Central Sensory Conduction Time Research Articles

Evoked potential response in patients with idiopathic Parkinson’s disease and atypical parkinsonian syndromes: A comparative study

Patients with idiopathic Parkinson’s disease (IPD) and atypical parkinsonian syndromes (APSs) suffer from a range of disorders, especially in balance and locomotion, which necessitate visual, auditory, and somatosensory inputs. In this study, IPD patients, APS patients, and healthy controls (HCs) (n = 50 per group) underwent a series of assessments for visual evoked potentials (VEP), brainstem auditory evoked response (BAER), and short-latency somatosensory evoked potentials (SSEP). Results showed that VEP P100 latency was prolonged in multiple system atrophy-cerebellar type (MSA-C), multiple system atrophy-parkinsonian type (MSA-P), and corticobasal ganglionic degeneration (CBD) patients. The latency of peaks III and V was prolonged in IPD, MSA-C, dementia with Lewy bodies (DLB), and Parkinson’s disease dementia (PDD). BAER I-III and I-V interpeak latency were prolonged in IPD, DLB, and PDD, whereas BAER I-III, III-V, and I-V interpeak latencies were increased and the V/I amplitude ratio was decreased in MSA-C. The central sensory conduction time (N20-N13) was increased in MSA-P and MSA-C in SSEP. IPD patients had prolonged VEP P100 latency (P < 0.001), lower VEP N75-P100 amplitude (P < 0.001), prolonged BAER I, II, II, IV, V peak latencies (P < 0.001), I-III, I-V interpeak latencies (P < 0.001), lower BAER V/I amplitude ratio (P < 0.001), and prolonged SSEP N13, N20, central sensory conduction time (N20-N13) (P < 0.001) than HCs. IPD patients also had prolonged BAER I, II, II, IV, V peak latencies (P < 0.001), prolonged I-III, I-V interpeak latencies (P < 0.001), and shorter SSEP N13, N20, central sensory conduction time (N20-N13) (P < 0.001) than APS patients. Moreover, APS patients had prolonged VEP P100 and N145 latencies (P < 0.001) and decreased N75-N145 amplitude (P < 0.001) compared to HCs. APS patients also had prolonged BAER II, II, IV, V peak latencies (P < 0.001), prolonged I-III, III-V, I-V interpeak latencies (P < 0.001), decreased V/I amplitude ratio, and prolonged SSEP N13, N20, central sensory conduction time (N20-N13) (P < 0.001) than HCs. Postural instability and gait disorder (PIGD) IPD had significantly prolonged BAER III, V peak latencies (P < 0.05), and prolonged III-V interpeak latencies (P < 0.05) compared to tremor-dominant IPD. Overall, the IPD and APS patients had significant VEP, BAER, and SSEP abnormalities of demyelination and axonal variety in the visual, auditory, and somatosensory pathways. The changes were also correlated with the disease duration and severity. Although the diseases are predominantly motor disorders with significant non-motor components, these electrophysiological abnormalities might open a new avenue to assess the non-motor symptoms.

Utility of the tibial nerve somatosensory evoked potentials in differentiating between neuromyelitis optica spectrum disorders and multiple sclerosis.

Somatosensory evoked potentials (SEPs) are widely used for the diagnosis and evaluation of neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS). However, whether the parameters of tibial nerve SEPs can help to distinguish NMOSD from MS remains unclear. Thus, the aim of this study was to investigate the utility of tibial nerve SEP parameters in differentiating patients with NMOSD and MS. The clinical data of patients with NMOSD or MS treated in our institution between 2005 and 2021 were retrospectively extracted from our electronic database. Additional inclusion criteria were presentation with sensory symptoms in the lower extremities with corresponding lesions in the magnetic resonance images as well as available data on anti-aquaporin-4 antibodies and tibial nerve SEPs. The Z-scores of the N21-P38 interval (central sensory conduction time), P38 latency, and P38 amplitude were compared between the patients with NMOSD and MS. The relationship of disease severity with the parameters of the tibial nerve SEPs was also evaluated. Twenty patients with NMOSD and 13 patients with MS were enrolled. The Z-scores of the N21-P38 interval and P38 latency were significantly higher in the MS group than in the NMOSD group (p < 0.05 and p < 0.01, respectively), whereas there was no difference in the Z-scores of the P38 amplitude between the two groups. In the MS group, only the N21-P38 interval and P38 latency were significantly correlated with disease severity (p < 0.05 and p < 0.01, respectively). In contrast, none of the tibial nerve SEP parameters were significantly correlated with disease severity in the NMOSD group. Evaluation of the N21-P38 interval and P38 latency in tibial nerve SEPs potentially helps in differentiating between NMOSD and MS.

A patient with McLeod syndrome showing involvement of the central sensorimotor tracts for the legs

BackgroundMcLeod syndrome is a rare X-linked recessive acanthocytosis associated with neurological manifestations including progressive chorea, cognitive impairment, psychiatric disturbances, seizures, and sensorimotor axonal polyneuropathy. However, no studies have investigated the functioning of central sensorimotor tracts in patients with McLeod syndrome.Case presentationA 66-year-old man had experienced slowly progressive chorea and gait disturbance due to lower limb muscle weakness since his early fifties. Blood examinations showed erythrocyte acanthocytosis and the reduction of Kell antigens in red blood cells. Brain magnetic resonance imaging showed atrophy of the bilateral caudate nuclei and putamen. The diagnosis of McLeod syndrome was confirmed by the presence of a mutation of the XK gene on the X chromosome. Somatosensory-evoked potential and transcranial magnetic stimulation studies demonstrated that the central sensory and motor conduction times were abnormally prolonged for the lower extremity but normal for the upper extremity.ConclusionsThis is the first report of the involvement of the central sensorimotor tracts for the legs in a patient with McLeod syndrome. The clinical neurophysiological technique revealed the central sensorimotor tracts involvements clinically masked by neuropathy.

Comparison between somatosensory-evoked potential parameters in patients with nonspecific versus specific chronic low back pain

Background: Modern pain neuroscience has revolutionized our understanding about pain, including the role of central sensitization in amplifying pain experiences with increased neuronal response to central nervous system stimuli. During external upper and lower limb perturbation, it has been shown that Chronic low back pain (CLBP) was associated with longer reflex response latencies of trunk muscles. One theoretic but rarely examined possibility for longer reflex latencies is related to modulated somatosensory information processing. Objectives: The objective of the study was to compare the somatosensory-evoked potential (SSEP) parameters of the right median and left tibial nerves between patients with nonspecific and specific CLBP. Materials and Methods: The study includes 102 CLBP patients, clinically and radiologically confirmed and divided into two groups: 48 patients with nonspecific pathology and 54 patients with specific pathology. During this SSEP study the right median and left tibial nerves of all patients were examined. Recorded parameters include the latency and amplitudes. Results: The means of the latencies of all the SSEP waves of the right median and left tibial nerves were only significant in the peripheral SSEP waves in the upper and lower limbs (N9 and N10, respectively) and highly significant in cortical right median N20 SSEP wave. Regarding the central sensory conduction time values, both in the median and tibial SSEP study, The significant differences was noted only in the median nerve SSEP study. Regarding the means of the amplitudes of differently studied SSEP components of the right median and left tibial nerves, it was only significant in the peripheral SSEP (N9) wave of the right median nerve and in the subcortical and cortical (P37 and N45) waves in the tibial nerve SSEP study. Conclusions: Results showed a significantly higher SSEP amplitude and latency in nonspecific CLBP patients as compared to their counterpart CLBP patients. This could reflect a higher excitability of sensory cortex and sensory pathways in patients with nonspecific CLBP as compared to their counterpart patients.

Age-related dynamics of the parameters of somatosensory evoked potentials in healthy children

The purpose of this study was to evaluate the parameters of somatosensory evoked potentials (SSEPs) in healthy children of different age groups (n = 94). The amplitudes of the main cortical peaks and the central sensory conduction time (CSCT) from n. medianus and n. tibialis in children aged under 12 months, 1–12 years, and 12–17 years were estimated and compared. No significant cortical peaks were recorded from the tibial nerve in five children younger than 1 year (5 out of 23, 22%). Significant differences in CSCT were observed between the children younger than 1 year and two other groups. The amplitudes did not significantly differ between the groups. Thus, SSEPs may be used for the evaluation of somatosensory pathways in children aged one month to 17 years. CSCT differs significantly between children younger than 1 year and other age groups. Age-related reduction in CSCT and elevation of the cortical peak amplitudes may reflect the myelination of somatosensory pathways and the improvement in nervous system integration.

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.

ID 369 – The effects of chronic arsenic exposure on somatosensory pathway

Objective From 1920 to 1962, a mining company at a small mountainous village called Toroku in Japan intermittently produced arsenic trioxide. Although many patients had severe whole-body surface and deep sensory disturbances, previous studies reported only slight axonal degeneration based on nerve conduction studies or sural nerve biopsy. Methods Subjects were six patients with chronic arsenic exposure in Toroku. All patients had moderate to severe whole-body surface and deep sensory impairments without any motor disturbances. Peripheral nerve conduction study and bilateral median nerve somatosensory evoked potentials were performed in all patients. Results In nerve conduction study, two patients showed mild decrease of sensory nerve action potentials. In somatosensory evoked potentials, the N9 was delayed in two patients. The N11 was not detected in any patients, while the P13/14 was detected only in two patients. The N20 was detected in all patients. Patients with chronic arsenic poisoning had a significantly longer central sensory conduction time (latency between N9 and N20) compared to normal subjects (p Conclusions Sensory disturbances in patients with chronic arsenic poisoning are related to not only peripheral neuropathy but also central nervous system impairment. Key message Chronic arsenic exposure may affect the central nervous system.

Prolonged central sensory conduction time in patients with chronic arsenic exposure

BackgroundMany patients from Toroku, Japan, who have chronic arsenic exposure demonstrate whole-body sensory disturbance that is slightly more pronounced in the extremities. Although previous research in this population showed a mild peripheral neuropathy, it is unknown whether these patients have central nervous system impairment. To investigate the lesion sites underlying sensory disturbance related to chronic arsenic poisoning, we analyzed somatosensory evoked potentials (SEP). MethodsClinical features, nerve conduction study results, and median and/or tibial SEP were analyzed in patients with chronic arsenic exposure (total, 13 patients; median & tibial, 4; median, 5; tibial, 4) retrospectively. The SEP findings in patients were compared with those in normal controls. ResultsThe median SEP results indicated a conduction delay between the proximal brachial plexus and the primary sensory cortex, and tibial SEP findings indicated a delay between the dorsal gray matter of the lumbosacral cord and the primary sensory cortex. ConclusionThis is the first study to identify an impairment of the central somatosensory pathway in patients with chronic arsenic exposure. Sensory disturbance in these patients is related not only to peripheral neuropathy but also to impairment of the central nervous system.

Isolated pyramidal tract impairment in the central nervous system of adult-onset Krabbe disease with novel mutations in the GALC gene

This report describes a 60-year-old female patient with Krabbe disease who presented with slowly progressive gait disturbance due to mild spastic paraplegia. Brain magnetic resonance imaging showed high-intensity lesions along the upper parts of the bilateral pyramidal tracts in fluid-attenuated inversion recovery images. Central motor conduction time was prolonged both in the upper and the lower extremities, while central sensory conduction time was normal. The reduced lymphocyte galactocerebrosidase (GALC) activity and two novel mutations in the GALC gene, p.G496S and p.G569S, proved the diagnosis of Krabbe disease. Our findings show that adult-onset Krabbe disease is characterized by isolated pyramidal tract impairment in the central nervous system, both neurophysiologically and radiologically.

Brain volume analyses and somatosensory evoked potentials in multiple system atrophy

We investigated a progression of brain atrophy and somatosensory system dysfunction in multiple system atrophy (MSA). Subjects were 21 MSA patients [12 MSA-C (cerebellar type) and 9 MSA-P (parkinsonism type)]. The relative volumes of cerebrum, brainstem and cerebellum to the intracranial volume were obtained from three-dimensional computed tomography (3D-CT) of the brain. The median nerve somatosensory evoked potentials (SEPs) were recorded, and the latencies and amplitudes of N9, N11, P13/14, N20 and P25 components were measured. We studied correlations between brain volumes, SEP and clinical features. The brainstem and cerebellar atrophies were aggravated with progression of the disease. The central sensory conduction time (CSCT) was progressively prolonged in parallel with the disease duration irrespective of the actual age of the patients. In MSA patients, the volume reductions of cerebellum and brainstem could be one of structural markers of disease progression, and the sensory pathway is progressively involved with the progression of disease processes.

Multimodality-evoked potential study of anti-aquaporin-4 antibody-positive and -negative multiple sclerosis patients

Neuromyelitis optica (NMO) is claimed to be a distinct disease entity from multiple sclerosis (MS) because of its strong association with NMO-IgG/anti-AQP4 antibody; however, the in vivo role of the antibody remains unknown. Therefore, we aimed to clarify whether the presence of anti-AQP4 antibody is associated with any abnormalities in multimodality-evoked potentials in 111 patients with relapsing–remitting or relapsing-progressive MS, including the opticospinal form of MS, 18 of whom were seropositive for anti-AQP4 antibody. More patients with anti-AQP4 antibody showed a lack of the P100 component on visual-evoked potentials (VEPs) than those without the antibody (11/17, 64.7% vs. 20/84, 23.8%, p = 0.003), whereas the frequency of delayed P100 latency was significantly higher in the latter group than in the former (1/17, 5.9% vs. 28/84, 33.3%, p = 0.021). The frequencies of non-responses and delayed central sensory conduction times in median and posterior tibial nerve somatosensory-evoked potentials (SEPs) were not significantly different between anti-AQP4 antibody-positive and -negative patients. In terms of upper and lower limb motor-evoked potentials (MEPs), the frequencies of non-responses and delayed central motor conduction times did not differ significantly based on the presence or absence of anti-AQP4 antibody. The frequency of optic nerve lesions on MRI was significantly higher in anti-AQP4 antibody-positive patients than in anti-AQP4 antibody-negative patients ( p = 0.0137). Multiple logistic analyses revealed that anti-AQP4 antibody positivity (OR = 8.406, p = 0.02) and unevoked VEP responses (OR = 35.432, p < 0.001) were significantly related to development of severe visual impairment. Such an association of anti-AQP4 antibody with disability was not found for either severe motor or sensory impairment. These findings suggest a distinctive nature of optic nerve lesions between anti-AQP4 antibody-positive and -negative patients; lesions are supposed to be more necrotic in the former group and more demyelinating in the latter.

Intra-cortical connectivity in multiple sclerosis: a neurophysiological approach

Multiple sclerosis is an autoimmune disease predominantly affecting the white matter of the CNS, causing--among functional sequelae-cortico--cortical partial or total disconnection. Since functional connectivity linking cerebral regions is reliably reflected by synchronization of their neuronal firing, in this study an electrophysiological parameter measured by magnetoencephalography was used to quantify an intra-cortical connectivity (ICC) index focused on the primary somatosensory cortical areas (S1). Twenty-one patients affected by mild (Extended Disability Scale Score, median 1,5) relapsing-remitting (RR) multiple sclerosis in the remitting phase without clinically evident sensory impairment were evaluated. Three dimensional MRI was used to quantify the lesion load, discriminating black hole and non-black hole portions, normalized by individual brain volumes. When matched with a control population, multiple sclerosis patients showed a reduced ICC combined with the complete loss of the finger-dependent functional specialization in S1 cortex of the dominant hemisphere. No association was found between ICC impairment and disease duration, or prolongation of the central sensory conduction time, presence of spinal cord lesions and ongoing disease modifying therapy. The ICC index slightly correlated with the lesion load. A local index of ICC in a circumscribed brain primary area was altered in mildly disabled RR-multiple sclerosis patients, also in absence of any impairment of central sensory conduction. In conclusion, the diffuse damage influencing the multi-nodal network subtending complex cerebral functions also affects intrinsic cortical connectivity. The S1 ICC index is proposed as a highly sensitive and simple-to-test functional measure for the evaluation of intra-cortical synchronization mechanisms in RR-multiple sclerosis.

TUO07 Somatosensory processing in very prematurely born infants recorded with magnetoencephalography

Methods: An electrophysiological parameter measured by Magnetoencephalography was used to quantify an Intra-Cortical Connectivity (ICC) index focused on the primary somatosensory cortical areas (S1). Twenty one patients affected by mild (Extended Disability Scale Score, EDSS, mean 1,7 range 0-3,5) relapsing-remitting multiple sclerosis (RR-MS) in the remitting phase without clinically evident sensory impairment were evaluated. Three dimensional magnetic resonance imaging (3D-MRI) was used to quantify the lesion load, discriminating black hole (BH) and non-BH portions, normalized by individual brain volumes. Results: When matched with a control population, MS patients showed a reduced ICC, combined with the complete loss of the finger-dependent functional specialization in left S1 cortex. No association was found between ICC impairment and disease duration, or prolongation of the central sensory conduction time, evidence of spinal cord lesions and disease modifying therapy. The ICC index slightly correlated with the lesion load. Conclusion:A local index of intra-cortical connectivity in a circumscribed brain primary area was altered in mildly disabled RR-MS patients, also in absence of any impairment of central sensory conduction. It is concluded that the diffuse damage influencing the multi-nodal network subtending complex cerebral functions also affects intrinsic cortical connectivity. S1 ICC is proposed as a highly sensitive and simple-to-test functional index for the evaluation of the widespread cerebral damage in RR-MS.

Median nerve somatosensory evoked potentials and their high-frequency oscillations in amyotrophic lateral sclerosis

Objective To investigate sensory cortical changes in amyotrophic lateral sclerosis (ALS), we studied somatosensory evoked potentials (SEPs) and their high-frequency oscillation potentials. Methods Subjects were 15 healthy volunteers and 26 ALS patients. Median nerve SEPs were recorded and several peaks of oscillations were obtained by digitally filtering raw SEPs. The patients were sorted into three groups according to the level of weakness of abductor pollicis brevis muscle (APB): mild, moderate and severe. The latencies and amplitudes of main and oscillation components of SEP were compared among normal subjects and the three patient groups. Results The early cortical response was enlarged in the moderate weakness group, while it was attenuated in the severe weakness group. No differences were noted in the size ratios of oscillations to the main SEP component between the patients and normal subjects. The central sensory conduction time (CCT) and N20 duration were prolonged in spite of normal other latencies. Conclusions The median nerve SEP amplitude changes are associated with motor disturbances in ALS. The cortical potential enhancement of SEPs with moderate weakness in ALS may reflect some compensatory function of the sensory cortex for motor disturbances. Significance The sensory cortical compensation for motor disturbances is shown in ALS, which must be important information for rehabilitation.

A distinct subgroup of chronic inflammatory demyelinating polyneuropathy with CNS demyelination and a favorable response to immunotherapy

To explore subclinical central nervous system (CNS) involvement in chronic inflammatory demyelinating polyneuropathy (CIDP), we recorded somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) using transcranial magnetic stimulation, to measure central sensory conduction time (CSCT) and central motor conduction time (CMCT) and examined brain and spinal cord MRI in patients with probable CIDP based on the American Academy of Neurology AIDS Task Force criteria. Eighteen patients with probable CIDP (12 males and 6 females; mean age at examination ± SD, 45.8 ± 17.0 years; range, 17–72) were included in the study. Of the 13 patients who underwent SEPs, one had prolonged CSCT (8%) and of the 13 who underwent MEPs, four had abnormal CMCT (31%). Cranial MRI revealed five of 18 patients had abnormal scans, only one of which showed multiple ovoid periventricular lesions suggestive of demyelination while none showed any intramedullary lesion on spinal cord MRI. Thus, 6 of the 18 patients were considered to have subclinical demyelinative CNS involvement which had lower disability on Global Neurological Disability Score (GNDS) ( p = 0.0061), a male preponderance (0.0537) and a larger compound muscle action potential (CMAP) amplitude in the median nerve ( p = 0.005) than those without. The decrease of GNDS with immunologic therapies was nearly significant in the former ( p = 0.0556) but not in the latter. The results of the present study suggest that subclinical CNS involvement in CIDP is not uncommon in Japanese patients and that CIDP with subclinical CNS involvement is more demyelinative thus responsive to immunotherapies while those without have more axonal damage and less responsive to immunotherapies.

DIFFERENTIAL SURGICAL TREATMENT OF CERVICAL SPINE STENOSIS

Objectives. To determine the efficacy of various procedures of precise differentiated surgical decompression for elimination of prevailing clinical manifestations of degenerative stenosis depending on a character and localization of morphological changes (degenerative or posttraumatic) in the cervical spine, the expediency and necessity of application of various fixation and stabilization techniques. Material and Methods. Eighteen patients included in the study were examined for degenerative stenosis in the cervical spine. All of them underwent decompressive surgery. International representative scales were used to estimate results depending on basic clinical syndrome. Results. The increase in latency and central sensory conduction time (according to somatosensory evoked potentials data) indicates that ischemic compression lesion is mainly caused by dorsal compression. In this case a laminectomy according to Hirabayashi was performed. The increase in central motor latency time (according to central transcranial magnetic stimulation) greater by 30 % than a norm indicates that ischemic lesion is caused by anterior vertebral artery compression. In this case a corporectomy was performed. Conclusion. Compression lesions in cervical spine stenosis have local ischemic character and correspond to blood supply basin of compromised spinal or segmental artery. There is a correlation of ischemic compression focus localization with a character of electrophysiological conduction and responses. Differential character of surgical decompression provides observation of minimal invasive principles and better neurological restoration of patients.

Prolonged central sensory conduction time in alcoholics with hypoactive aldehyde dehydrogenase-2.

People who have a Glu487Lys mutation (single nucleotide polymorphism) in the aldehyde dehydrogenase-2 (ALDH2) gene are slow to metabolize the alcohol breakdown product acetaldehyde. The P13/14-N20 interval of the median nerve somatosensory evoked potential was significantly longer in alcoholic patients with a hypoactive ALDH2 (n = 27) than in those with an active ALDH2 (n = 43). This suggests that acetaldehyde accumulation due to hypoactive ALDH2 is associated with a prolongation of the central sensory conduction time between pons and primary sensory cortex. The present result indicates that an elevated blood concentration of acetaldehyde must cause the central sensory tract involvement and that acetaldehyde is one of factors producing brain damage in alcoholics.

Cognitive impairment and diffuse white matter atrophy in alcoholics

Objective Diffuse brain white matter atrophy is often seen in chronic alcoholics, but its relation with cognitive impairment remains to be solved. In order to address this issue, in alcoholics with cognitive impairment at different levels, we studied relations of the central sensory conduction time (CSCT) or brain magnetic resonance imaging (MRI) findings with the cognitive function. Methods Subjects were 35 alcoholics with mild cognitive impairment (mini-mental state examination score, MMSE, ≥24; mean±SD, 27.7±1.9), 12 with moderate to severe cognitive impairment (MMSE<24; 20.3±2.7), 15 with Alzheimer's disease (AD) (MMSE, 18.9±4.3) (disease control) and 20 healthy volunteers (MMSE, 28.5±1.6) (normal control). Median nerve SEPs were recorded in the all subjects, and the latencies and amplitudes of their N9, N11, P13/14, N20 and P25 components were measured. The ventriculocranial ratio (VCR) and the width of cortical sulci were measured on MRIs. These physiological parameters and MRI findings were compared between the 4 groups of the subject, and correlations between those all features were also analyzed. Results CSCT and VCR were significantly greater in alcoholics with moderate to severe cognitive impairment than those in the other 3 groups. Pearson's product–moment correlation analyses of the alcoholics disclosed that both the CSCT and VCR had significant negative correlations with the MMSE score. Moreover, the CSCT and VCR were positively correlated. Conclusions Both physiological and morphological estimates of the white matter function (CSCT and VCR) had a significant correlation with the cognitive dysfunction. Significance The diffuse white matter atrophy may be one of the factors causing cognitive impairment in chronic alcoholics.

Myelopathy and amnesia following accidental electrical injury

Documentation of MRI and neurophysiological changes following accidental electrical injury. Tertiary care referral teaching hospital at Lucknow, India. A 30-year-old lady developed amnesia and spastic paraparesis with loss of pin prick sensation below the second thoracic spinal segment following electrocution. Her spinal MRI was normal and cranial MRI revealed T2 hyperintensity in the right putamen. Peroneal, sural and electromyography were normal. Tibial central sensory conduction time was normal but central motor conduction time to lower limbs and right upper limb was prolonged. Neurophysiological study and MRI may help in understanding the pathophysiological basis of neurological sequelae following electrical injury.

Clinical and physiological significance of abnormally prolonged central motor conduction time in HAM/TSP

We measured the central motor conduction time (CMCT), central sensory conduction time (CSCT), F wave and mean F wave/M wave amplitude ratio in patients with HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) and controls. CMCTs in upper (U) and lower (L) limbs were significantly prolonged in HAM/TSP. L-CSCT was significantly prolonged in HAM/TSP, but U-CSCT in HAM/TSP and controls were not significantly different. CMCT and CSCT were significantly correlated in HAM/TSP. U-CMCT, but not L-CMCT, correlated with the clinical severity of HAM/TSP. Although F wave conduction velocity and its occurrence were normal in HAM/TSP, U- and L-mean F wave/M wave amplitude ratio tended to be higher in HAM/TSP, and the L-mean F wave/M wave amplitude ratio was significantly correlated with the L- and thoracic CMCT. These findings demonstrate that the prolongation of CMCT sensitively reflects the extension of the lesions and the disinhibition to the anterior horn cells in HAM/TSP.