Central Conduction Abnormalities Research Articles

Central conduction abnormalities in patients receiving levodopa-carbidopa intestinal gel infusion.

In recent years, several studies have reported a relatively high frequency of polyneuropathy in patients with Parkinson's disease (PD), in particular, in patients receiving levodopa-carbidopa intestinal gel (LCIG) infusion. In spite of the several patients investigated with nerve conduction studies, no study has prospectively explored a possible central nervous system involvement of patients receiving LCIG infusion. We prospectively evaluated eight PD patients receiving LCIG infusion, who underwent neurophysiological evaluations with nerve conduction studies, visual, somatosensory and motor evoked potentials before LCIG infusion, and 1 and 6months after. At 6months follow-up, we found significant reduction in sural nerve SNAP amplitude, increase of central sensory conduction time N22-P40, and increases of central motor conduction time recorded from I dorsal interosseous and tibialis anterior. In PD patients with LCIG infusion, we found a subclinical neurophysiological impairment of both peripheral and central nervous system.

Spinal cord involvement in patients with cirrhosis

A severe spinal cord involvement may rarely occur in patients with cirrhosis and other chronic liver diseases; this complication is usually associated with overt liver failure and surgical or spontaneous porto-systemic shunt. Hepatic myelopathy (HM) is characterized by progressive weakness and spasticity of the lower extremities, while sensory and sphincter disturbances have rarely been described and are usually less important. The diagnosis is assigned in the appropriate clinical setting on clinical grounds after the exclusion of other clinical entities leading to spastic paraparesis. Magnetic resonance imaging is often unremarkable; however, also intracerebral corticospinal tract abnormalities have been reported recently. The study of motor evoked potentials may disclose central conduction abnormalities even before HM is clinically manifest. HM responds poorly to blood ammonia-lowering and other conservative medical therapy. Liver transplantation represents a potentially definitive treatment for HM in patients with decompensated cirrhosis of Child-Pugh B and C grades. Other surgical treatment options in HM include surgical ligation, shunt reduction, or occlusion by interventional procedures.

Visual evoked potentials for the evaluation of CNS impairment in type 1 diabetes in children

Central nervous system (CNS) impairment is common in diabetic patients even in the early stage of the disease and it could be associated with peripheral neuropathy. Nevertheless, less attention has been directed toward the chronic effects of diabetes on the CNS. The aim of the study was to investigate the changes of central nerve conduction in children with insulin-dependent diabetes mellitus prospectively using the visual evoked potentials (VEP) and to know how those results were related to clinical risk factors and parameters of peripheral nerve conduction studies (NCS). A total of 75 diabetics (29 males) aged 5-26 years (mean 14.3±4.7) underwent VEP and NCS annually for 5 years. For comparison, 52 healthy children were studied. Out of 75 patients, 25 patients completed annual studies for 5 years. The latencies of P100 were prolonged at the study entry when compared with controls (P< 0.001). Significant positive correlations were found between the VEP latency and the glycosylated hemoglobin level. The values of latency and amplitude were inversely related with the age of patients and the duration of the disease. The values of latency were not related with parameters of NCS. Only a few parameters of NCS were weakly associated with the amplitudes of P100. Poor glycemic control proved to be an important risk factor over 5 years as related to the development of subclinical central neural pathway abnormality. VEP could be considered as a valid noninvasive tool for detecting early diabetic central conduction abnormalities such as retinopathy or optic neuropathy.

Central Fatigue in Multiple Sclerosis (MS)

In MS patients fatigue is manifested as a decrease in motor function, often associated with exercise. This decrease in muscle function is caused by inadequate central activation rather than peripheral abnormalities. Transcranial magnetic stimulation (TMS) studies have been used to detect central conduction abnormalities in subjects with definite MS. Previous work in our laboratory has demonstrated that these conduction changes are accentuated after fatiguing exercise. PURPOSE: To determine if cortical excitability is altered following fatiguing exercise in MS patients vs healthy controls. METHODS: Cortical excitability was assessed during motor tasks (finger flexion and extension) before and after fatiguing exercise (3-min maximal hand grip) using functional magnetic resonance imaging (fMRI). MS patients (n=5, mean age = 39.5 yr, Expanded Disability Status Score ranging from 1 to 6) were compared to controls (n=6, mean age 35.7). RESULTS: Activated cortical volume in the motor strip was significantly greater in MS patients compared to controls before (3947 ± 1073 vs 1624 ±227) and after (3150 ± 1042 vs 1774 ± 617) the fatigue paradigm. Cortical activation in MS patients was 143% and 77% higher for pre- and post-exercise, respectively, (p <0.05). Increased activated volume observed in MS patients is consistent with magnetic resonance spectroscopic imaging studies that demonstrate adaptive changes in the cerebral cortex consistent with axonal injury. Although pre- to post-exercise changes were not statistically significant, controls remained fairly stable while MS patients demonstrated a decrease in activated volume following exercise. The largest decreases were observed in the MS patients with greater disability. These results support previous TMS studies that indicate a reduction in cortical excitability with fatigue in individuals with MS. CONCLUSION: A similar study should be completed with a larger sample to verify these results. It may be possible to assess the effects of therapies (drug and rehabilitation) on development and recovery of central fatigue using this method.

THE ROLE OF SOMATOSENSORY EVOKED POTENTIALS IN THE DIAGNOSIS OF AIDS‐ASSOCIATED MYELOPATHY

BACKGROUND: Although AIDS‐associated vacuolar myelopathy is detected in&gt; 50% of autopsy cases, it is often unrecognized during life. The clinical assessment is often difficult because of concurrent peripheral neuropathy and lack of specific diagnostic markers. Somatosensory evoked potentials (SEPs) have been successfully used to evaluate central conduction in a number of diseases involving the spinal cord. OBJECTIVES: To assess the diagnostic yield of SEPs in AIDS‐associated myelopathy. METHODS: We recorded tibial and median nerve SEPs in 69 HIV‐infected subjects referred for evaluation of lower extremity neurologic abnormalities. Stimulation of the peroneal nerve at the popliteal fossa was performed in patients with absent response to ankle stimulation. RESULTS: HIV‐infected subjects had significantly delayed latencies of both peripheral and central potentials, suggesting a combination of peripheral and CNS abnormalities. Analysis of peripheral and central latencies allowed us to discriminate between neuropathy and myelopathy in individual patients. Abnormalities of tibial central conduction time (CCT) correlated with clinical diagnosis of myelopathy. There was no significant difference in median CCTs between patients and controls, suggesting that conduction abnormalities were restricted to the thoracolumbar spinal cord. A derived spinal conduction time was a sensitive indicator of central conduction abnormalities in AIDS patients with myelopathy. CONCLUSIONS: The combination of median, posterior tibial, and peroneal SEPs is a valuable tool in the diagnosis of AIDS‐associated myelopathy, particularly when myelopathy and peripheral neuropathy coexist. The use of a derived spinal conduction time improves the diagnostic yield of SEPs in AIDS‐associated myelopathy.

Peripheral And Central Conduction Abnormalities In Diabetes Mellitus

Objectives: To investigate peripheral and central somatosensory conduction in diabetic patients. Methods: We recorded sensory nerve action potentials and 5‐channel somatosensory evoked potentials (SEPs) with non‐cephalic reference after median nerve stimulation in 55 diabetic patients and 41 age/height matched normal subjects. We determined onset latencies of the spinal N13‐P13 and the cortical N20‐P20 components, and obtained the central conduction time (CCT). Results: Onset latencies of all SEP components were prolonged in diabetic patients. The mean onset CCT in the diabetic group was 6.3 ± 0.5ms (mean ± SD), being significantly longer than that in the control group (6.1 ± 0.2 ms). The peripheral sensory conduction velocity was also decreased in the diabetic group, but there was no significant correlation between peripheral conduction slowing and the onset CCT prolongation. Conclusions: Diabetes affects conductive function in the central as well as peripheral somatosensory pathways. The CCT abnormality does not coincide with lowering of the peripheral sensory conduction. The present results do not favor the hypothesis that a central‐peripheral distal axonopathy plays an important role in development of diabetic polyneuropathy.

Peripheral and central conduction abnormalities in diabetes mellitus.

To investigate peripheral and central somatosensory conduction in patients with diabetes. The authors recorded sensory nerve action potentials and 5-channel somatosensory evoked potentials (SEPs) with noncephalic reference after median nerve stimulation in 55 patients with diabetes and 41 age- and height-matched normal subjects. The authors determined onset or peak latencies of the Erb's potential (N9) and the spinal N13-P13 and the cortical N20-P20 components, and obtained the central conduction time (CCT) by onset-to-onset and peak-to-peak measurements. Both onset and peak latencies of all SEP components were prolonged in patients with diabetes. The mean onset CCT in the diabetic group was 6.3 +/- 0.5 msec (mean +/- SD)-significantly longer than that in the control group (6.1 +/- 0.2 msec)-whereas no significant difference was found in the peak CCT. The amplitudes of N9 and N13-P13 components (but not N20-P20) were significantly smaller in the diabetic group. The peripheral sensory conduction velocity was also decreased in the diabetic group, but there was no significant correlation between peripheral conduction slowing and the onset of CCT prolongation. Diabetes affects conductive function in the central as well as peripheral somatosensory pathways. The CCT abnormality does not coincide with lowering of the peripheral sensory conduction. The current results do not favor a hypothesis that a central-peripheral distal axonopathy plays an important role in development of diabetic polyneuropathy.

Dissociation of somatosensory and motor evoked potentials in non-comatose patients after head injury

Objectives: This study was performed to evaluate the clinical value of combined use of somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) in patients with different brain lesions after head trauma.Methods: A total of 64 patients with minor and moderate head injury were investigated by means of SEPs recorded over the parietal and frontal areas and MEPs following single-pulse transcranial magnetic stimulation (sTMS) and slow-rate repetitive transcranial magnetic stimulation (rTMS).Results: In almost 50% of the patients, a dissociated impairment of somatosensory and motor evoked potentials was found. This dissociation was related to different distribution of SEP and MEP abnormalities in head injury subgroups. The higher threshold to sTMS and increased variability of the MEP amplitude during slow-rate rTMS were the most prominent features in patients with focal brain contusions, suggesting impairment of the cortical excitability. SEP abnormalities, as well as central conduction impairments, were more noticeable in patients with diffuse brain injury.Conclusions: A combined analysis of SEPs and MEPs may improve the assessment of cortical dysfunctions and central conduction abnormalities in non-comatose patients with head injury. A slow-rate rTMS may be considered as a complementary technique to the evaluation of the threshold in assessment of the excitability of the motor cortex in minor and moderate head injury.

Exploration par les potentiels évoqués moteurs (PEM) des tumeurs intrarachidiennes : corrélations avec les données des potentiels évoqués somesthésiques (PES)

Motor evoked potentials (MEPs) assessment of central motor conduction in intraspinal tumors: a study of 43 patients. MEPs to transcutaneous magnetic stimulation have been recorded in 43 patients with an intraspinal tumor documented by MRI. The tumor was extramedullary in 18 patients and intramedullary in 25. MEPs were abnormal in 62.8% of patients. There were no significant differences in the rate of MEP abnormalities according to the lesion site or the histological findings, except for meningiomas which showed abnormal MEPs in all eight patients included in this series. The percentage of patients with abnormal MEPs was 9.3% despite the absence of any clinical symptom of central motor pathway dysfunction. Infraclinical MEPs abnormalities were observed in 24% of explored limbs. Median and tibial nerves somatosensory evoked potentials (SEPs) were recorded in 41 patients and showed abnormalities of central conduction or of segmental spinal responses in 65.9% of the cases. When combining data from MEP and SEPs, abnormalities were observed in 70.7% of patients ( 29 41 ). Five patients (12.2%) had abnormal MEPs, but normal SEPs, and four other patients (9.8%) had abnormal SEPs, but normal MEPs. This finding suggests that both MEPs and SEPs should be recorded for presurgical evaluation of intraspinal tumor.

Somatosensory evoked potentials and nerve conduction studies in patients with Guillain-Barré syndrome

Somatosensory evoked potentials, F-waves, and nerve conduction studies (NCS) were performed to determine their usefulness in detecting electrophysiologic abnormalities in 23 children in the acute stage of Guillain-Barré syndrome. The studies were performed on average 8.3 days after the onset of neurological symptoms, before the period of maximal weakness. All patients had at least one abnormal test. Somatosensory evoked potentials (SEP) showed most abnormalities: 91% abnormal recordings with posterior tibial nerve (PTN) stimulation and 68% with median nerve (MN) stimulation. The nerve conduction velocities were abnormal in 76% and 67% with PTN and MN stimulation, respectively. The F-waves were abnormal in 66% (PTN) and 56% (MN). The SEP studies were helpful in detecting proximal and central conduction abnormalities in 26% of patients, and they were more sensitive in detecting an abnormality when compared with F-wave recordings. Furthermore, in one patient with normal NCS and F-waves the prolonged lumbar potential-P35 conduction time of the PTN-SEP was the only abnormality found. SEP can detect an abnormality and thus support the clinical diagnosis of Guillain-Barré syndrome in the acute stage when the results of more conventional tests are inconclusive.

Somatosensory pathway dysfunction in uremic children

Neurophysiological studies have shown defects in peripheral conduction in up to 75% of adults with end-stage renal disease (ESRD), though abnormalities of central conduction seem more variable. There are no comparable pediatric data. We therefore measured median nerve somatosensory evoked potentials (SEPs) in 10 children with ESRD, maintained by hemodialysis, who had no neurological signs or symptoms, and compared the results with those for age-matched controls. The latencies of N9, P14, N20 and P22, and interpeak latencies, N9-N20, N9-P14 and P14-N20, were not significantly different between the two groups (Student's t test). However, the children with ESRD were significantly retarded in growth and when arm length was taken into account, a significant difference in peripheral conduction was revealed. There was no correlation with other indexes of disease severity (parathormone, aluminium, Hb, Na, K, Cl, BUN and creatinine). SEPs appear to reflect subclinical changes in peripheral conduction in sensory pathways in children with ESRD which are not correlated with other measures of disease severity.

Neurophysiology of the Striated Urethral Sphincter in Multiple Sclerosis

Urethrovesical dysfunction is common in patients with multiple sclerosis. We present the results of urodynamic and neurophysiological studies in a series of 24 patients with multiple sclerosis associated with urinary symptoms. Urethral sphincter electromyography showed only minor abnormalities but studies of central conduction demonstrated abnormal sensory conduction in 88% and abnormal motor conduction in 80% of the patients studied. These abnormalities of central conduction correlated well with the urodynamic findings.

Abnormalities of parietal and prerolandic somatosensory evoked potentials in Huntington's disease

Cervical, parietal and prerolandic somatosensory evoked potentials (SEPs) to median nerve stimulation at the wrist were recorded with an earlobe reference in 24 patients with Huntington's disease (HD) and in 24 age-matched normal controls. Cortical responses of abnormal wave form and reduced amplitude were constantly observed in HD patients. SEP changes affected more severely the prerolandic (P22/N30) pattern, which could not be recognized in two-thirds of patients, than the parietal (N20/P27) pattern, which could be identified in all cases. The N20 latency and the central conduction time (N13–N20 interval) were significantly increased. The occurrence of abnormalities of central conduction and of a predominant involvement of the prerolandic SEP pattern suggests an impairment of impulse transmission along the somatosensory lemniscal pathway at subcortical, possibly thalamic, level in HD.

Slow recovery of central axons in acrylamide neuropathy

To study the differential vulnerability of central versus peripheral axons, we observed serial changes in conduction over comparable segments of central and peripheral axons of the primary sensory neuron in 17 rats with acrylamide neuropathy using somatosensory evoked potentials. Central conduction abnormalities persisted even after peripheral conduction and clinical abnormalities had recovered. Morphometric studies showed prompt restoration of the largest-diameter fibers in the peripheral nerve after clinical recovery but persistent or even more severe loss of large- and medium-sized fibers in the cervical gracile tract. This finding suggests that recovery from central-peripheral distal axonopathy begins in the largest peripheral axons, perhaps even at the expense of central axons, and that clinical recovery can occur at a time when central conduction remains abnormal. The selective central axonopathy found in certain chronic degenerative disorders may be a consequence of this slow central recovery process associated with chronic or intermittent metabolic derangements.