EMG of paraspinal muscles in LBP

ABSTRACTS PS. Single fiber composition of motor unit potentials in neurogenic and myopathic disorders. - T. Salmi (Lab. Clinical Neurophysiology, Helsinki University Hospital, Helsinki, Finland) The altered shape of motor unit potentials (MUPs) (increased number of polyphasic MUPs, increased fiber density) in EMG is a very sensitive diagnostic sign of neuromuscular diseases. It is caused by the altered distribution of the muscle fibers correlating with the histological changes in the muscle. A new computerized method was used to analyze quantitatively the single fiber composition of MUPs in different neuromuscular disorders. The signals recorded with a single fiber (SF) or concentric needle electrode are high-pass filtered at 500 Hz. The number of time-locked spikes exceeding 200 #V detection level is counted for each MUP and the statistical result expressed as 'computerized fiber density' (cFD) is calculated on-line. In healthy subjects the mean cFD was quite identical (mean: 1.15-1.20, S.D.: 0.05-0.08) in extensor digitorum communis (EDC) and tibialis anterior (TA) with both SF and concentric electrodes. The number of the time-locked spikes was significantly higher in 66 patients with neurogenic disorders. In patients with ALS, vincristine neuropathy and peripheral neuropathy, all patients had abnormal cFD (1.35-2.40). All patients (n = 10) with nemaline body myopathy had pathological cFD in EDC. In other myopathies and myositis cFD in EDC or TA was abnormal in all patients (1.35-2.20). The method is computer-based, quantitative and on-line. The calculated index was pathological in all patient groups. The method can not discriminate neurogenic from myopathic changes. It is, however, sensitive and fast. Therefore, the method is found to be useful in clinical practice.

PS. Cutaneous and meningeal changes secondary to transcranial electrical stimulation evoking motor potentials in the rabbit. - G. Sancesario *, S. Petrillo **, R. Massa *, S. Correr * * and P.M. Rossini * (* Institute of Neurology, Univ. Tor Vergata, Rome, and * * Institute of Anatomy, Univ. La Sapienza, Rome, Italy) Ultrastructural changes provoked in the leptomeninx by high-current transcranial stimulation were investigated in the rabbit by means of scanning electron microscopy (SEM). Six animals were examined at 2, 24 and 48 h after stimulations. Unifocal anodal square stimuli with a duration of 0.2-2 msec and intensity of 14-30 mA were employed. A total of 320-640 stimuli were delivered in each animal. Tissutal changes included cutaneous edema and subcutaneous hemorrhages in the areas beneath the pericranial cathode. Hemorrhagic petechiae were observed on the skull and the dura mater in the area beneath the stimulating anode. Leptomeninges appeared macroscopically normal in all the animals. However, at the SEM, in 4 out of the 6 animals, swollen leptomeningeal cells, intercellular breaks and macrophages infiltrations were found. The morphological changes affected a roundish area about 1-2 mm

$91 in diameter in each animal, beneath the stimulating anode. These results may indicate the limited spread of the stimulating field created by unifocal arrangements. The severity of the cutaneous and meningeal changes appeared dependent more on the duration of the stimulation pulse than on the intensity and the number of the delivered stimuli. SEM resulted extremely useful in detecting localized damages on the meninges.

PS. Additional evidence that the clinical deterioration in Friedreich's ataxia is unrelated to the peripheral neuropathy. - L. Suntor~ C. Crisci, R. Massini, A. Perretti and G. Caruso (Dept. Clin. Nem'ophysiol., 2nd School of Medicine, University of Naples, Naples, and Fondazione Clin. Lavoro, Centro Medico, Campoli M.T., Italy) We have previously reported that the progressive clinical deterioration of Friedreicli's ataxia patients is unrelated to the degenerative process along peripheral nerve fibres. In fact, the same electrophysiologlc and histologic picture has been observed in patients with a 2 year history of the disease as in patients with a 20-year history and with a completely different clinical picture. In 15 Friedreich's ataxia patients motor and sensory conduction velocity values were re-measured 2-6 years after the first study, and in 2 patients sural nerve biopsy was contralaterally repeated after 6 years. Motor and sensory conduction velocity values obtained at the second examination were practically identical to those observed at the first one. This was true for both individual values and mean values. Moreover, in both patients the second biopsy showed the same severe reduction of large myelinated fibers and the same aspects of regeneration after axonal degeneration as seen in the previous study. This study supports the hypothesis that systems other than the peripheral nervous system must be involved in the progression of the disease.

PS. EMG of paraspinal muscles in LBP. - I. Sarova-Pinhas and O. Pinhas-Hamiel (Dept. of Neurology, The Edith Wolfson Medical Center, Holon, Israel) Forty-four patients with LBP have been examined, generally, neurologically, neuroradiologically and electrodiagnostically. The electrodiagnostic tests included: NCV of the lower limbs nn., F-wave, H-reflex, EMG of tib. ant. and EHL mm and EMG of the lumbar paraspinal ram. The results of the paraspinal mm EMG were correlated with parameters of clinical examination (duration of the LBP, intensity of the pain, Lastgue sign, reflexes, sensation), with the neuroradiological findings and with the results of the other electrodiagnostic examinations. It was found that the EMG of the lumbar paraspinal muscles demonstrated abnormal findings in 77.3% of the patients; the EMG of lower limb mm was abnormal in 38.6%. An especially good correlation was found between the paraspinal mm EMG and the myelography. Because of the special anatomical innervation of the paraspinal mm, the EMG

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VllI CONGRESS OF EMG AND RELATED t_ LINICAL NEUROPHYSIOLOGY

may demonstrate the level of the lesion. We suggest to use the paraspinal mm EMG in routine EMG, not only as a complementary examination in the electrodiagnosis, but as a diagnostic tool, that may replace the E M G of the lower limb's mm and the NCV in case of LBP. The examination is useful because it may demonstrate either the need of further investigations or the needlessness to proceed with them. We concluded that the EMG of paraspinal mm is helpful for a better management of the patient with LBP.

SY. Pathophysiologicai mechanisms of deafferentation pain. J.W. Scadding (The National Hospital for Nervous Diseases and Instltute of Neurology, Queen Square, London WCIN 3BG, U.K.) Pathophysiological mechanisms of possible importance in peripheral and central deafferentation pains will be reviewed. Peripheral sensory nerve injury (PNI) leads to a brief injury discharge, followed by the development of a chronic afferent discharge, extensively studied in experimental neuromas. Ectopic impulse generation, mechanical sensitivity, noradrenaline sensitivity and ephaptic transmission all occur in neuromas, with evidence for a local interaction between noradrenergic sympathetic and somatosensory fibers. In addition after PNI, some dorsal root ganglion cells generate ectopic impulses. Injured dorsal root fibers become highly mechanosensitive. Central changes in the dorsal horn (DH) after PNI include a decrease in inhibitory surrounds with partial deafferentation, reduced presynaptic and postsynaptic inhibitions and disinhibition of completely deafferented DH cells. These decreases of inhibition increase the effect of the reduced sensory input in deafferentation states. Some DH cells take on new receptive fields after deafferentation becoming responsive to nearby intact peripheral nerves. C fiber afferents appear to play an important rote in the maintenance and changes of connectivity. With central lesions causing myelopathic and thalamic pain there is little direct evidence for loss of inhibitions, ectopic impulse generation, abnormal chemical sensitivities, or the development of alternative sensory pathways, though these mechanisms seem most likely to explain these painful states.

33 and 24, respectively. For histological evaluation of the sciatic nerve, semithin sections were used. Edema and subsequent leukocyte infiltration with demyelination paralleled both clinical disease and electrophysiological alterations. Demyelination was quantified conveniently by looking at remyelination on day 60. Our results show that long-term simultaneous clinical, electromyographic, evoked potential and histological studies are essential to fully monitor EAN.

PS. Subclinical hypoesthesia: the value of sensory quantitation. - W. Schady and S. Mitchell (Dept. of Neurology and Medicine, Manchester Royal Infirmary, Manchester MI3 9WL, U.K.) Bedside testing of sensation is notoriously unreliable. We have employed simple, commercially available, techniques of sensory quantitation to demonstrate unsuspected hypoesthesia in patients with both central and peripheral disorders. Nineteen patients with scleroderma, none of whom had neurological symptoms, were subjected to tests of thermal (warm-cold limen and heat pain), vibratory (Vibrameter. Somedic AB) and tactile (von Frey hairs and two-point discrimination) thresholds in the dominant hand and foot. Thermal and pain thresholds were no different from those of controls, but tactile thresholds were significantly higher in patients: 6.8 mN in the index finger and 12.3 mN in the big toe. Two-point discrimination was also significantly impaired in patients, but vibration perception, assessed on the dorsum of the hand and foot, was not. The findings suggest that acral sensory impairment in scleroderma results from damage to intradermal afferent terminals. Fifteen mobile non-edematous patients with hereditary spastic paraplegia (HSP) without clinically demonstrable sensory loss were similarly tested. Whereas all tactile and vibratory thresholds were normal, the warm-cold limen was markedly increased in lower but not in upper limbs. This indicates that HSP is not a pure motor disorder and that spinothalamic tract involvement is likely.

PS. Monitoring of experimental allergic neuritis (FAN). M. Schabet, K.-J. Schott, A. Stevens and H: Wiethrlter (Neurologische Univ.-Klinik, 7400 Ttibingen, F.R.G.)

PS. The value of sensory neurography and compression tests in juvenile, insulin-requiring diabetics. - H.W. Scharafinski, J. J/irg and H J, Lelanann (Dept. of Neurology, University Medical School, GHS Essen, F.R.G.)

Therapeutic trials require good methods for monitoring and investigating the 'spontaneous' course of EAN. We have followed Lewis rats clinically, electrophysiologically and histologically for up to 60 days after immunization with 1 mg bovine myelin. Clinical disease (grade I = limp tall, 2 = abnormal gait, 3 = paraparesis, 4 = tetraparesis or paraplegia) commenced around day 12 and peaked on day 20. Recovery took up to 2 months. Evoked integrated muscle activity of the m. triceps surae and spinal somatosensory evoked potentials of the tibial nerve were recorded on days 0, 14, 18, 24, 33 and 60. The most prominent pathological changes were found on days

Sensory neurography with single and double stimuli at intervals of 3 msec at the right median nerve as well as nerve conduction velocities of the sural nerve were performed in 20 juvenile diabetics without and 15 diabetic patients with neurologic deficits. In addition, we investigated whether abnormal liability of the peripheral nerves to ischemia and compression constitutes the most sensitive indicator of functional disturbance in peripheral nerves. The NAPs of the median nerve were measured immediately before compression up to 60 min at maximum. Compression was released after disappearance of NAPs and sensor-NAPs were measured after decompression