scanty attention. The purpose of this study was to evaluate objectively the functional changes in the peripheral nervous system in COPD by different electrophysiological parameters and to determine the frequencies of these changes in patients with COPD.AimAssessment of peripheral nerve conduction by evaluation of the motor and sensory nerve conduction (SNC) in COPD patients.Patients and methodsIn this case–control study, we recruited 25 COPD patients and matched 25 healthy controls. Motor and SNC studies for ulnar and median nerves were evaluated by means of electrophysiological nerve study. Motor nerve conduction velocity and sensory nerve conduction velocity (SNCV), distal latencies (DLs), and amplitude of compound motor action potential were recorded. Arterial blood gases including partial pressure of oxygen and carbon dioxide (PaO2and PaCO2), oxygen saturation (SaO2), and arterial pH were measured. Pulmonary function test was done and forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio were measured.ResultsThere was a significant difference between COPD patients and the control group in all spirometric and gasometric parameters recorded, except for the arterial pH. On studying motor nerve conduction through median and ulnar nerves, there was an increase in DL, decrease in motor nerve conduction velocity, and longer F-wave latency in the COPD group than in the control group in both nerves. SNC study of the median nerve revealed a decrease in SNCV and an increase in DL in the COPD group than in the control group. Median nerve motor neuropathy was proved in 28% of patients, ulnar nerve motor neuropathy was proved in 36% of patients, whereas sensory nerve study of median nerve proved that 68% of patients have sensory axonal neuropathy and 12% have demyelinating sensory neuropathy. Median nerve Distal Latency (DL) shows negative correlation with FEV1and FEV1/FVC ratio. SNCV of the median nerve was positively correlated to oxygen tension level.ConclusionThe incidence of neuropathy is high. The rate of axonal neuropathy was significantly higher than other types. Our study showed a significant positive correlation between the degree of hypoxemia and severity of neuropathy, whereas it showed negative correlation between spirometry parameters (FEV1and FEV1/FVC ratio) and median nerve DL.

Electrophysiological changes in sensorimotor nerves in diabetes mellitus & usefulness of nerve conduction studies for early diagnosis of diabetic neuropathy

Background: Diabetes Mellitus(DM) a metabolic disorder is the most common cause of peripheral neuropathy. Nerve conduction studies(NCS) are commonly employed to detect the neuropathy. The present study was undertaken to find out the utility of NCS as an early indicator of neuropathy in diabetic patients. Materials & methods: Study was carried out in 50 diagnosed DM patients attending OPD in Medicine, Civil Hospital, Ahmedabad. Diabetic subjects were selected having FBS >110 mg/dL with duration of DM > 5 years. Their HbA1c levels were measured for glycaemic control. Diabetic patients with good glycaemic control were grouped in group A & that with poor glycaemic control in group B. 25 age matched non-diabetic & healthy subjects were selected for control group C. NCS was performed at Institute of Spine, Civil Hospital Campus, Ahmedabad. Nerve conduction parameters like compound muscle action potential(CMAP), sensory nerve action potential(SNAP), nerve conduction velocity(NCV) & distal latency(DL) were studied. Results: In our study there is increase in DL of peroneal, sural; median & ulnar sensory nerves in group B subjects. NCV of sensorimotor nerves is significantly decreased in group B subjects. SNAP of all nerves is reduced in group A & B. CMAP is reduced significantly in all nerves in group B. Conclusion: As DM progress further, it increases risk of neuronal involvement which can be accelerated by poor glycaemic control. Our result indicates demyelinating type of neuropathy with some changes of axonopathy. Therefore NCS is done for early detection of neuropathy in DM patients.

Neurophysiological Changes in Rats Subchronically Treated with Styrene or Its Metabolites

Neurophysiological Changes in Rats Subchronically Treated with Styrene or Its Metabolites: Junichi Misumi, et al. Department of Public Health and Hygiene, Oita Medical University—The purpose of this study was to clarify the causative agent(s) in the peripheral neuropathy induced by styrene. Styrene 600 or 300, and its metabolites; hippuric acid 600 or 300; mandelic acid 300; styrene oxide 100; mg/kg were subcutaneously injected into rats for 10 to 12 wk. The changes in maximum sensory conduction velocity (SCV), maximum motor conduction velocity (MCV), and motor distal latency (DL) in the rat's tail nerve were tested. Compared with the control group, decreases in MCV, SCV, and an increase in DL were observed in the rats injected with styrene 600, styrene oxide 100 and mandelic acid 300 mg/kg. No significant changes were found in the rats treated with hippuric acid 300 or 600 mg/kg. The MCV and SCV values in the styrene oxide 100 and mandelic acid 300 mg/kg groups were significantly lower, and DL values were significantly longer than those in the styrene 600 mg/kg group. It is presumed that the neuropathy caused by styrene is related to the neurotoxicity of its intermediate metabolites, namely mandelic acid and styrene oxide. It appears that the neurotoxicity of mandelic acid needs to be further evaluated in styrene‐produced neuropathy.

N-hexane neuropathy in offset printers.

In an offset printing factory with 56 workers, 20 (36%) developed symptomatic peripheral neuropathy due to exposure to n-hexane. Another 26 workers (46%) were found to have subclinical neuropathy. The initial change in the nerve conduction study was reduced amplitude of the sensory action potentials, followed by reduced amplitude of the motor action potentials, reduction in motor conduction velocities and increase in distal latencies. These changes indicate primary axonal degeneration with secondary demyelination. Sural nerve biopsy in a severe case showed giant axonal swellings due to accumulation of 10nm neurofilaments, myelin sheath attenuation and widening of nodal gaps. The development of neuropathy bore no direct relationship to the duration of exposure, hence factors such as individual susceptibility may be important. Optic neuropathy and CNS involvement were uncommon and autonomic neuropathy was not encountered.

Silicone Gel Infiltration of a Peripheral Nerve and Constrictive Neuropathy following Rupture of a Breast Prosthesis

Following rupture of a subpectoral breast prosthesis, massive amounts of silicone gel migrated into the arm of a patient. The patient developed painful paresthesias and decreased sensation in the cutaneous distribution of the superficial radial nerve. Nerve conduction studies showed both an increase in distal latency and decreased amplitude in this nerve compared with the normal opposite side. Subsequent neurolysis confirmed dense fibrosis surrounding the nerve. Silicone droplets also were observed within the thickened epineurium of the median nerve, but no electrophysiologic evidence of neuropathy occurred. Multiple debridements of the subcutaneous tissue of the arm were necessary. In one of these specimens, histologic sections demonstrated silicone gel infiltration of a subcutaneous nerve. This is the first reported case of silicone gel infiltration of a nerve and constrictive neuropathy associated with a prosthesis rupture.

Further Evidence of Involvement of Central and Peripheral Sensory Pathways in Olivopontocerebellar Atrophy

We report the electrophysiological findings of the central and peripheral somatosensory pathways in 20 patients with olivopontocerebellar atrophy. Changes in sensory action potentials of the median nerve were observed in 14 patients and consisted of reduced sensory potential amplitudes associated in 10 cases with an increase in distal latencies. Sixteen out of 20 patients also showed changes in somatosensory evoked potentials after stimulation of the median nerve, consisting of decreased amplitude of N13 (13 cases) and N20 (16 cases) components, associated with increased N9-N13 interpeak latency in 9 and N13-N20 in 14 patients. The origin of these alterations is discussed.

Nerve conduction during Wallerian degeneration in the baloon.

Conduction in the lateral popliteal nerve of the baboon was studied during the course of Wallerian degeneration. Six nerves were examined. In each case the muscle response to nerve stimulation and the ascending nerve action potential were recorded daily until the nerve became inexcitable. The muscle response to nerve stimulation disappeared after four to five days, but ascending nerve action potentials could be recorded for a further two to three days. There was no change in maximal motor conduction velocity or in distal latency until the muscle response to nerve stimulation was severely reduced in amplitude. At this stage there was a consistent increase in distal latency, sometimes associated with a mild reduction in maximal motor velocity in the leg. There was no change in the velocity of ascending nerve action potentials. Histological studies confirmed the presence of degeneration in the terminal parts of the intramuscular nerve fibres at a time when the proximal parts of the same fibres were relatively normal.