Search

The purpose of this study was to evaluate the effect of additional light hand contact (F<1 N) in the region of the hypothenar eminence on forward movement of the center of pressure (COP) and dominant hand. Subjects sled their hypothenar eminence on a vertically-oriented pressure sensitive board while reaching forward beyond their arm length. In the two separate experiments forty nine healthy, college-aged volunteers participated in the study. Thirty subjects (mean age of 22.2±2.4 years, 6 male and 24 female) participated in the experiment on level ground and nineteen subjects (22±2.6 years, 5 male and 14 female) in the experiment on an elevated surface. The forward displacement of the COP was significantly larger (p = 0.002) when subjects were allowed to slide with the hand as compared to no contact when the activity occurred on level ground (84±10 mm and 79±11 mm, respectively), and on a one meter elevated surface (71±17 mm and 65±21 mm, respectively). The maximal forward reach of the dominant hand was significantly greater when subjects were allowed to slide with the hypothenar eminence as compared to the no contact condition on the level ground (336±35 mm and 344±38 mm, respectively, p<0.02), and on the one meter elevated surface (298±58 mm and 307±58 mm, respectively, p<0.01). This data indicate that subjects were able to use additional haptic information from the hypothenar region to bring their COP and dominant hand further forward while standing on level ground as well as on a one m elevated surface.

Jitter measurement with axonal microstimulation was used to study synaptic function at 115 neuromuscular junctions (NMJs) of normal subjects at various stimulation rates. Jitter was lowest at 0.5 Hz; it increased slightly at 1, 2, and 5 Hz and remained at that level at 10 Hz (a light work load) and 20 Hz (a heavy work load); and it increased further at 50 Hz (an extreme load). This pattern was seen for the majority of the NMJs, suggesting a high safety factor of neuromuscular transmission maintained rather uniformly over a wide range of discharge rates. A proportion of the normal NMJs had relatively large jitter; these tended to show prominent facilitation as the rate was raised from 5 or 10 to 20 Hz. Similar but more dramatic facilitation improving the safety factor was seen at most NMJs in myasthenia, which was studied for comparison. Such facilitation was not found at normal NMJs with low jitter., (Copyright 2002 Wiley Periodicals, Inc.)

We report a 35-year-old patient with megaloblastic anemia who presented with features of subacute combined degeneration of the cord. Electrophysiological studies showed features of axonal neuropathy. In addition, there was evidence of prominent focal proximal conduction block in several nerves. After treatment with cyanocobalamin the neuropathy improved, and the peripheral nerve conduction block detected earlier disappeared. Reversible nerve conduction block as a feature of vitamin B12 deficiency in man, to our knowledge, has not been reported in literature, so far.

Acetylcholinesterase (AChE) mRNA levels are severalfold higher in fast rat muscles compared with slow. We hypothesized that AChE mRNA levels and AChE activity in the neuromuscular junction depend on a specific nerve-induced pattern of motor unit activation. Chronic low-frequency stimulation, mimicking the activation pattern in slow muscles, was applied to fast muscles in rats. Molecular forms of AChE were analyzed by velocity sedimentation, and AChE mRNA levels were analyzed by Northern blots. AChE mRNA levels in stimulated fast muscles dropped to 10-20% of control after 1 week and became comparable to those in slow soleus muscles. The activity of the junctional A12 AChE form in 35 d stimulated fast muscles decreased to 56% of control value, reaching that in the soleus muscle. Therefore, synaptic AChE itself depends on the muscle activation pattern. Complete inactivity after denervation also decreased the AChE mRNA level in fast muscles to <10% in 48 hr. In contrast, profuse fibrillations observed in noninnervated immature regenerating muscles maintain AChE mRNA levels at 80% of that in the innervated fast muscles. If protein synthesis was inhibited by cycloheximide, AChE mRNA levels in 3-d-old regenerating muscle, still containing myoblasts, increased approximately twofold. No significant increase after cycloheximide application was observed either in denervated mature fast muscles or in normal slow muscles. Low AChE mRNA levels observed in those muscles are probably not caused by decreased stability of AChE mRNA as demonstrated in myoblasts.

Forty one patients with the clinical diagnosis of Behçet's syndrome from two teaching hospitals in Kuwait were studied. There were 34 male and seven female patients. Age at presentation ranged from 14 to 48 years. Neurological manifestations were present in 24 patients. Eleven patients showed evidence of increased intracranial pressure, and 10 of these had radiologically confirmed dural sinus thrombosis. Five patients presented with a meningoencephalitic or meningomyelitic picture, three with a stroke-like picture, and three with primarily brain stem signs. One patient developed trigeminal neuritis, and five patients exhibited (along with other features) variable degrees of psychological manifestations. All patients with neurological involvement were treated with steroids, and some also had courses of other immunosuppressant drugs and colchicine. The disease took a relatively benign course, except those patients with meningoencephalitic and meningomyelitic presentation, one of whom died from the disease. Those treated early had a better prognosis. The incidence of dural sinus thrombosis in this series of patients is unusually high. In most patients, the course of the disease was more favourable than reported in the literature. This may be attributed to early and aggressive treatment.

The use of single fibre electromyography (SFEMG) in the study of neuromuscular transmission across individual motor endplates in situ is reviewed. The neuromuscular jitter can be studied both during voluntary contraction and electrical activation of the muscle fibre. The differences, pitfalls and advantages of these methods are discussed. Findings in myasthenia gravis and other disorders of the neuromuscular transmission are examined.

Single fiber EMG recordings from patients with myasthenia gravis obtained during axonal microstimulation revealed an occasional bimodal distribution of response latencies. This phenomenon could be dependent on stimulus strength, however, in a way different from that in the axon reflex. It is suggested to be due to dual neuromuscular junctions (NMJs) supplied by two different motor neurons. Some cases of bimodal jitter were not dependent on stimulus strength and are assumed to be due to dual innervation by the same neuron. The phenomenon could only be demonstrated at abnormal NMJs with partial impulse blocking. It is suggested to reflect multiple reinnervation of muscle fibers that had undergone functional or structural denervation in the course of the immune attack against the original NMJ. This study suggests that the coexisting NMJs from the same or different motor neurons may be functional at the same time.

Single-fiber electromyography (SFEMG) allows precise study of the microphysiology of the human motor unit under normal conditions. The physiological parameters that can be quantified include impulse transmission along the intramuscular axon collaterals, pre- and post synaptic events at the neuromuscular junction, and muscle fiber membrane properties. This chapter illustrates some of the advantages of SFEMG in studies of neuromuscular fatigue in normal muscle, as well as in disorders of neuromuscular transmission, and conditions associated with disturbed muscle fiber depolarization-repolarization.

Controversy regarding the nosological position of the syndrome of ophthalmoplegia, ataxia and areflexia (Miller Fisher syndrome) exists. The oculomotor dysfunction was presumed to represent an unusually symmetrical peripheral cranial nerve dysfunction. To investigate the neuro-ophthalmic manifestations in this rare syndrome we reviewed 109 reports describing 243 cases. The ophthalmoplegia was remarkable in its constant association with a cerebellar type ataxia. It was described to be remarkably symmetrical at all stages of development and recovery. From the early description of the syndrome by Fisher the ophthalmoplegia was observed to evolve as a symmetrical failure of upgaze followed by loss of lateral gaze and last by downgaze, recovery develops in the opposite pattern. Despite the severe nature of the ophthalmoplegia, 58 patients were reported to have sparing of downgaze and 192 (79%) had relative sparing of the eye lids. Active lid retraction and preserved Bell's phenomenon, despite upgaze paralysis, were described in 22 and 15 patients respectively. Upper lid jerks were described in 2, Parinaud's syndrome in 2, convergence spasm in 6, internuclear ophthalmoplegia in 15 and horizontal dissociated nystagmus in 11. Interestingly 23 were reported to present with paralysis of abduction progressing to lateral gaze paralysis and 5 had paralysis of abduction and contralateral gaze paralysis. Four had defective vestibulo-ocular reflex despite recovery of upgaze, 10 had central type nystagmus including rotatory, retractory and rebound nystagmus. Relative preservation of optokinetic nystagmus and preservation of vestibulo-ocular reflex despite an otherwise complete ophthalmoplegia were reported in 6 and 2 patients respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

The neuro-ophthalmological manifestations of 20 patients with the syndrome of ophthalmoplegia, ataxia and areflexia are described. The symmetrical nature of the ophthalmoplegia and the associated cerebellar ataxia point to centrally placed lesions. Several supranuclear, nuclear and internuclear ophthalmological signs are identified. Some of these, like partial sparing of the levator palpebrae and normal downgaze in the presence of severe ophthalmoplegia are noted too frequently to be just unusual signs of peripheral oculomotor dysfunction. Other identified features included upper lid retraction on attempted upgaze and preserved Bell's phenomenon in the presence of paralysis of the latter, as well as several other central ophthalmological signs. These findings contrast with those seen in the Guillain-Barré syndrome and, thus, the syndrome of ophthalmoplegia, ataxia and areflexia is not a mere variant of it.

Fifteen patients with the classical syndrome of ophthalmoplegia, ataxia, and tendon areflexia (SOAA) were studied in an attempt to clarify the mechanisms of ataxia and myotatic hyporeflexia. All showed features of cerebellar rather than sensory ataxia. Peripheral nerve conduction studies, including F-waves, were normal in a majority of the patients, as was needle EMG. Low-amplitude compound sensory nerve potentials were seen in four patients only, and mild slowing of sensory conduction velocity in two. Three had abnormal blink reflex studies, suggestive of a central lesion in two, and another two showed a transient delay of N5 peak of brainstem auditory evoked potentials. Somatosensory evoked potentials were normal. Despite clinically depressed or absent tendon jerks, T-waves were elicited at normal latencies. These findings do not support the prevailing view that the neurological abnormalities in SOAA are due to involvement of sensory fibres in the peripheral nerves and dorsal roots. We suggest that lesions scattered in the brainstem tegmentum and in the cerebellar peduncles are responsible for the ataxia and the depressed tendon jerks.

While recording activity from individual muscle fibers by single fiber EMG (SFEMG), stimulated either through their axons or directly, the length of the recorded muscle fiber was changed--stretched or made shorter--by manipulating the recording needle or by passive joint movements. This resulted in significant changes of latency corresponding to an increase in propagation velocity on shortening of the muscle fiber and to a slowing of its lengthening. The maximum increase in velocity was estimated to 33% and slowing to about 22%. These length-dependent changes of muscle fiber propagation velocity are suggested to contribute to the supernormal phase of propagation velocity recovery function and to be responsible for an important part of the myogenic, interdischarge interval-dependent, jitter.

Stretch reflexes of posterior tibial (PT) and triceps surae (TS) muscles were studied electrophysiologically in 27 children with unoperated unilateral congenital equinovarus deformity, in an attempt to evaluate changes in tone of the leg muscles as a possible pathogenetic factor. Significantly reduced latency of the PT responses on the affected side was recorded in a majority of patients. In most patients the amplitudes of the PT responses were asymmetrical; however, lateralization was inconsistent. The TS responses were asymmetrical in a smaller proportion of the patients, though still significantly different from the controls. The findings suggest an asymmetrical increase in excitability level of the PT motoneuron pool on the affected side.

Electrical microstimulation of motor axons in conjunction with single fiber EMG (SFEMG) is increasingly used to measure the jitter of the motor endplates. This study examines the jitter of the stimulation site on the axon when stimulus strength is at threshold. In the absence of spurious blocking, this was found to be 5 microseconds on the average. With intermittent blocking, however, a mean additional jitter of 40 microseconds was obtained. The latter is considered to result from changing propagation velocity in the muscle fiber due to irregularity of activation rate. In clinical jitter studies, inadvertent threshold stimulation can result in significant error when associated with intermittent blocking.

Single fiber EMG (SFEMG) with axonal micro-stimulation is a convenient method to study the neuromuscular jitter at the individual motor end-plates. Compared to the original method of jitter measurement in voluntarily activated muscle, it has the advantage of perfect control of the discharge rate, including pauses in activity, useful in quantitative estimation of the neuromuscular transmission defect. It obviates the need to search for muscle fiber pairs. It can be used in young children and in uncooperative patients, as well as those with impaired voluntary motor control. It is useful in animal experiments as well as veterinary medicine. The technique eliminates the possibility of overestimating the jitter due to unrecognized interdischarge interval dependent jitter, as well as that of underestimating it due to unrecognized low jitter in split muscle fibers. The technique has certain pitfalls causing under- or overestimation. The paper gives practical guidelines and hints as to how to avoid some of these, particularly errors due to overlooked threshold stimulation and to unrecognized direct muscle fiber stimulation.

This article reviews the essential technical principles and findings with electrical microstimulation as used in conjunction with single-fiber electromyography (SFEMG). It highlights the details in the microphysiology of the motor unit that can be conveniently studied with these methods, particularly the neuromuscular transmission at the individual motor endplates, muscle fiber recovery functions, and a variety of late responses. The differences, advantages, and disadvantages of the stimulation method of jitter measurement, compared to the original method, in the voluntarily activated muscle are described. Special attention is given to the pitfalls of the technique. Indications for clinical use of stimulation SFEMG in the electromyography laboratory are suggested.

Direct electrical stimulation with paired pulses at varied intervals was used to study the propagation velocity and action potential amplitude recovery functions (VRF and ARF) of single muscle fibers. Following a subnormal period with slowed conduction, most of the muscle fibers tested in healthy subjects showed a period of supernormal propagation velocity starting at 3 to 12 ms, with a peak between about 5 and 15 ms, a mean increase of 7%, and an approximately logarithmic decay toward 1 second. The onset of supernormality was earlier in muscle fibers from patients with muscular dystrophy and significantly delayed in those from denervated muscles. Denervated muscle fibers also had a significantly longer refractory period.

The jitter and frequency of blocking was studied at single motor end-plates in 10 patients with myasthenia gravis (MG) and in a patient with Lambert-Eaton myasthenic syndrome (LEMS), using single fiber EMG (SFEMG) with axonal microstimulation at rates varying from 0.5 Hz to 20 Hz. While some myasthenic motor end-plates showed lowest degrees of transmission disturbance at the lowest rates and most pronounced abnormality at the highest rates of stimulation, over one-half were most abnormal at intermediate rates and improved at higher rates. In 1 patient, all end-plates behaved in this way. On the other hand, all end-plates in the LEMS patient showed the expected improvement of the abnormal jitter and blocking on increasing the stimulation rate. It is argued that improvement of jitter and blocking at higher rates, unless dramatic, does not necessarily suggest a presynaptic abnormality.

Twelve patients with Wilson's disease, aged 11-25 years, underwent brainstem auditory evoked potential (BAEP) study. The results were correlated to clinical, neuroradiological and laboratory data. Ten had prominent to severe neurological manifestations, suggestive of involvement of one or several CNS structures, and 2 were neurologically free. All had evidence of abnormal copper metabolism, and 8 had CT scan evidence of brain atrophy, or hypodense areas in basal ganglia, or both. The 2 patients without neurological manifestations as well as one with neurological signs had normal BAEP. One patient with neurological signs had increased N1 latency due to cochlear hearing loss, but normal interpeak intervals, while 8 of 10 patients with prominent neurological symptoms and signs had abnormal BAEPs (prolongation of NIII-NV interpeak interval). The value of NIII-NV interpeak interval correlated with the number of different neurological signs (neurological score) attributable to involvement of different CNS structures (r = 0.64 at P = 0.001). Abnormal BAEPs do not seem to be an early finding in Wilson's disease.

One hundred and fifty children with febrile convulsions (FC) were followed up for 3-10 years. They were divided into two groups: group A consisted of 120 children whose disorder was under control, and group B 30 patients in whom the disorder was not under control. Risk factors for uncontrolled FC and later development of epilepsy were looked into. In group A, 8 patients (6.6%) developed epilepsy, while another 3 (2.5%) had a single afebrile seizure. In group B, 10 (33.3%) children developed epilepsy, while 1 (3.3%) had a single afebrile seizure. The difference in the later occurrence of epilepsy between the two groups was statistically significant.

Direct stimulation of muscle fibres with a regular 10 Hz rate, three computer generated random rhythms and a sequence of voluntary discharges was used to quantify the interdischarge interval (IDI) dependent jitter due to velocity recovery function (VRF). This jitter was found to depend on conduction time and strength of VRF, but not on propagation velocity. The results suggest that in the usual jitter study in voluntarily activated muscle fibre pairs, with moderately irregular discharge rate and interpotential intervals below 3 ms the IDI dependent jitter contributes on average less than 10 microseconds, but can be so large as to produce false abnormal values at more irregular rates, longer interpotential intervals and pronounced differences in VRF. It can be effectively removed by mathematical algorithms or, better still, by using electrical stimulation.

Reflex responses were elicited in the biceps femoris muscle of patients with cervical spinal cord lesions by stimulating the sural nerve and recording from single motor neurones by single fibre EMG technique. The consecutive responses within the surface-recorded early component displayed a latency jitter between 500 and 600 microsec (S.D.), suggesting an oligosynaptic reflex arc. These responses were rarely seen; they were suppressed by increasing the stimulus strength. The surface-recorded late component consisted in the single fibre EMG recordings of repetitive discharges of individual motor neurones. The latency jitter of the earliest of these discharges was about 1440 microsec, and it progressively increased in the later discharges, reflecting increasingly more variable central conduction time. Ischaemia of the leg made some of the late discharges at a latency of about 0.5 sec remarkably stable and reduced their jitter. They may represent responses to the activity of slowly conducting afferent fibres, normally suppressed by inflow along the fast conducting fibres. Stimulation of dorsal columns through epidurally placed electrodes at T1 and T2 levels resulted in a complete suppression of repetitive discharges, outlasting the actual stimulation. TENS and light stroking of the skin below the level of the spinal cord lesion, as well as subthreshold stimuli to the sural nerve, had a similar effect. These results suggest that the late component of the flexion reflex may share some of the neural mechanisms responsible for feeling pain.

The technique of electrical stimulation of the brain through intact scalp was applied to activate the corticospinal tract (CST) of healthy human volunteers. Single motoneurone responses were picked up by a special (single fibre EMG) needle electrode. Our finding of relatively small latency variation of consecutive single motor unit responses seems to support the concept of predominantly monosynaptic transmission at the spinal level. The alternation between several discrete latencies seems to reflect a complexly shaped spinal motoneurone excitatory postsynaptic potential (EPSP), which could be due to either alternating direct/indirect (via other cerebral neurones) activation of the corticospinal tract (CST) neurones, or alternating mono- or oligosynaptic transmission at the spinal level, or multiple CST impulses in response to a single stimulus.

A single fiber EMG (SFEMG) study was performed in 51 patients with idiopathic juvenile scoliosis of moderate degree (mean 23.8 degrees of Cobb), aged 7-18 years (mean 13.2 years). The findings in the extensor digitorum communis muscle (EDC) include a moderate but significant increase in fiber density (mean 2.02, +/- 0.21, P less than 0.001), a mild but significant (P less than 0.001) neuromuscular transmission abnormality (7.6% of fibers showed increased jitter and 4.5% intermittent blocking), and a moderately prolonged mean interspike interval (mean 0.98 msec, +/- 0.20, P less than 0.005) in EDC. Five of the patients had normal fiber density, 9 had a normal jitter study, and further 7 had a normal mean interspike interval. However only one had all the parameters normal. The paraspinal and intercostal muscles at the apex of the scoliotic curvature examined in some of the patients showed similar abnormalities. The study thus suggests the existence of a subclinical systemic neuromuscular disorder in nearly all of our patients with idiopathic scoliosis, which might have a pathogenetic significance.

A technique is described of measuring the motor end plate jitter in the orbicularis oculi muscle activated by extra-muscular nerve stimulation, standardised for routine use in diagnosis and evaluation of neuromuscular transmission disorders. Among the advantages of the technique are comparatively quick and easy sampling of adequate number of single motor end-plates, convenient control of discharge rate between less than 1 and up to 20 Hz, absence of direct muscle fibre responses, and little discomfort for the patient. The jitter in the orbicularis oculi is significantly lower than that in the extensor digitorum communis muscle. There is a positive correlation between the jitter and the latency of the individual muscle fibre responses, possibly indicating that smaller diameter muscle fibres have slightly lower safety factor of neuromuscular transmission. The data collected in a group of healthy volunteers suggest the following upper normal limits for the mean of absolute consecutive difference of the latency: 30 microseconds for individual motor end plates (one out of 20 values may be higher), and 18 microseconds for a median of 20 motor end plates.

Measurement of motor and sensory conduction velocities, amplitude of M-wave and sensory nerve action potentials, and coaxial needle EMG were used to evaluate function of grafts bridging defects in median, ulnar, and radial nerves in 73 patients. The results show values only moderately lower than the normal limits.

The vibration reflex was studied in 49 patients with traumatic spinal cord lesions. It was elicited in all patients, even after presumably complete division of the cord. The vibration relfex consisted of a short-latency, brief outburst of phasic activity of motor units, followed by rapidly decreasing phasic component and a later slowly declining tonic component. When periods of vibration were repeated at short intervals of 2 to 10 seconds, the responses showed an approximately exponential decline, although the beginning of each subsequent response was always larger than the end of the preceding response. A large part of this decline can be characterized as a habituation of the vibration reflex. In comparison with the vibration reflex in normal subjects, the phasic component was increased and the tonic one reduced. The tonic component was especially susceptible to potentiation and dishabituation by voluntary effort to contract the vibrated muscle, even in some patients with no other evidence that the lesion was incomplete. We suggest that the tonic component of the human vibration reflex depends, at least in part, on segmental interneurons and their descending spinal pathways, while the phasic component depends mainly on the excitability level of spinal motoneurons.

The paper describes computer-aided measurement of interpotential intervals in single fibre eletromyography (SFEMG), a diagnostic and research method in clinical medicine. The method is based on analysis of consecutive intervals in pairs of single muscle fibre action potentials. The most important parameter obtained is the mean value of absolute differences of consecutive interpotential intervals, which reflects the reliability of impulse conduction along the terminal branches of motor axons and across the neuromuscular junction. The interface units, in combination with amplifers, binary counters and pulse amplitude-to-pulse width converters, allow not only direct analogue-to-digital conversion but also recognition of potentials. This enables the computer system to make decisions. The results are computed in less than 1 sec after analysis, and are immediately displayed in a graphic and alpha-numberical form on a screen at the measurement site. This provides an immediate visual feedback for the investigator thus both increasing the diagnostic efficacy and reducing the discomfort to the patient. Simultaneous printout by a teletype is used for documentation. The computer system consists of an HP 2116C computer with standard periphery and the program has been written in FORTRAN IV language with subroutines in FORTRAN IV and ASSEMBLER languages.

SFEMG recordings were carried out in patients with amyotrophic lateral sclerosis, progressive muscular atrophy, familial spinal muscular atrophy and syringomyelia. The fibre density was increased in all conditions, especially in progressive muscular atrophy indicating marked collateral sprouting. The duration of the action potential was increased indicating a mixture of hypertrophic and atrophic fibres and slowly conducting newly formed nerve sprouts. The action potentials were unstable with varying degree of impulse blocking especially in the more progressive cases (ALS), representing recent re-innervation. The SFEMG method is used to characterize the functional status of the motor unit and helps in diagnosis and in predicting prognosis. In addition, SFEMG recordings reveal abnormalities in clinically and electromyographically normal muscles.

Latency variation of consecutive responses of single orbicularis oculi motoneurones in the first component of the electrically elicited blink reflex was 2.6 times larger than that of the H reflex of the soleus muscle fibres. Some motoneurones showed bimodal latency distribution or double responses or both at an interval of about 4-5 ms. Typical first component responses were sometimes obtained by contralateral stimulation. Central conduction time in the brainstem, estimated for 15 motoneurones, was between 2.4 and 6.6 ms. It is concluded that the first component of the blink reflex is conducted through an oligosynaptic arc including one or more interneurones.

With the aim of studying peripheral physiological mechanisms involved in transcutaneous electrical nerve stimulation (TENS) for the suppression of pain, the authors have examined 14 healthy volunteers in the perceptual part and 8 in the microneurographic part of this study. For pain suppressing stimulation they have used ring electrodes and stimulators capable of producing rectangular, sine wave, triangular and hybrid wave forms. Pain was induced with electrical stimuli on the distal phalanx of the middle finger. TENS with rectangular, sine wave and triangular pulses activates mainly A beta, but also some A delta fibres. Pain suppressing capacity of different wave forms used was the same and was achieved with stimuli close to the threshold for pain. Pain was most effectively diminished when noxious and pain suppressing stimuli were applied to the same finger; this effect was smaller with the two stimuli on neighbouring fingers and very weak when pain suppressing stimulus was applied to the contralateral hand. Increases in stimulus frequency resulted in an increased and variable latency as well as intermittent blocking of those spike components which had been near threshold at low frequency stimulation. This interpreted as being due to local changes in excitation threshold. In surface-recorded averaged electroneurograms this effect was seen as amplitude decrement and increased response duration, but was not due to impulse transmission failure in A delta fibres as seen microneurographically. On continuous high frequency stimulation, the intensity of sensation elicited diminished, although there was no change in the microneurogram. The authors conclude that the peripheral contribution to the analgesic effects of TENS seems to be unimportant.

Statokinesimetric characteristics were analysed in patients with scoliosis which had developed in the course of degenerative neuromuscular disorders and in patients with adolescent idiopathic scoliosis. Patients with Duchenne and limb- girdle muscular dystrophy and spinal muscular atrophy showed markedly decreased oscillations of the body's centre of gravity, in addition to a forward shift of its mean position. Thus the postural equilibrium in neuromuscular patients with scoliosis is even more efficiently controlled than normal. On the other hand, patients with idiopathic scoliosis did not show any significant changes as compared with normal subjects. The present study therefore does not support the suggestion that the pathogenesis of scoliosis, at least in neuromuscular patients, is triggered by an impairment of descending postural control.

Motor end plate jitter was studied by single fibre EMG in the orbicularis oculi muscle of eight patients with facioscapulohumeral dystrophy activated by extramuscular nerve stimulation. The jitter was found to be slightly larger in comparison with the normal controls, although still within the normal limits in each patient. The findings are considered to indicate absence of any significant neuromuscular transmission disturbance, inflammatory or regenerative process, or reinnervation in progress. There was no evidence of muscle fibre conduction abnormality even in very weak muscle.

Hundred-seventy patients with the 4 commonest degenerative neuro-muscular disorders (limbgirdle and Duchenne muscular dystrphy, Kugelberg-Welander's spinal muscular atrophy and peroneal muscular atrophy) were screened for scoliosis, which was found in 56%. Of 76 patients in the early stages of their respective disorders (stages 1-6 of Gardner-Medwin and Walton), scoliosis was found in 72%. The incidence of scoliosis was not related to the duration or degree of clinical weakness. Morphologically, scoliosis in these disorders was not found to differ from idiopathic scoliosis. Neither side nor site of the scoliosis were related to the distribution of muscle weakness as determined by manual testing.

Single fibre EMG recordings were made from 152 fasciculating motor units in 17 patients with motor neuron disease. All recordings showed abnormal jitter, many (75%) displayed intermittent blocking, and most had abnormal fibre density (mean 4.3), demonstrating considerable degrees of collateral sprouting supported by the fasciculating motor units, and varying degrees of functional immaturity of the new axonal twigs and the motor end plates. The SFEMG abnormalities reflecting both the degree and the recency of collateral reinnervation correlated with the mean interdischarge interval, suggesting that the properties of the generator site depend on the functional state of the fasciculating motor unit as a whole.

This single fibre EMG study compares the standard method of neuromuscular jitter measurement in voluntarily activated muscle to that by intramuscular electrical stimulation of motor axons in a group of normal subjects. The latter method avoids the interdischarge interval-dependent jitter, as well as a possible failure to recognise split muscle fibres. The mean MCD on axonal stimulation was only 5.2 microseconds less than in the voluntary activation study and was thus 8% more than theoretically expected for single motor end plates. The difference could be due to an axonal jitter and some other factors. Axonal stimulation has proved to be a relatively easy and reliable method for routine estimation of neuromuscular jitter, provided that the resolution of time measurement is better than 2 microseconds, so that low jitter due to occasional direct muscle fibre stimulation is not mistaken for a normal reading. The upper normal limits for the extensor digitorum communis muscle suggested by the present study are 40 microseconds (individual muscle fibres) and 25 microseconds (mean of 30 muscle fibres).

Twelve patients with neurobrucellosis and 17 patients with systemic brucellosis without neurological involvement underwent a brainstem auditory evoked potentials (BAEP) study. All neurobrucellosis patients (100%) showed abnormalities in their BAEP recordings, suggestive of brainstem lesions at various levels. On the other hand, only 5 (29%) of the 17 patients with systemic brucellosis had mild unilateral BAEP abnormalities, while the remaining 12 had normal responses. Comparison of pooled data between the systemic brucellosis and neurobrucellosis groups showed highly significant differences in all BAEP parameters. The recording of BAEP is thus considered a sensitive supplementary method to reveal CNS lesions in patients with neurobrucellosis.