H reflexes from the tibial and median nerves. The International Federation of Clinical Neurophysiology.
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Biomedical subjects
Publications and source records attributed to P Fuhr.
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Little is known about nociceptive reflex mechanisms in the upper limb in humans. To investigate nociceptive effects on spinal motoneurone excitability, a conditioning noxious stimulus was applied to the index finger of five healthy subjects. Motor evoked potentials (MEPs) following contralateral transcranial magnetic stimulation (TMS) were recorded from thenar eminence (TE) and biceps brachii (BB) muscles ipsilateral to finger stimulation. TMS was randomly applied alone or combined with preceding finger stimulation at an interstimulus interval of 100 ms. MEP amplitudes were profoundly suppressed in TE and augmented in BB. We conclude that nociception produces a differential effect on different spinal motoneurone pools, which may be part of a complex protective reflex mechanism in the upper limb of humans.
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The case of a patient with a 2-day history of symptoms suggesting acute carpal tunnel syndrome is presented. However, an urgent electroneurographic examination revealed median nerve compression at the forearm and magnetic resonance imaging confirmed compression by a mass proximal to the carpal tunnel. Surgical exploration showed a recently thrombosed aneurysm of an epineural vessel. Histological and, later, general and angiological investigations could not reveal the underlying cause of this aneurysm. Preoperative electrodiagnostic examination is recommended in acute peripheral nerve compression to prevent decompression at an incorrect site. If atypical nerve compression is suspected, magnetic resonance imaging may be indicated to detect localized nerve compression and its underlying cause.
The early diagnosis of Parkinson's disease (idiopathic parkinsonism) is important for two reasons. Some never drugs possibly have a neuroprotective effect, which can be utilized maximally only with early onset of treatment. Moreover, diagnostic mistakes may occur early in the course of the disease. Although the hallmark of Parkinson's disease is a syndrome of movement disorders, slight cognitive deficits, depression, or pain with or without paresthesias can be present at an early stage. Therefore, symptoms at the time of the first diagnosis and at the beginning of the first clinical manifestation of Parkinson's disease are often not identical. The diagnosis can be made only clinically, since no biological marker is available up to now. However, in unclear cases pharmacological tests constitute a valuable extension of the clinical examination.
The purpose of this study was to investigate the value of clinical testing of distance stereopsis. Distance stereopsis was assessed with the Mentor Binocular Vision Testing System (B-VAT) system for 45 patients with ocular deviations of 6 delta or more at distance (heterophoria and intermittent strabismus) and for 36 patients with orthophoria. On the average, distance stereopsis was better for patients with the smaller ocular deviations than for those with the larger ocular deviations. The mean distance stereoacuities, both contour and global, for the orthophores were 53 and 81 sec arc, for the heterophores 93 and 100 sec arc, and for the intermittent strabismics 95 and 169 sec arc. Although the average size of the deviation at distance and near for the heterophoric and strabismic patients was nearly the same, distance stereopsis tended to be poorer than near stereopsis. There was a significant difference between the proportion of orthophores and the proportion of intermittent strabismics exhibiting distance stereopsis with both contour and global stereo targets (p < 0.05).
This study tested the hypothesis that patients with Parkinson's disease are impaired when they must rely on internal information to generate a response. Choice reaction times of control subjects and patients with Parkinson's disease, on and off their medication, were measured in tasks in which the motor demands were constant but which varied in the degree to which the stimuli held intrinsic information about the required response. A dopaminergic deficit was observed only in the tasks which employed stimuli compatible with the response and not in a task employing stimuli arbitrarily associated with the response. The data do not support the hypothesis that patients are differentially impaired in using internalized stimulus-response relationships.
Reciprocal inhibition of the H-reflex in the wrist flexors elicited by stimulation of the radial nerve provides insight into the pathophysiology of different kinds of dystonia and may become a diagnostic tool for some movement disorders. Some of the results have been conflicting, however, owing presumably to differences in the technique. The present study in normal subjects shows that the amount of inhibition increases with decreasing amplitude of the unconditioned H-reflex and with increasing intensity of the radial nerve stimulus. Duration of the stimulus is important: stimuli of short duration are ineffective, and stimuli of long duration produce inconsistent inhibition.
The motor cortex and the proximal part of the peripheral nervous system can be stimulated by a rapidly changing magnetic field. The procedure is simple, painless and safe. It allows to quantify the function of the most rapidly conducting corticospinal fibers. It is possible to detect subclinical lesions. The use of this technique for the study of lesions of the proximal parts of the peripheral nervous system is as of yet largely experimental.
Five patients from a kindred with hereditary hyperekplexia had physiological testing. The surface-recorded electromyographic pattern of audiogenic muscle jerks was identical to that of the normal acoustic startle reflex. Testing at graded stimulus intensities indicated an increase in the gain of the acoustic startle reflex. Nose-tap stimuli resulted in short-latency generalized electromyographic bursts that were similar to the R1 component of the blink reflex. Electrical stimulation of peripheral nerves elicited a pattern of generalized muscle jerks that was similar to that of the acoustic startle reflex. Somatosensory evoked potentials, brainstem auditory evoked potentials, and cortical auditory evoked potentials were normal. The primary physiological abnormality in hereditary hyperekplexia is widespread elevated gain of vestigial withdrawal reflexes in the brainstem and possibly the spinal cord, most likely resulting from increased excitability of reticular neurons.
The physiology of rigidity in Parkinson's disease (PD) can be investigated by the study of reflexes. Cutaneous reflexes (CR) were measured in 10 patients with PD and in 10 age- and sex-matched normal volunteers. EMG activity was recorded from the first dorsal interosseous muscle with surface electrodes, rectified and averaged. The index finger was stimulated with an intensity four times the sensory threshold. The subjects abducted the index finger with 20% of maximal force. While the latencies of the different reflex components and the amplitudes of the excitatory peaks were not different in the two groups, the first inhibitory component was less pronounced in patients with PD as compared with normals. This effect is partially reversed with dopaminergic drug treatment. The results are compatible with the loss of an inhibitory spinal mechanism elicited by cutaneous afferents, and can be a partial explanation for increased tone in PD.
We recorded motor evoked potentials (MEPs) from deltoid, biceps brachii, abductor pollicis brevis and flexor carpi radialis muscles of 5 normal volunteers during transcranial magnetic stimulation. With the subjects at rest, an 8-shaped magnetic coil was used to deliver 30 stimuli to different scalp positions 0.5 or 1.0 cm apart. The variability in amplitude and latency of MEPs was studied as a function of the scalp position stimulated, the number of stimuli at each position, and the percentage of maximal peripheral M responses (%M) elicited. The results were used to estimate the optimal number of stimuli at each position and the optimal spacing of scalp positions for topographic mapping of the human motor cortex. The amplitude and latency variability of MEPs were higher when suboptimal scalp positions were stimulated. Consequently, a larger number of stimuli were required to determine representative MEP amplitudes at suboptimal positions. In addition, there was an inverse relationship between %M recruited by transcranial magnetic stimuli in different subjects and the variability in MEP amplitude and latency. Latency variability was less pronounced than amplitude variability. Optimal sampling conditions are required to produce the best topographic maps, particularly to show subtle reorganization patterns in the human motor cortex.
It is now known that amputation results in reorganization of central motor pathways, but the mechanism for the changes is unclear. One possibility is alteration of the excitability of the alpha motoneurons. We studied motor reorganization and excitability of alpha motoneurons to Ia input in 6 subjects with unilateral lower limb amputation. A Cadwell MES-10 stimulator was used to deliver transcranial magnetic stimuli through a circular coil centered on the sagittal axis 4 cm anterior to Cz and through an 8-shaped coil positioned over scalp locations 1 cm apart along the coronal axis. Surface EMG was recorded bilaterally from quadriceps femoris, the first muscle immediately proximal to the site of amputation. Excitability of the spinal alpha motoneuron pool to Ia afferents was assessed by determining the ratio of the maximal H reflex to the maximal M response (H/M ratio) elicited in the quadriceps femoris. Stimuli of equal intensity delivered to optimal scalp positions recruited a larger percentage of the alpha motoneuron pool in muscles ipsilateral to the stump than in those contralateral to the stump (P less than 0.01). Mean onset latencies of motor evoked potentials were shorter in ipsilateral muscles than in contralateral muscles (P less than 0.01). Muscles ipsilateral to the stump showed a trend toward activation from a larger number of scalp positions than those contralateral to the stump (P = 0.06). There was no difference in the quadriceps H/M ratios (7.2% ipsilateral vs. 10.9% contralateral). The absence of changes in the excitability of the alpha motoneuron pool in the presence of motor reorganization targeting muscles proximal to the stump suggests that reorganization occurs proximal to the alpha motoneuron level.
We report on a 25-year-old patient with hyporeflexia, progressive segmental hypohidrosis and dry, scaly skin mimicking tinea manuum on the affected palm. This case is the fourth with Ross syndrome and skin manifestations as a result of segmental hypohidrosis.
We recorded motor evoked potentials (MEP) to transcranial magnetic stimulation from abductor pollicis brevis (APB), flexor carpi radialis (FCR), biceps brachii and deltoid muscles at rest and during slight voluntary activation. An 8-shaped coil connected to a Cadwell MES-10 magnetic stimulator was positioned over different scalp positions 1 cm apart. At least 24 stimuli were delivered at each location. Latencies of MEPs were compared with those obtained by electrical and magnetic stimulation during muscle activation. Progressively longer MEP latencies were obtained in 5 groups depending on the type and position of stimulation. The shortest latencies were obtained with (1) electrical stimulation during muscle contraction and (2) non-focal magnetic stimulation during muscle contraction; magnetic stimulation at rest produced longer latencies with stimulation of (3) an optimal position, (4) a suboptimal position, and (5) a non-optimal position. Mean latency differences between successive groups were 1.9, 2.0, 1.6, and 2.6 msec for APB. Similar latency differences were found for the other arm muscles. The results are compatible with the hypothesis that the different latencies evoked by stimulation at different scalp locations are determined by the summation at spinal motoneurons of excitatory postsynaptic potentials generated by successive numbers of I waves.
During tonic voluntary muscle contraction, a period of electromyographic silence follows the motor evoked potential produced by transcranial stimulation of the contralateral motor cortex. We studied the silent period in the wrist flexors of 3 normal volunteers and a deafferented patient during 20% of maximal contraction. To test the excitability of the spinal motor neuron pool during the period of silence, the H-reflex was evoked in the normal subjects at different intervals after cortical stimulation. The amplitude of the H-reflex in the silent period was expressed as a percentage of the amplitude during complete muscle relaxation. The H-reflex was profoundly depressed at the beginning of the silent period (13.5-27% of the control measurement), but showed a clear tendency to recover toward the end of the silent period despite continued absence of muscle activation (71-84% of the control). Moreover, the silent period in the deafferented patient was of longer duration than can be accounted for by segmental mechanisms. These findings imply, at least in the late part of the silent period, that a reduction in the excitability of the spinal motor neuron pool plays only a minor role in determining the phenomenon and that it is probably caused by lack of cortical drive.
Basic principles of magnetic stimulation of biological tissues are reviewed. Noninvasive magnetic stimulation of the brain delivered over sensorimotor areas evokes movements and less commonly paresthesias in contralateral limbs. We have evaluated the maps of motor outputs in patients with (1) congenital mirror movements, which resulted in marked derangement of the map of outputs of distal hand muscles with enlarged and ipsilateral representations; (2) amputations, which resulted in plastic reorganization of motor outputs targeting muscles immediately proximal to the stump; (3) spinal cord injury, which also resulted in enlargement of the map of outputs targeting muscles proximal to the lesion level; and (4) hemispherectomy performed at an early age for intractable seizures, which resulted in the remaining hemisphere controlling ipsilateral arm muscles. These results demonstrate the potential for reorganization in motor systems following lesions in the peripheral as well as in the central nervous system.
We studied the effects of transcranial magnetic stimulation of the motor cortex on ipsilateral upper extremity muscles in six normal men. Stimulation had inhibitory and excitatory effects on the muscles during voluntary activation. Transient inhibition, an ipsilateral silent period (ISP), occurred in all muscles tested, often without any preceding excitatory response. Motor evoked potentials (MEPs) occurred ipsilaterally in the proximal muscles of some subjects. Ipsilateral MEPs and ISPs were delayed relative to the MEPs evoked by the same stimulus in the corresponding contralateral muscles. The excitability of the alpha motoneuron pool, assessed during the period of the ISP by eliciting H-reflexes, showed no change, suggesting that ipsilateral inhibition acts at a level above the alpha motoneuron. Connections from motor cortex to ipsilateral muscles could be via the corpus callosum and contralateral hemisphere or via purely ipsilateral pathways.