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Biomedical subjects

M Sonoo

Publications and source records attributed to M Sonoo.

At least 19 recordsLinked to original sources
PubMed2006

Spread of the radial SNAP: a pitfall in the diagnosis of carpal tunnel syndrome using standard orthodromic sensory conduction study.

OBJECTIVE: To investigate the occurrence of the spread of the radial sensory nerve action potential (SNAP) among patients with carpal tunnel syndrome (CTS) during standard median orthodromic sensory conduction study (SCS) using index finger stimulation. METHODS: We prospectively examined 74 hands in 56 CTS patients. We stimulated the index finger using ring electrodes. SNAPs were recorded at wrist over median and radial nerves. RESULTS: A spread of radial SNAP was clearly identified over the median nerve despite its small amplitude, in 72/74 hands during stimulation of the base of the index finger. In hands with delayed median SNAP, two peaks were observed; however in hands with absence of genuine median SNAP, only one peak of the spread was noticed. The proximal interphalangeal joint (PIP) stimulation still elicited an identifiable spread in 47/74 hands. CONCLUSION: This spread phenomenon is a previously undescribed pitfall during the standard median orthodromic SCS, frequently occurring in CTS patients. SIGNIFICANCE: In severe CTS cases, one may make wrong conclusion of normal median sensory latency if unaware of this pitfall.

Action Potentials↗
PubMed2005

Reduced amplitude of the sural nerve sensory action potential in PARK2 patients.

The authors performed nerve conduction studies in nine PARK2 and eight idiopathic Parkinson disease patients and found a significant reduction of sural sensory nerve action potential (SNAP) amplitude in eight PARK2 patients who mostly remained asymptomatic. These data suggest that sensory axonal neuropathy may be a common clinical feature of PARK2 and a reduced amplitude of sural SNAP could be a diagnostic indicator of PARK2.

Action Potentials↗
PubMed2005

New and reliable MRI diagnosis for progressive supranuclear palsy.

OBJECTIVE: To evaluate the area of the midbrain and pons on mid-sagittal MRI in patients with progressive supranuclear palsy (PSP), Parkinson disease (PD), and multiple-system atrophy of the Parkinson type (MSA-P), compare these appearances and values with those of normal control subjects, and establish diagnostic MRI criteria for the diagnosis of PSP. METHODS: The authors prospectively studied MRI of 21 patients with PSP, 23 patients with PD, 25 patients with MSA-P, and 31 age-matched normal control subjects. The areas of the midbrain tegmentum and the pons were measured on mid-sagittal MRI using the display tools of a workstation. The ratio of the area of the midbrain to the area of the pons was also evaluated in all subjects. RESULTS: The average midbrain area of the patients with PSP (56.0 mm2) was significantly smaller than that of the patients with PD (103.0 mm2) and MSA-P (97.2 mm2) and that of the age-matched control group (117.7 mm2). The values of the area of the midbrain showed no overlap between patients with PSP and patients with PD or normal control subjects. However, patients with MSA-P showed some overlap of the values of individual areas with values from patients with PSP. The ratio of the area of the midbrain to the area of pons in the patients with PSP (0.124) was significantly smaller than that in those with PD (0.208) and MSA-P (0.266) and in normal control subjects (0.237). Use of the ratio allowed differentiation between the PSP group and the MSA-P group. CONCLUSION: The area of the midbrain on mid-sagittal MRI can differentiate PSP from PD, MSA-P, and normal aging.

Aged↗
PubMed2005

Tibial nerve SEPs localized the lesion site in a patient with early tabes dorsalis.

There is controversy regarding the initial pathology of tabes dorsalis. In a patient with early tabes dorsalis, tibial nerve somatosensory evoked potentials elicited normal P15, a delayed traveling peak in the lumbar bipolar leads, and absent subsequent components. Based on the comparison with normative data and stimulation at different intensities, the authors conclude that only the slower conducting antidromic motor volleys are preserved, whereas the dorsal root is damaged at its distal end.

Adult↗
PubMed2004

N10 component in median nerve somatosensory evoked potentials (SEPs) is not an antidromic motor potential.

OBJECTIVE: To test the hypothesis that the N10 far-field potential in median nerve somatosensory evoked potentials is generated by the motor axons by examining patients with amyotrophic lateral sclerosis (ALS). METHODS: Subjects were 5 ALS patients showing pronounced or complete denervation of median-innervated small hand muscles. We evaluated N10 over scalp, and proximal plexus volleys (PPVs) at lateral or anterior cervical electrode. RESULTS: N10 and PPVs were definitely preserved for every ALS subject. N10 amplitudes of ALS subjects were even significantly larger than control subjects. In one ALS patient completely lacking motor axons, N10 was larger than the largest one among control subjects. CONCLUSIONS: Present results clearly indicate that N10 is not predominantly generated by motor axons but by the whole median nerve dominated by sensory axons. We propose a theory that N10 is a junctional potential generated by the entrance of the median nerve into bone at the intervertebral foramen, producing a positive pole at the non-cephalic reference electrode. Significantly larger N10 in ALS subjects may be due to the lack of cancellation by slower motor axons. SIGNIFICANCE: The hypothesis that N10 is generated by motor axons is refuted, and a new theory of its generation is presented.

Aged↗
PubMed2004

Abductor sign: a reliable new sign to detect unilateral non-organic paresis of the lower limb.

OBJECTIVES: To test a new neurological sign, the "abductor sign," which can distinguish between organic and non-organic leg paresis using synergic movements of the bilateral hip abductors. METHODS: The subjects were 33 patients presenting with paresis of one leg, 17 of organic origin and 16 of non-organic origin (hysteria). To test the abductor sign, the examiner told the patient to abduct each leg, and opposed this movement with his hands placed on the lateral surfaces of the patient's legs. The leg contralateral to the abducted one showed opposite actions for organic paresis and non-organic paresis: for example, when the paretic leg was abducted, the sound leg stayed fixed in organic paresis, but moved in the hyperadducting direction in non-organic paresis. Hoover's sign was used for comparison in the same patients. RESULTS: The abductor sign gave the correct classification for all 33 cases. Hoover's sign was reliable if the results were carefully interpreted, but it was non-diagnostic for 16 patients because of strong hip extensors and in two because of strong hip flexors. Two patients with non-organic paresis succeeded in tricking the examiner by pretending full effort to lift the paretic leg. CONCLUSIONS: The abductor sign is a useful test to detect non-organic paresis, because (1) it is difficult for a hysterical patient to deceive the examiner, (2) the hip abductor is one of the most commonly involved muscles in pyramidal weakness, and (3) the results are easily visible as movement or non-movement of the unabducted leg.

Adult↗
PubMed2001

Single fiber EMG and repetitive nerve stimulation of the same extensor digitorum communis muscle in myasthenia gravis.

OBJECTIVE: To compare voluntary single fiber electromyography (v-SFEMG) and repetitive nerve stimulation (RNS) at the same extensor digitorum communis (EDC) muscle in myasthenia gravis (MG). METHODS: We examined v-SFEMG and RNS successively on the same day in the same EDC muscle. We studied 45 examinations of both v-SFEMG and RNS in 29 patients suffering from MG, together with examinations of RNS in 30 control subjects. RESULTS: Forty-one of 45 (91%) v-SFEMGs showed abnormal results, whereas only 18/45 (40%) RNSs showed an abnormal decrement. The percentage of decrement showed similar correlations with 3 v-SFEMG parameters: percentage of abnormal pairs, percentage of blocking pairs, and the mean MCD value. Examinations showing a significant decrement in RNS had at least 60%, and usually no less than 90%, abnormal pairs, and 10-80% blocking pairs. Some muscles without a decrement had up to 50% blocking pairs. CONCLUSIONS: These results suggest that the blocking phenomenon observed in v-SFEMG is not a direct counterpart of the decrement in RNS. This must be partly because fibers contributing to the decrement are continuously blocked during voluntary contraction, and partly, because smaller motor units explored by v-SFEMG are probably more abnormal in MG than larger motor units mainly contributing to a decrement. Both factors make v-SFEMG much more sensitive than RNS.

Adult↗
PubMed2001

Lower cervical origin of the P13-like potential in median SSEPS.

The authors studied the origin of the scalp P13-like potential in median somatosensory evoked potentials, which have been reported to be preserved in patients with cervicomedullary lesions or in brain death. There were five patients with high to middle cervical lesions (C2/3 or C3/4 level). Small P13-like potentials after P11 were identified for all patients with a noncephalic reference but not with an ear reference. Their onset latencies were slightly earlier than the expected latency of the true P13/14 onset. In two patients, delayed true P13/14s followed by N18s were identified with both noncephalic and ear references. The authors argue that the P13-like potential observed in these patients is a different entity from scalp P13 in normal subjects. Because the C3/4 vertebral level corresponds to the C5 cord level, the origin of the P13-like potential must be below C5, contradicting the previous opinion that it is generated at the cervicomedullary junction or at the high cervical dorsal column. The authors named this potential lower cervical P13 (or lcP13), and present an opinion that it is generated by the beginning of the second spinal ascending volley, which has been described by direct-recording studies in humans.

Adult↗
PubMed2000

Anatomic origin and clinical application of the widespread N18 potential in median nerve somatosensory evoked potentials.

N18 is a broad negativity, with a duration of approximately 20 msec after positive far-field potentials and is recorded widely over the scalp using a noncephalic reference. Its origin has been controversial but its preservation after pontine or upper medullary lesion while loss after high cervical lesions suggested its medullary origin. Comparison with animal studies and direct recording studies in humans leads the authors to conclude that N18 is most likely generated at the cuneate nucleus by primary afferent depolarization. Namely, dorsal column afferents send collaterals to interneurons within the cuneate nucleus, which in turn synapse on presynaptic terminals of dorsal column fibers and depolarize them as a mechanism of presynaptic inhibition. In this way, an electrical sink is formed on presynaptic terminals, whereas their dorsocaudally situated axons serve as a source. The ventrorostral negative pole of the resultant dipolar potential must correspond to N18. The authors obtained a measure to evaluate medullary function objectively, and therefore N18 may be useful as a diagnostic tool for brain death. Usage of a C2S reference is essential for the accurate estimation of N18. Origins of other somatosensory evoked potential components related to the cuneate nucleus are also discussed.

Afferent Pathways↗
PubMed1999

N18 in median somatosensory evoked potentials: a new indicator of medullary function useful for the diagnosis of brain death.

OBJECTIVES: To record N18 in median somatosensory evoked potentials (SEPs) for deeply comatose or brain dead patients and to demonstrate the usefulness of N18 for the diagnosis of brain death in comparison with auditory brain stem responses (ABRs) and P13/14 in median SEPs, which have been conventionally used as complementary tests for the diagnosis of brain death. METHODS: Subjects were 19 deeply comatose or brain dead patients. Thirteen recordings were performed in deeply comatose but not brain dead conditions, and 12 recordings were performed in brain death. N18 was evaluated in the CPi-C2S lead (or other scalp-C2S leads) to obtain a flat baseline. RESULTS: N18 was preserved in 12 of 13 non-brain dead comatose recordings whereas it was completely lost for all of the 12 brain death recordings. P13/14 in median SEPs was preserved for all the comatose recordings, whereas apparent P13/14-like potentials, usually of low amplitude, were seen in nine of 12 brain death recordings-that is, frequent false positives. The ABRs already showed features which were characteristic for brain death (loss of components other than wave 1 or small wave 2) for four comatose recordings, in three of which N18 was preserved. The last result not only corresponds with the fact that ABRs can evaluate pontine and midbrain functions and not medullary function, but further supports the medullary origin of N18. In the four patients followed up for the course of progression from coma to brain death, N18s preserved in normal size during the comatose state were completely lost after brain death was established. CONCLUSIONS: The N18 potential is generated by the cuneate nucleus in the medulla oblongata in the preceding studies. N18 is suggested to be a promising tool for the diagnosis of brain death because there were no false positives and rare false negatives in the present series for detecting the remaining brain stem function.

Adult↗
PubMed1998

P9 in median nerve SEPs is a junctional potential generated by the change of the volume conductor size between trunk and neck.

OBJECTIVES: We aimed to investigate the origin of P9 in median SEPs by applying the junctional potential theory. METHODS: We studied the distribution over the body surface with contralateral shoulder reference in 4 normal subjects. RESULTS: A stationary potential field P9/tN9 (=truncal N9) was recorded: P9 over head and neck (the smaller part), tN9 over trunk (the larger part), the boundary being located between trunk and neck. This polarity agreed with that expected from simulation studies. CONCLUSIONS: P9 is a junctional potential generated by the change of the volume conductor size between trunk and neck.

Body Surface Potential Mapping↗
PubMed1997

Detailed analysis of the latencies of median nerve somatosensory evoked potential components, 2: Analysis of subcomponents of the P13/14 and N20 potentials.

Detailed analysis of P13/14 and N20 wavelets was performed for 62 normal subjects and patients with various lesions along the somatosensory pathway. A histogram of the latencies of all the identified P13/14 wavelets (measured from P13/14 onset) demonstrated three latency-groups, which were named P13, P14a and P14b subcomponents. The relationship between the three newly identified subcomponents and the conventional naming of P13 and P14 was inconstant, indicating the ambiguity of the latter. P14b was most prominent in the contralateral central region, and therefore a P15 positivity slightly after P14b was often recorded in the CPc-Fz and CPc-CPi leads (CPc and CPi are centroparietal electrodes contralateral and ipsilateral to the stimulation). P14b/P15 was lost even in patients with cortical lesions, and thalamocortical fibers were assumed for its origin. The CPc-Fz and CPi-Fz leads registered a low negativity named broad N13', suggesting frontal predominance of the overall P13/14 complex. Both P13 and P14a were identified in a patient with a pontine lesion, and a caudal brainstem origin for both was suspected due to the onset of two repetitive bursts of the ascending lemniscal volley. We refuted the presynaptic origin of the scalp P13 potential and pointed out that a prolonged and/or polyphasic P11 frequently observed in patients with high cervical lesions can be mistaken as scalp P13. A histogram of the latencies of all the identified negative wavelets of N20 in the CPc-Fz lead (measured from N20 onset) revealed five definite latency-groups, which were named N20a, N20b, N20c, N20d and N20e subcomponents. The highest peak of N20 actually corresponded to either N20b, N20c or N20d, and this uncertainty, which must be related to intracortical processes, resulted in a large instability of the N20 peak latency as well as the age and sex dependence of the N20 onset-peak interval, both of which were demonstrated by our preceding study (Sonoo, M., Kobayashi, M., Genba-Shimizu, K., Mannen, T. and Shimizu, T. Detailed analysis of the latencies of median nerve SEP components, 1: selection of the best standard parameters and the establishment of the normal values. Electroenceph. clin. Neurophysiol., 1996b, 100: 319-331). Negative subcomponents in the CPc-NC lead and positive subcomponents in the Fz-NC lead constituted mirror images of each other, which suggested that these subcomponents were generated within area 3b.

Adult↗