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N Kohara

Publications and source records attributed to N Kohara.

At least 19 recordsLinked to original sources
PubMed2000

High-frequency SEP components generated in the somatosensory cortex of the monkey.

To investigate the origin of high-frequency somatosensory evoked potential (SEP) components, we recorded median nerve SEPs from the scalp and the depth in six monkeys. Laminar field potentials were analyzed in area 3b (N10; corresponding to human N20) and area 1 (P12; corresponding to human P25). After digital filtering (300-900 Hz), 4-6 components were identified, and the 1st to 4th peaks in area 3b (7-11 ms in latency) and the 3rd to 5th in area 1 (9-13 ms) showed clear polarity reversals between the surface and the depth of the cortex. These results provide direct evidence for intracortical origin of early high-frequency components in area 3b and of late ones in area 1.

Action Potentials↗
PubMed2000

Effect of maturation on nerve excitability in an experimental model of threshold electrotonus.

Threshold electrotonus (TE) is a new tool for investigating axonal function noninvasively in vivo. To increase its potential clinical value, we developed a rat model of TE, and examined the effects of maturation and pharmacological intervention. We recorded TE in 92 male rats (body weight 90-650 g) by stimulating the motor nerve in the tail, and applying 100-ms conditioning currents. Motor conduction velocities increased up to a body weight of 330 g, and remained constant thereafter. TE in mature rats was similar to that in humans, and two parameters were analyzed: TEd(10-20) or the mean threshold reduction 10-20 ms after the onset of the depolarizing conditioning current at 40% of threshold intensity; and TEh(10-20) or the corresponding threshold decrease on hyperpolarization. Like latency, the absolute value of TEh(10-20) decreased up to 330 g, and then stabilized thereafter, probably reflecting the progressive increase in the axonal diameter and relative reduction in internodal impedance. In contrast, TEd(10-20) gradually decreased up to 330 g, and then jumped to a higher level, which was maintained for animals of >400 g. 4-Aminopyridine, a blocker of fast potassium channels, selectively increased TEd(10-20) only in the immature or young (<330 g) rats. This suggests that, in the mature animals, fast potassium channels become sequestrated from the nodal membrane and not activated in response to nodal depolarization. These findings indicate that mature rats (>400 g) may provide a useful experimental model for interpreting abnormal TE responses in humans, and provide evidence for nonlinear maturation of potassium channel function in myelinated axons.

4-Aminopyridine↗
PubMed2000

Chronic motor axonal neuropathy associated with antibodies monospecific for N-acetylgalactosaminyl GD1a.

We report on three patients with chronic motor neuropathy who had elevated titers of immunoglobulin (Ig)G antibodies against N-acetylgalactosaminyl GD1a (GalNAc-GD1a) and normal titers of antibodies against other gangliosides. Presenting with progressive muscular atrophy, fasciculations, and no sensory deficits, the patients had been diagnosed to have motor neuron disease. Electrodiagnostic features were predominantly axonal. Two patients clinically improved after intravenous Ig infusion and cyclophosphamide therapy. Increased titers of IgM antibodies to GalNAc-GD1a were also found in two of 15 patients with multifocal motor neuropathy with conduction block but were associated with concomitant rise of anti-GM1 antibodies. These three cases represent a chronic motor axonal neuropathy in which antibody testing for a minor ganglioside was helpful for instituting therapy.

Action Potentials↗
PubMed2000

F-wave latency serves as the most reproducible measure in nerve conduction studies of diabetic polyneuropathy: multicentre analysis in healthy subjects and patients with diabetic polyneuropathy.

AIMS/HYPOTHESIS: For use in future drug development for diabetic polyneuropathy, we conducted multicentre trials to assess the reproducibility of nerve conduction studies. METHODS: All measurements were repeated twice at a time interval of 1-4 weeks in 132 healthy subjects (63 men) and 172 patients (99 men) with diabetic polyneuropathy. Using a standardised method, 32 centres participated in the study of control subjects and 65, in patients with diabetic polyneuropathy. Motor nerve conduction studies consisted of stimulating the left median and tibial nerves and recording the compound action potential from abductor policis and adductor hallucis for measuring amplitude, terminal latency and minimal F-wave latency. For sensory conduction studies, sensory nerve action potentials were recorded antidromically from the second digit and the posterior aspect of the lateral malleous after distal stimulation of the left median and sural nerves. We also calculated motor conduction velocity, F-wave conduction velocity and sensory conduction velocity. The relative intertrial variation and intraclass correlation coefficient were used as an index of reproducibility. RESULTS: Of all the measurements, F-wave latency yielded the highest intraclass correlation coefficient with the smallest relative intertrial variation for both median and tibial nerves in both groups. CONCLUSION/INTERPRETATION: Median and tibial F-wave latency provide the most reproducible measures for a nerve conduction study, serving as one of the best measures in multicentre drug trials for diabetic polyneuropathies.

Adult↗
PubMed2000

Membranous lipodystrophy presenting with palilalia: a PET study of cerebral glucose metabolism.

A case of membranous lipodystrophy (Nasu-Hakola disease; NHD) associated with palilalia was reported. A 38-year-old Japanese woman developed walking difficulty in her twenties. At age 35 she manifested neuropsychiatric symptoms characterized by euphoria, palilalia and dementia. A bone marrow biopsy showed periodic acid Schiff-positive membranous cystic lesions in the adipose tissue. Positron emission tomography with (18F)-2-fluoro-2-deoxy-D-glucose disclosed that regional cerebral glucose metabolism was decreased in the bilateral frontal white matter with mild hypometabolism in the thalamus and basal ganglia; all predominantly on the right. Taken together with the previous postmortem findings, it is postulated that frontal lobe hypofunction, predominantly in the right hemisphere, produced the unique neuropsychiatric symptoms in this patient.

Adult↗
PubMed2000

Activity-dependent conduction block in multifocal motor neuropathy.

Patients with multifocal motor neuropathy may complain of muscle fatigue, even though the degree of conduction block assessed at rest has improved with treatment. To explore the mechanism involved, we examined changes in muscle force during maximum voluntary contraction (MVC) and monitored conduction block before and after MVC in five patients with multifocal motor neuropathy. The results were compared with those for the contralateral unaffected homonymous muscles. For one patient, who had bilateral involvement, a normal subject of a similar age and stature served as the control. Results of conduction studies were also compared with those from six patients with amyotrophic lateral sclerosis (ALS) with similar compound muscle action potential (CMAP) amplitudes after proximal stimulation. During MVC for 60 s, the affected muscles developed prominent fatigue; the force at the end of contraction compared with the initial force was significantly lower for the affected muscles [42 +/- 19% (mean +/- standard deviation) of the initial force] than for the control muscles (94 +/- 9%; P = 0.01). After MVC, the amplitude ratio of CMAPs after proximal versus distal nerve stimulation transiently decreased to 19 +/- 14% of that before MVC in the affected muscles, but not in the control muscles (94 +/- 3.8% of that before MVC) and in patients with ALS (95 +/- 6.7%). In one patient with a focal lesion in the forearm, nerve excitability was monitored at the lesion site before and after MVC for 120 s. There were significant increases in axonal threshold (approximately 48%) and supernormality (approximately 135%) immediately after MVC, suggesting that the axonal membrane had undergone hyperpolarization and, by extrapolation, that this had precipitated the conduction block. This study is the first to show that activity-dependent conduction block plays a role in human disease by causing muscle fatigue.

Action Potentials↗
PubMed2000

Role of primary sensorimotor cortices in generating inhibitory motor response in humans.

To clarify the mechanism by which inhibitory motor responses such as cortical negative myoclonus are generated in humans, three patients with medically intractable partial epilepsy (two with frontal lobe epilepsy and one with parietal lobe epilepsy) were studied by means of direct cortical stimulation with a single electric pulse through subdural electrodes. All underwent chronic long-term video/EEG monitoring, cortical mapping by 50 Hz electric cortical stimulation and recording of cortical somatosensory evoked potentials with chronically implanted subdural grid electrodes (3 mm in diameter and centre-to-centre distance of 1 cm) to map both epileptogenic and functional zones. After these clinical evaluations, cortical stimulation by single electric pulse (0.3 ms duration, 1 Hz) was carried out through pairs of subdural electrodes located at the primary sensorimotor area (MI-SI), pre-supplementary motor area (pre-SMA) and lateral negative motor area (lateral NMA), while surface EMG was recorded from the muscles of the contralateral hand. The results showed that (i) in all subjects, single pulse stimulation of MI-SI elicited a motor evoked potential (MEP) followed by a silent period (SP) in the contralateral distal hand muscles, the latter lasting 300 ms after the stimulus. The duration of SP was proportional to the size of the preceding MEP. In one subject, SP without any preceding MEP was elicited, and, in another subject, there was a short SP immediately before MEP in the contralateral thenar muscle. (ii) Following the stimulation of either pre-SMA or lateral NMA, no SP was observed. It is concluded that the inhibitory mechanism within the MI-SI, but probably not in the non-primary motor areas, either closely linked to or completely independent of excitation, most likely plays an important role in eliciting brief negative motor phenomena such as cortical negative myoclonus or SP.

Adult↗
PubMed2000

Abnormal premovement gating of somatosensory input in writer's cramp.

One characteristic of focal dystonia is the sensory trick, by which sensory input to a certain area of the body can reduce abnormal contractions in muscles nearby. This suggests that adjusting the link between sensory input and movement allows motor commands to be issued more effectively from the brain. To explore this sensorimotor link, we studied the attenuation (gating) of somatosensory evoked potentials (SEPs) before and during hand movements in patients with writer's cramp. For premovement gating, 10 patients and 11 age-matched normal subjects were given a warning sound followed 1s later by an electric stimulus to the right median nerve at the wrist. The latter served both as a reaction signal to start a finger extension task and as the input to evoke SEPs over the scalp. Because reaction times always exceeded 70 ms, short-latency SEPs thus obtained were unaffected by the afferents activated by the movement. The amplitudes of frontal N30 components were significantly decreased over the frontal leads compared with SEPs elicited at rest (P: < 0.002) in the normal group, whereas significant gating was found not for N30 but for frontal P22 (P: = 0. 002) in the patient group. For midmovement gating studies, SEPs to the right median nerve stimulation were recorded in 16 patients and 12 age-matched normal subjects at rest, and during active and passive finger extension-flexion movements. In contrast to the premovement SEPs, the frontal N30 was equally gated during active and passive movements both in the patient (P: < or = 0.002) and the normal group (P: < or = 0.003). These findings indicate that in writer's cramp the sensitivity of sensory input channels from the hand is wrongly set by the central command to move. Perhaps the sensory trick, by supplying additional input not usually present during unobstructed movement, is a manoeuvre to correct this imbalance. Dystonia may result not only from abnormalities in the central motor command but also from disturbed central processing of sensory input.

Adult↗
PubMed1999

Pre-movement gating of short-latency somatosensory evoked potentials.

Somatosensory evoked potentials (SEPs) are reduced in amplitude during movement (gating). The mechanism involves central gating of afferent input and competition from other afferents activated by the movement. We distinguished these two by giving 11 normal subjects a warning sound followed 1 s later by an electric stimulus to the right median nerve at the wrist. The latter served both as a cue to start a finger movement and as stimulation to evoke SEPs. Gating effects were widespread in frontal (N30) and central (N60) areas, but were also seen, albeit to a lesser extent, in the recordings at P3 (P30). Since finger movement began after the stimulus, such gating must have been purely central in origin, presumably reflecting motor preparation.

Adult↗
PubMed1999

Cortical distribution of Bereitschaftspotential and negative slope potential preceding mouth-opening movements in humans.

Cortical potentials associated with the voluntary movement of various body parts are known as movement-related cortical potentials, which allow evaluation of the cortical efferent function and other higher functions controlling voluntary movement. The cortical potentials have three main components: the Bereitschaftspotential (or 'readiness potential'), the negative slope and the motor potential. Here, the cortical potentials preceding mouth-opening movements were recorded to investigate which of these components could be observed. Electroencephalograms (EEGs) were recorded from 11 electrodes placed over the scalp (F3, Fz, F4, T3, C3, Cz, C4, T4, P3, Pz and P4) according to the international 10-20 system. Electromyograms (EMGs) were recorded from the anterior belly of the digastric and the masseter. The 10 healthy participants were requested to make brisk and self-paced mouth-opening movements. All data were digitized with a sampling frequency of 200 Hz and stored for off-line analysis. Movement-related cortical potentials were obtained by averaging the EEG, using the digastric EMG onset as a trigger signal. The Bereitschaftspotential was recorded as a gradually increasing, bilaterally widespread negativity starting 1.7 s (mean) +/-0.23 s (S.D.) before the onset of the opening movement. The amplitude, which was measured at movement onset, was maximum at Cz (3.8 +/- 1.3 microV). The negative slope was observed 500-600 ms before the movement onset, and the motor potential was not clearly identified, because of postmotion artefacts. The cortical maps of the Bereitschaftspotential and negative slope combined together before to the mouth opening showed a symmetrical distribution with a maximum at the vertex region. The study reveals that the Bereitschaftspotential and the negative slope, two components of the movement-related cortical potentials, can be observed preceding mouth-opening movements and are similar to those associated with other voluntary movements. Findings such as distribution, amplitude and onset of the potentials could provide important information for studying the cortical control of mandibular movements.

Adult↗
PubMed1999

An electrophysiological study of the corticospinal projections in amyotrophic lateral sclerosis.

OBJECTIVE: To elucidate the pattern of corticospinal tract involvement in patients with amyotrophic lateral sclerosis (ALS), we analyzed motor evoked potential (MEP) waveforms and their relationship to the behaviour of single motor units using the peristimulus time histogram (PSTH) technique. METHODS: Abnormality of the corticospinal pathways was studied in 35 ALS patients using MEPs. PSTHs were also constructed to assess the effect of magnetic cortical stimulation on the discharge pattern of a voluntarily activated motor unit. RESULTS: MEPs showed a complex waveform in 10 out of 18 (56%) ALS patients with upper motor neuron signs (UMN). PSTHs revealed double primary peaks (PPs), PP1 and PP2, in 6 out of 16 motor units (38%) in ALS with UMN, as compared to only 2 out of 16 (13%) motor units in multiple sclerosis or cerebrovascular disease with UMN. None of the patients with lower motor neuron diseases or ALS without UMN had these abnormalities. The late component of complex MEPs showed a good correlation to PP2 (P < 0.0001), both probably being mediated by relatively preserved slower conducting corticospinal volleys. CONCLUSIONS: These findings suggest preferential involvement of the fast conducting direct corticospinal tracts, sparing the slower or polysynaptic projections in ALS.

Adult↗
PubMed1999

[Abnormal hyperexcitability in ALS].

The defect of neuromuscular transmission is one of the important signs in ALS. The amplitude of a single motor unit potential from patients with ALS often decrease during tonic voluntary contraction. This phenomenon is closely correlated with fatigue seen in the patient. Overfunctioning of Ach release in the nerve terminal might cause the failure of neuromuscular transmission in ALS. Fasciculations is an another characteristic sign and considered mainly to be peripheral axons in origin. It is postulated that the dysfunction of potassium channel in ALS axons makes the hyperexcitability of the axon membrane, causing fasciculations. Magnetic cortical stimulation sometimes evokes the same potentials as fasciculations, implying the hyperexcitability might be present also in spinal motoneurons or even in pyramidal neurons in ALS. All of these findings lead to the hypothesis that hyperexcitability or overactivity of central and peripheral motoneurons is an essential feature in ALS.

Amyotrophic Lateral Sclerosis↗
PubMed1999

[Myasthenia gravis with electrophysiological features of Lambert-Eaton myasthenic syndrome: usefulness of serum autoantibodies assay and neuromuscular junction biopsy].

A 60-year-old man with a 40-year history of seronegative ocular myasthenia gravis (MG) developed generalized weakness cumulating crisis over 2 years. On admission, ophthalmoplegia, severe ptosis and marked generalized weakness were observed without autonomic symptoms and signs. The deep tendon reflexes were decreased, but were normalized after repeated muscle contractions. EMG of the abductor digiti minimi muscle showed low amplitude in compound muscle action potentials (0.6 mV), waxing phenomenon (292%) with 20 Hz repetitive nerve stimulation (RNS), waning phenomenon (34%) in 3 Hz RNS, and posttetanic facilitation (393%). Stimulated single fiber EMG showed reduced jitter with higher stimulation rates. Serum anti-P/Q-type voltage-gated calcium channel antibodies were negative with no evidence of malignancy. Sensitive assay of acetylcholine receptor antibody in serum revealed a positive titer, while conventional assay was negative. A muscle biopsy was performed and immune complex deposition was demonstrated at the endplate. A nearly complete clinical remission and normalization of electrophysiological features followed immunoadsorption and prednisolone therapy. A sensitive immunoassay of acetylcholine receptor antibodies and immunolocalization of complement at the endplate are useful diagnostic tools in cases presenting with features of myasthenia gravis and Lambert-Eaton myasthenic syndrome.

Autoantibodies↗
PubMed1998

Effect of ultrahigh-dose methylcobalamin on compound muscle action potentials in amyotrophic lateral sclerosis: a double-blind controlled study.

To develop a symptomatic treatment for amyotrophic lateral sclerosis, we compared the effects of ultrahigh-dose and low-dose (25 and 0.5 mg/day, intramuscularly, for 14 days) methylcobalamin on averaged compound muscle action potential amplitudes (CMAPs) in a double-blind trial. No significant changes in CMAP amplitude were found in 12 patients who had the low-dose treatment at either 2 or 4 weeks after start of treatment. By contrast, 12 patients assigned to the ultrahigh-dose group demonstrated a significant increase at 4 weeks. This method may provide a clinically useful measure to improve or retard muscle wasting, if a larger extended trial fulfills its promise.

Action Potentials↗
PubMed1998

Electrophysiological studies of early stage corticobasal degeneration.

We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic-rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon-emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor-evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input from the sensory cortex.

Aged↗