Safety of radio frequency (RF) electromagnetic fields (EMF) is commonly discussed in terms of specific absorption rate (SAR). Phantoms are useful for the dosimetry on energy absorption of RF-EMF exposures. SAR is estimated from measurements of an increase in temperature within the phantom over a short period of time following the exposure. In the past study, a method for visualizing the three-dimensional (3D) distribution of temperature due to RF-EMF energy absorption was reported. A difficulty of this method is that it can only visualize the temperature higher than the clouding point. We focused our interest on capsulate liquid crystal that has been used for visualization of temperature distribution within fluids. The objective of this study is to make a phantom containing capsulate liquid crystal so as to develop a method to visualize 3D distribution of electromagnetic power absorption. We have investigated suitable materials for the transparency phantom and discussed the method to adjust the dielectric properties of the phantom.

We describe a patient with acute cholecystitis and duodenitis associated with Churg-Strauss syndrome. A 36-year-old male, who had been healthy, had abdominal pain following high fever. He had marked hypereosinophilia of 17,000/mm3. Radiographs of the chest disclosed a transient infiltrated lesion in the left lower lung. Ultrasonographic and gastroendoscopic examinations revealed acute cholecystitis and duodenitis, respectively. Endoscopic retrograde cholangiopancreatography demonstrated a filling defect suspecting aberrant ascariasis in the common bile duct. The patient suddenly developed distally dominant mononeuritis multiplex, especially in the upper limbs. Muscle biopsy revealed vasculitis of intramuscular arteries with infiltration of eosinophils. These findings fulfilled the diagnostic criteria of Churg-Strauss syndrome. Corticosteroid dramatically resolved the abdominal symptoms. Cholecystectomy and removal of the foreign body were performed. Histological examinations revealed that necrosis of the gallbladder was caused by occlusion due to thrombosed arteries and that the foreign body in the common bile duct was an aggregate of necrotic epithelium of the bile duct wall surrounded by inflammatory cells. Although abdominal complaints rarely appeared as an initial symptom in the patients with Churg-Strauss syndrome, this syndrome should be taken into consideration for an accurate diagnosis when the patients with abdominal pain of unknown origin had eosinophilia, asthma, or allergic rhinitis.

OBJECTIVE:To investigate spatiotemporal features of the isofrequency bands for 400 and 4000 Hz tones in human auditory cortex and on the hemispheric differences in the arrangement of isofrequency bands.METHODS:We recorded auditory evoked magnetic fields (AEFs) to 400 or 4000 Hz tone pips presented at right or left ear from 31 normal subjects. The dipole location for the N100m sources was successively calculated from the AEFs obtained from the hemisphere contralateral to the stimulated ear.RESULTS:In the right hemisphere, the current sources for 400 and 4000 Hz moved toward the anterolateral direction before the N100m peak, showing parallel arrangement of the isofrequency bands (4000 Hz in medial location). In the left hemisphere, the movement direction of 400 Hz dipoles was anterolateral, while that of 4000 Hz dipoles was lateral.CONCLUSIONS:This difference in the organization of isofrequency bands between right and left auditory cortices reflects distinct functional roles in auditory information processing such as pitch vs. language discrimination.SIGNIFICANCE:This work is the first to disclose isofrequency bands in human auditory cortex based on the analysis of magnetoencephalography.

Diabetic polyneuropathy is a specific form of peripheral nerve disorder, in which distal nerve axons degenerate insidiously under hyperglycemia of diabetes mellitus. Although all types of peripheral nerve fibers are involved, it is usually sensory dominant with eventual involvement of autonomic and motor nerve fibers. Its manifestation ranges from subclinical changes in nerve conduction to painful and severe motor and autonomic disabilities. Once established, it is irreversible. Early identification is, therefore, of clinical importance.

The dipole orientation of equivalent current source for the high frequency oscillations (HFOs) above 300 Hz and that for the underlying N20m were compared. Somatic magnetic fields were recorded over the left hand somatosensory area to right median nerve stimulation at the wrist with a wide-bandpass (0.1–2000 Hz). The HFOs and underlying N20m were extracted by digital filtering of 300–900 Hz and 1–300 Hz, respectively. We found that the orientation of the HFOs and underlying N20m current sources differs and that the HFO source orientation shows a more divergent pattern than the N20m. These results suggest that the somatosensory HFOs are not generated from the pyramidal cell population in area 3b which produces the underlying N20m and that they may reflect activities of the non-pyramidal neuron population.

Diabetic amyotrophy is a relatively rare condition in which unilateral or bilateral muscular weakness acutely or subacutely develops mainly around the hip and thigh in mild type 2 diabetes (1). It often accompanies pain around the buttock and hip, while paresthesia and allodynia are lesser symptoms. Although the name bears the condition like a myogenic disorder, it is a genuine neuropathic condition. To describe this condition, varieties of terms have been applied; proximal diabetic neuropathy (PDN), diabetic femoral neuropathy, and diabetic lumbosacral plexopathy are popular terms to describe this disorder. Dyck et al (2) proposed the term of diabetic lumbosacral radiculoplexus neuropathy, since it seems the most accurate for the knownanatomical distribution of the lesion in this condition. The pathogenesis of PDNhas been understood to be due to nerve/plexus ischemia as a consequence of diabetic micro-angiopathy. Evidence provided by a histological study showing multifocal infarcts of the proximal nerve trunks and lumbosacral plexus strongly supports the ischemic pathogenesis of PDN (3). Multifocal nerve fiber loss has been frequently described in the biopsied cutaneous nerve, too. In 1994 Said et al (4) found necrotizing vasculitis in the cutaneous nerves biopsied from two patients with PDN, and perivascular infiltrates in four patients, in addition to multifocal fiber loss attributed to nerve ischemia. Other investigators then reconfirmed the presence of vasculitis or perivasculitis in biopsied nerves from PDN(5, 6). On the other hand, Pascoe et al (7) reported that inflammatory infiltrates were less commonin the sural nerve specimen from 44 PDNpatients of MayoClinic. Since minor foci with cellular infiltrates in and around the perineurium were sometimes seen in any peripheral neuropathies, many investigators wondered if these changes were due to some kind of metabolic effects of diabetes. Recently, Dyck et al (2) prospectively studied distal cutaneous nerves (sural and superficial peroneal) of 33 PDNpatients in Mayo, and confirmed perivascular inflammation in all nerves examined, vessel wall inflammation in 15 nerves, and previous bleeding in 19 nerves, all of which suggested microscopic vasculitis as a primary event of PDN.Small arterioles, venules, or capillaries were mainly involved. Kelkar et al (8) found polymorphonuclear small-vessel vasculitis affecting epineurial vessels and IgM deposits along the endothelium and in affected vessels. Activated complementdeposition was seen along the endothelium of small vessels. From these distinct findings, an immune-mediated inflammatory theory has rapidly emerged as the primary event in PDN. In this issue Ogawa(9) reported the dramatic effect of highdose intravenous immunoglobulin (IVIg) on the proximal muscular weakness of a 49-year-old patient with PDN.

Clinical spectrum of diabetic neuropathy is variable; it may be asymptomatic, but once established as polyneuropathy, it is irreversible and may finally be disabling. To estimate the prevalence of subclinical diabetic polyneuropathy in the UAE, we undertook a pilot study by means of nerve conduction study (NCS) of peroneal motor and sural sensory studies in 60 diabetics with no symptoms of neuropathy. Neurological examination revealed clinical abnormalities suggesting polyneuropathy in 26 patients, 43% of the patients. NCS revealed abnormal values in 63% of the whole patients. Abnormal NCS was confirmed in 88% of the positive sign group. As to the negative sign group 44% had abnormalities in NCS. Prolonged F-wave latency was seen in 29% in no sign group and in 66% of the patients with positive signs. We found close association between neurological deficit score and abnormalities in NCS. Among various parameter of systemic nerve conduction study in subclinical patients, prolonged F-wave latency seems the commonest abnormality suggesting morphological changes in subclinical diabetic nerve. Decrease in amplitude of compound sensory action potential of sural nerve is another earlier abnormality, which is, then, accompanied by a fall in motor amplitude of peroneal nerve in advanced patients. Recently, our own group of Hirosaki has demonstrated that somatosensory central conduction time (CCT) between the spinal cord entry time and the arrival time to the sensory cortex is prolonged in diabetics. This abnormality might be partly responsible for the irreversible sensory deficits of diabetic neuropathy.

Our recent study showed that the overall prevalence of CIDP was estimated as 2.2 per 100,000 population in Aomori Prefecture, in Northan Honshu of Japan. In our series of more than 80 cases with CIDP, a chronic acquired inflammatory demyelinating polyneuropathy, nearly 30% showed clear laterality of weakness, and electrophysiologic laterality or multifocality was apparent in almost all cases. Nearly 90% of patients were able to walk without walking aids or other assistance. Sixty% showed distal dominant muscular weakness. In 12 patients with age of onset under 15, pes cavus deformity was seen in 5. Two thirds complained numbness in the extremities during progressive phase. Four cases initially showed severe sensory ataxia associated with motor conduction block. It should be, thus, reminded that clinical spectrum of CIDP is enormously wide: chronic acquired demyelinating multiple mononeuropathy showing asymmetric involvement (Lewis-Summer syndrome) should be put on one side of the clinical presentation of CIDP. Multifocal motor neuropathy (MMN) is, on the other hand, an unique syndrome mimicking amyotrophic lateral sclerosis (ALS). There may be, however, true association syndrome of CIDP and ALS presenting both peripheral nerve demyelination and pyramidal sign with progressive bulbar involvement. Recently, several atypical varieties of CIDP showing only one-limb involvement, upper limb weakness rather than lower limb power loss, or proximal weakness, etc ... have been reported in the literature. To realize such clinical variations of chronic acquired demyelinating neuropathy is important for early diagnosis and commencement of treatment of CIDP. Clinical guideline for suspicion of CIDP could be useful for general physicians and neurologists unfamiliar to peripheral neuropathies.

I. Ozaki, Y. Yaegashi, T. Kimura, M. Baba, M. Matsunaga, I. Hashimoto (Japan) 41 Lysyl oxidase, the extracellular matrix-forming enzyme, in rat brain injury sites GM Gilad, HM Kagan, VH Gilad (Israel, USA) 45 Bisphenol-A differently affects estrogen receptors-a in estrous-cycling and lactating female rats AM Aloisi, D. Della Seta, I. Ceccarelli, F. Farabollini (Italy) 49 Peripheral capsaicin receptors increase in the inflamed rat hindpaw: a possible mechanism for peripheral sensitization SM Carlton, RE Coggeshall (USA) 53

Objectives: To investigate peripheral and central somatosensory conduction in patients with diabetes. Methods: 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. Results: 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. 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 current results do not favor a hypothesis that a central-peripheral distal axonopathy plays an important role in development of diabetic polyneuropathy.

(CIDP) is a chronic demyelinating disorder presenting with progressive, stepwise, or relapsing muscle weakness (1). It is characterized by the presence of multifocal areas of demyelination in the peripheral nervous system including the spinal nerve roots. Cranial nerves are also involved occasionally (2). Since the causal mechanismsare not yet understood, some authors (3) approve of using the word 'idiopathic' in place of 'inflammatory' for the T of 'CIDP'. To recognize CIDP is important in any neurological units, because this disorder is basically treatable. It is, however, often difficult or impossible to differentiate from other neuropathies on the basis of the phenotypic expression in an individual patient. Clinical diagnosis totally depends on skilled peripheral nerve conduction study; electrophysiological evidence of active or ongoing multifocal demyelination, or motor nerve conduction block associated with considerable conduction delay, is essential (1). Since the early recognition of this disorder, peripheral nerve thickening has been noted by some careful observers. In the late 50's, Austin first described palpable thickened nerves in his classic steroid-dependent case (4). He mentioned interstitial edemato be an important cause of enlarged nerves, although true interstitial hypertrophy associated with onion bulb formation could develop after recurrent demyelination and

To elucidate the effect of proximal constriction on motor nerve terminals, silk ligations were placed around the tibial nerve in the thigh of rabbits. The ligatures were tight enough to cause Wallerian degeneration in most of the large myelinated fibers; we studied those which remained unaffected. A week after operation, 9 animals showed a fall in amplitude of medial plantar muscle action potential to less than 30% of the pre-operative value on tibial nerve stimulation at the ankle. They were killed after keeping the constriction from 10 to 100 days, and the medial plantar muscles were removed for histological studies on the motor terminals of the medial plantar nerve. AChE-silver staining showed many nerve endings without terminal axons, and "junctional" terminals showing preservation of the continuity proximal to complete degeneration from 10 days to the 40 days after ligation. A few terminal and nodal sproutings were found 10 days after ligation. Transverse sections of the intramuscular portion of the medial plantar nerve showed a decrease in number of the large myelinated fibers. While the ratio of axonal caliber/external diameter of large myelinated fibers (g-ratio) was reduced, g-ratio of small myelinated fibers were varied but as high as that in normal controls from 40 days after ligation. These results indicate distal axonal degeneration (dying back) of the terminal fibers besides the Wallerian degeneration at the level of the ligature and inhibited distal sproutings, which are probably caused by a local disturbance of axonal transport resulting from proximal constriction.

We reported a case of Isaacs' syndrome with abnormal F response detected electrophysiologically. A 14-year-old female was admitted to Hirosaki University Hospital with complaints of progressive myokymia and muscle cramp. PHT and CBZ were partially effective, but discontinued for drowsiness. A neurological examination revealed prominent myokymia and muscle cramp in the legs. The myokymia were worsened by exercise, bathing and diet. An electrophysiological examination showed characteristic F-response; high amplitude, long duration and increased number of phases. The epidural nerve block brought about a disappearance of the myokymia and an improvement of the abnormal features of F response. After repeated double filtration plasmapheresis, the myokymia and abnormal features of F response were remarkably reduced. Although Isaacs' syndrome is thought to have a hyperexcitability at the site of distal peripheral nerve, we suggested that the hyperexcitability might exist at the site of proximal region, and that immunological mechanisms underlie the cause of myokymia and unusual F-response in this case.

Fifty patients with CIDP were treated with cortico-steroids (CS), plasmapheresis (PP) and human immunoglobulin (IG). Objective improvements in strength and in nerve conduction occurred in 53% of the patients after CS. In 50% of the non-responders to CS showed objective improvements after PP, and 40% of them responded to IG. Complete remission was achieved in only one patient. Around 15% of the patients showed poor response to any treatments. Azathioprine combined with CS induced little objective improvements.

Demyelinating conduction block is an important hallmark to distinguish chronic inflammatory demyelinating polyneuropathy (CIDP) from hereditary neuropathies, motor neuron disease and other axonal type neuropathies. The electrodiagnostic criteria of partial conduction block proposed by Asbury and Cornblath, more than 20% drop in CMAP amplitude between proximal and distal sites (e.g. elbow and wrist), may be inadequate, because 20% to 30% drop sometimes occurs in cases with hereditary demyelinating neuropathies. Rhee et al showed that pure temporal dispersion can produce amplitude reduction up to 50% without conduction block. This reduction between elbow and wrist is equivalent to 2% drop/cm. Since lesions are multifocal in CIDP, more than 2% drop/cm in relatively short segments could be a convincing finding of conduction block of CIDP or multifocal motor neuropathy. Our inching study has revealed that chance of lesion is equal from distal to proximal along the nerves of CIDP. However, it is not true in AIDP; most distal sites, roots, and physiological entrapment sites are more fragile, and early demyelination and secondary axonal degeneration start there. Axonal degeneration easily makes demyelinating conduction changes; therefore, in diagnosis of axonal form of AIDP, the possibility of early Wallerian degeneration has to be ruled out by careful follow-up, and delayed F-wave or long-latency units definitely go against the primary axonal pathology.

Following flu‐like illness a 75 year old man developed pure sensory neuropathy that reached a peak at 3 weeks. Cerebrospinal fluid protein was elevated with no increase in cell count The sensory deficits started to improve 4 months later, and were completely resolved 12 months later. Compound sensory nerve action potential, which had been absent initially, became detectable 8 months after the onset The revived sensory potentials progressively increased their size during the 2 year period. A variant of acute inflammatory demyelinating polyneuropathy may be part of a syndrome of acute sensory neuropathy.

Muscle & NerveVolume 18, Issue 1 p. 114-116 Short Report Scal-recorded p14 in median nerve SEPs is abolished by cuneate nucleus lesion Isamu Ozaki MD, Corresponding Author Isamu Ozaki MD Third Department of Medicine, Hirosaki University School of Medicine, Hirosaki, JapanThird Department of Medicine, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki 036, JapanSearch for more papers by this authorHideki Shimamura MD, Hideki Shimamura MD Third Department of Medicine, Hirosaki University School of Medicine, Hirosaki, JapanSearch for more papers by this authorMasayuki Baba MD, Masayuki Baba MD Department of Neurology, Hirosaki University School of Medicine, Hirosaki, JapanSearch for more papers by this authorMuneo Matsunaga MD, Muneo Matsunaga MD Department of Neurology, Hirosaki University School of Medicine, Hirosaki, JapanSearch for more papers by this author Isamu Ozaki MD, Corresponding Author Isamu Ozaki MD Third Department of Medicine, Hirosaki University School of Medicine, Hirosaki, JapanThird Department of Medicine, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki 036, JapanSearch for more papers by this authorHideki Shimamura MD, Hideki Shimamura MD Third Department of Medicine, Hirosaki University School of Medicine, Hirosaki, JapanSearch for more papers by this authorMasayuki Baba MD, Masayuki Baba MD Department of Neurology, Hirosaki University School of Medicine, Hirosaki, JapanSearch for more papers by this authorMuneo Matsunaga MD, Muneo Matsunaga MD Department of Neurology, Hirosaki University School of Medicine, Hirosaki, JapanSearch for more papers by this author First published: January 1995 https://doi.org/10.1002/mus.880180117Citations: 6AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume18, Issue1January 1995Pages 114-116 RelatedInformation

A 9 year old boy had chronic progressive motor-sensory neuropathy that started in early infancy. He had enlarged nerves and pes cavus deformity. Motor conduction studies showed very dispersed, polyphasic compound muscle action potentials with conduction velocities around 2 m/s. A sural nerve biopsy showed severe loss of myelinated fibres. Two months of treatment with corticosteroids restored muscle power. During this time the enlarged nerves became normal and electrophysiological recovery was achieved. Chronically acquired neuropathy in infancy is strikingly similar to genetically determined neuropathy.

Four cases presenting with posterior interosseous nerve syndrome (PIS) in the early period of acute Guillain-Barré syndrome (GBS) are described. The characteristic signs of PIS, consisting of finger extension inability, partial loss of power in wrist extension, and radial deviation during attempted wrist extension were demonstrated bilaterally. Radial nerve conduction study revealed a fall in of compound muscle potential amplitude after proximal stimulation. The signs of PIS became indistinguishable during the course of the illness; this was due to further progression of the forearm weakness veiling the syndrome in some patients, or recovery following plasmapheresis in others. Three of them were amateur sportsmen, in whom active supination-pronation of the forearm was probably responsible for this particular presentation.