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Biomedical subjects

M Sonoo

Publications and source records attributed to M Sonoo.

At least 37 records · Page 2Linked to original sources
PubMed1997

[A case of left subclavian artery occlusion with transient ischemic attacks probably in the internal carotid artery system].

The subclavian steal syndrome is known to steal blood flow from the vertebrobasilar system. However, we experienced a case of subclavian artery occlusion presenting transient ischemic attacks in left internal carotid system. A left handed 41-year-old man developed transient dysarthria and right hemiparesis including face several times when he physically used his arms. He had no symptoms of the vertebrobasilar system. A brain MRI revealed an old cerebral lacuna at the left putamen supplied by perforating arteries of the middle cerebral artery. The angiography demonstrated a complete occlusion of the proximal portion of the left subclavian artery without a reverse flow from the vertebral artery. Instead, descending cervical branches and deep cervical branches of the ipsilateral external carotid artery supplied collateral pathways to the occluded subclavian artery. On the basis of above observations, we speculated that he developed symptoms of the internal carotid system due to the steal through the collateral network of the cervical arteries directed to the subclavian artery. We should consider not only the vertebrobasilar system but also the internal carotid system, especially its cervical artery network, when exploring collateral pathways for the subclavian steal syndrome.

Adult↗
PubMed1996

Preserved widespread N18 and progressive loss of P13/14 of median nerve SEPs in a patient with unilateral medial medullary syndrome.

Median nerve somatosensory evoked potentials (SEPs) in a patient with unilateral medial medullary syndrome of recent onset having an MRI-confirmed lesion at upper medulla were investigated. Cortical N20 following stimulation of the affected limb was extremely depressed and delayed, whereas widespread N18, which was best manifested by the CPi-C2S lead (CPi is centroparietal electrode ipsilateral to the stimulation), showed no significant difference regarding amplitude and duration between affected and non-affected sides. The result supported our previous opinion that the principal part of N18, the broad negativity lasting around 20 ms, originates from the cuneate nucleus at the medullary level. Less steep onset of N18 on the affected side suggested that some structures rostral to the cuneate nucleus, possibly the termination of the overall ascending volley, may contribute to the earliest part of N18. P13/14 on the affected side normally preserved at the first examination progressively declined and finally disappeared after 4 months, which suggested that the major part of P13/14 is generated within caudalmost medial lemniscus, as well as the occurrence of retrograde degeneration of lemniscal fibers.

Electrophysiology↗
PubMed1996

[Dystrophin abnormality in a patient with polymyositis associated with primary biliary cirrhosis and myocardial injury].

We have reported a 58-year-old Japanese female with polymyositis, primary biliary cirrhosis (PBC) and arrhythmia. In contrast to the previously reported 13 cases of polymyositis associated with PBC, symptoms and laboratory data abnormalities responded to oral administration of predonisolone. Interestingly, immunohistochemical and immunoblot analyses of biopsied skeletal muscle revealed diminished expression of dystrophin carboxyl-terminal domain in the sarcolemma, suggesting that, in analogy to Duchenne muscular dystrophy, secondary abnormality of the link between the basal lamina and cytoskeleton via the dystrophinglycoprotein complex may have played a role in the molecular pathogenesis of muscle fiber degeneration in this patient.

Arrhythmias, Cardiac↗
PubMed1995

Multi-MUP EMG analysis--a two year experience in daily clinical work.

A new quantitative motor unit potential (MUP) analysis method, called multi-MUP analysis, is described. Multi-MUP analysis is a type of decomposition analysis of the EMG signal. At each site 6 different MUPs may be recorded during an epoch of 4.8 sec. Calculation time is about 3 sec. A study of 20-30 MUPs including editing takes 4-8 min. Compared to many earlier MUP analysis methods it is faster and more user friendly, therefore it can be used in daily routine EMG analysis. The accuracy and reliability of the method are good. The differences from methods based on manual analysis, spike triggered averaging, template matching and decomposition are discussed. The main advantages of multi-MUP analysis are: (1) quick acquisition of many MUPs; (2) simultaneous collection of several MUPs at one recording site; (3) possibility to analyze not only low threshold MUPs; (4) less bias in the selection of MUPs; and (5) the reproducibility of the results that allow the same reference values to be used in different laboratories. So far we have successfully used this method for 2 years on more than 2000 patients.

Electromyography↗
PubMed1994

Assessment of variability in the shape of the motor unit action potential, the "jiggle," at consecutive discharges.

A method for quantifying shape variability, the jiggle, or motor unit potentials (MUPs) recorded with conventional EMG electrodes is presented. Amplitude variability at each point of time of the MUP was analyzed. Two new parameters are proposed: the normalized value of the consecutive amplitude differences (CAD), and the cross-correlational coefficient of the consecutive discharges (CCC). Simulations showed that increased jitter of the constituent single fiber potentials increases the jiggle as expressed by an increase in CAD and decrease in CCC values. Even when the jitter value of each component was fixed, increased temporal dispersion increased the jiggle whereas an increased number of fibers decreased the jiggle. This new method has been applied in normal subjects, patients with chronic neurogenic diseases and patients with ALS. Jiggle was significantly increased in the ALS group, in agreement with visual observations. We believe that this method for quantifying jiggle will increase the information obtainable from routine EMG investigations.

Action Potentials↗
PubMed1993

The ability of MUP parameters to discriminate between normal and neurogenic MUPs in concentric EMG: analysis of the MUP "thickness" and the proposal of "size index".

The ability of a motor unit potential (MUP) parameter or a set of parameters to discriminate between control MUPs and MUPs from muscles with severe to moderate inactive neurogenic changes was investigated using discriminant analysis. As a single parameter, area gave rather good discrimination, while amplitude, duration and area/amplitude did not give good discrimination. Only 15-30% of MUPs from neurogenic muscles were judged to be abnormal by duration alone. The combination of amplitude and the area/amplitude ratio (area/amp; MUP thickness) improved the discrimination considerably and around 70% of MUPs in the neurogenic group were judged to be abnormal. A simple assigned discriminant function, 2 x log 10(amp) + area/amp, gave similar good results for both biceps brachii and tibialis anterior muscles, and this value was named as "size index." The experiment of manual scanning of an MUP revealed that area/amp increases, that is, the MUP becomes thicker, as the amplitude decreases for each MUP with increasing recording distance, while the size index remains almost constant for each MUP irrespective of the electrode position. The new parameter, size index, is promising since it is more stable and gives better discrimination results than duration.

Adult↗
PubMed1991

[Mono-radiculopathy multiplex--multiple infarction of the cauda equina caused by intravascular lymphomatosis].

A 55-year-old man had felt numbness of the bilateral peroneal sides of legs for 6 months. Then hepatosplenomegaly, anemia, body weight loss and fever developed, and a diagnosis of malignant histiocytosis (MH) was made by revealing the presence of innumerable atypical histiocytes with hemophagocytosis in the bone marrow. Soon later, sensory disturbance of bilateral peroneal sides of legs (right side dominant) developed and aggravated with painful dysesthesia and weakness of the legs for the last 2 weeks before death. Electrophysiologically, sensory conduction velocity of the sural nerve was normal and somatosensory evoked potentials from tibial nerve were normal before P15 but were not evoked at all after the lumbar potential, suggesting lumbosacral radiculopathy. Autopsy showed multifocal ischemic lesions and secondary degeneration of the lumbosacral nerve roots associated with necrosis and fibrosis of the radicular vessels and intravascular infiltration of atypical mononuclear cells which were positive for B cell markers. The neurological manifestations and the distribution of ischemic lesions, which were similar to those of vasculopathic mononeuropathy multiplex, would deserve the name of "monoradiculopathy multiplex".

Cauda Equina↗
PubMed1991

[Diagnostic criteria of conduction block and the spectrum of diseases which is accompanied with conduction block].

To establish the criteria of conduction block is essential for its clinical application. Nerve conduction studies were performed on 15 normal controls. Peak-to-peak amplitude, negative wave area and negative wave duration were measured and their ratios between proximal and distal stimulation were estimated. The results were summarized in Table. Decrease of amplitude and area was the more conspicuous in the longer segment, and therefore it was suspected to be due to the duration-dependent phase cancellation. Since area reduction was less than the amplitude reduction, the area was a more useful parameter than the amplitude. The importance to provide different normal values for the different nerve segment was emphasized. The diseases which are known to be accompanied with conduction block include AIDP, CIDP and entrapment neuropathy. Multifocal motor neuropathy with conduction block associated with anti-GM1 antibody is recently noticed and we presented the cases we experienced. By contrast, it has been demonstrated that HMSN type 1 does not show conduction block. We examined diabetic and uremic neuropathies and showed that they do not have conduction block. These facts suggest that the demyelination does not always produce conduction block.

Demyelinating Diseases↗
PubMed1990

[Motor-dominant neuropathy with multifocal conduction block].

Patient 1 was a 39-year-old man; patient 2, a 42-year-old woman; patient 3, a 78-year-old man. Leading symptoms were chronic asymmetrical weakness in all three cases, which started in a distal portion of the upper extremities. Muscle atrophy was often less prominent than would be expected from the power of the muscle. Fasciculations were observed in two patients and the initial symptom of patient 2 was painful cramp of the right thumb. Patient 1 initially had mild transient dysesthesia of the right fingers. The other two patients had no sensory symptoms or signs. General laboratory tests revealed no particular abnormalities except that patient 3 had mild diabetes mellitus, although the type of neuropathy in patient 3 was quite different from diabetic neuropathy. Total protein concentrations in the cerebrospinal fluid were 34, 32 and 43 mg/dl in three patients, respectively (normally, less than 40 mg/dl). Motor nerve conduction studies revealed conduction block in more than one nerve in every case. Conduction velocities were generally normal in those segments of nerve where conduction block was not detected. Serum anti-ganglioside antibodies were investigated by Enzyme-linked immunosorbent assay (ELISA). Glycolipids used as the antigen include GM1, GM2, GM3, GD1b, GD3, GT1b, GQ1b, GA1 and galactocerebroside. Strong IgM antibody activity against GM1, GD1b and GA1 was noted in patient 1. Weaker but significant IgM antibody activities against GM1 and GA1 were detected in patient 2 and 3. Thin-layer chromatography immunostaining also confirmed these results. Muscle biopsy in patient 1 revealed a lot of target fibers and profuse polyglucosan bodies in the axons of intramuscular nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Readiness potential associated with an athetotic movement].

A 28-year-old man was admitted to our hospital because of focal seizures probably generated by the right sensorimotor cortex with secondary generalization for 3 months. He had 5 years history of keratoconjunctivitis and iriditis. Physical examination revealed minimal hemiparesis and hyperreflexia in the left side and left papillitis. Cerebrospinal fluid analysis showed 75 cells per cubic-millimeter (all lymphocytes) and 88 mg/dl protein. Computerized tomography of the brain revealed elimination of the sulcus and vague enhancement of the cortex in the right cerebral hemisphere. The symptoms and the laboratory data improved spontaneously in a few months. Slow, athetotic movements were observed in the left forearm extensor muscles for about 10 days period. Electromyography (EMG) of these movements showed bursts of 300-800 sec in duration which repeated almost regularly at a varying frequency of 0.3-0.5 msec. The electroencephalographic (EEG) studies revealed slow background activities over the right hemisphere. The simultaneous recording of EEGs and EMGs demonstrated no EEG activity correlated with the athetotic movements. In the jerk-locked averaging (JLA) recorded with the time constant of 0.3 sec, no spiky or sharp EEG activities were detected before the EMG discharges of the left forearm extensor muscles. However, JLA with the time constant of 3.2 sec disclosed a slow negative shift which preceded the athetotic movement by about 500 msec. This negative potential was fairly localized in the right central area, which was thought to be consistent with the hand area of the motor cortex contralateral to the muscles showing the athetotic movements. The present case had a wide-spread, mainly unilateral lesion in the cerebral hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMedDate not supplied

Posterior cervical N13 in median nerve SEP has two components.

Somatosensory evoked potentials (SEPs) to median nerve stimulation were investigated in normal controls and patients with cervical lesions. Attention was paid primarily to the N13 and P13 components in the posterior and anterior cervical records with non-cephalic references. In normal subjects the CV2 and CV6 electrodes registered N13 with almost the same amplitude. Dissociation between N13 at the CV2 electrode (ucN13) and N13 at the CV6 electrode (lcN13) was observed in the patients. In 4 patients with cervical dorsal column lesions, lcN13 was preserved but ucN13 was almost completely absent. Anterior cervical P13 (acP13) was preserved. In a patient with syringomyelia, lcN13 and acP13 were greatly attenuated while ucN13 was relatively well preserved. These results suggested that the origins of ucN13 and lcN13 are different. The generator of lcN13-acP13 was assumed to be the postsynaptic potential of the dorsal horn interneurons. Upon comparison with previous animal studies and intraoperative studies, it was concluded that the generator of ucN13 is the postsynaptic potential of the cuneate nucleus.

Adult↗
PubMedDate not supplied

Widespread N18 in median nerve SEP is preserved in a pontine lesion.

Widespread N18 potential to median nerve stimulation was preserved in a patient who had profound unilateral disturbance of deep sensation and a lesion of the pontine medial lemniscus confirmed by MRI. It was concluded from this result that at least a significant part of the N18 potential was generated caudal to the pontine level or at higher levels via extralemniscal pathways. Careful review of studies in man with intraoperative recordings seemed to support that the N18 potential already exists at the medullary level. We suggested that the potential generated at the cuneate nucleus which was described in cats may correspond to part of the N18 potential.

Brain Diseases↗
PubMedDate not supplied

SEPs in two patients with localized lesions of the postcentral gyrus.

Scalp distributions of median nerve SEPs were studied in normal controls and 2 patients with localized lesions of the postcentral gyrus. In controls, parieto-occipital electrodes registered N20-P27 while frontal electrodes registered P20-N27. Other small components, parieto-occipital P22 and frontal N22, were recognized in about half of the control records. The wave forms at a frontal and a parieto-occipital electrode, both distant from the central region, formed exact mirror images of each other concerning N20-(P22)-P27 and P20-(N22)-N27. Electrodes near the central region contralateral to the stimulation registered cP22-cN30 (central P22 and central N30). When the postcentral gyrus was damaged, N20/P20-P27/N27 and cP22-cN30 were eliminated and the only remaining components were a frontal negative wave (frN) and a contralateral parieto-occipital positive wave (poP). Digital nerve stimulation also evoked poP and frN in both cases. In case 2, poP coincided with P22 of the non-affected side. The following generators were proposed; N20/P20-P27/N27: area 3b, cP22-cN30: areas 1 and 2, poP/early frN (= P22/N22): area 4 at the anterior wall of the central sulcus (due to direct thalamic inputs to motor cortex), late frN: uncertain (SMA?, SII?).

Adult↗
PubMedDate not supplied

Origin of the widespread N18 in median nerve SEP.

The widespread N18 potential in median nerve SEP was studied in normal subjects and in patients with high cervical, brain-stem and thalamic lesions who had profound disturbances of deep sensation. N18 was well identified in the HSi-CV2 derivation in every normal subject as a broad elevation from the baseline lasting about 20 msec. The cortical N20 was absent in all patients. N18 was absent in a patient with a dorsal column lesion at C1-2 level. The amplitude and configuration of N18 were normal in all other patients with brain-stem and thalamic lesions, including a patient with a lesion at the ponto-medullary junction. The sagittal distribution of N18 was studied in a patient with a thalamic lesion and an oblique distribution with the maximum region between Cz and nasion was demonstrated. The present results indicate that at least the greater part of N18 is generated at the caudal most brain-stem or through branches from this level. Taking previous animal and intraoperative studies into consideration, we think it most probable that the main part of N18 corresponds to the ventro-rostral negative pole of the dipolar potential generated at the cuneate nucleus by the primary afferent depolarization of presynaptic terminals of dorsal column fibers.

Adult↗