Search PubMed⌕ Search

Biomedical subjects

M R Magistris

Publications and source records attributed to M R Magistris.

52 records · Page 3Linked to original sources
PubMed1994

Magnetic transcranial and electrical stylomastoidal stimulation of the facial motor pathways in Bell's palsy: time course and relevance of electrophysiological parameters.

Facial nerve motor neurography was performed at various times after the onset of Bell's palsy in 97 patients. Stimulation of the facial nerve was performed (1) electrically in the fossa stylomastoidea (ElStim), and (2) magnetically in the labryinthine segment of the facial canal (MagStim), evaluating different coil positions over the skull. Additionally, the face-associated motor cortex was stimulated magnetically in 47 patients (CxStim). A marked reduction of the amplitudes of the compound muscle action potentials (CMAP) evoked by MagStim on either m. nasalis or mentalis, or both, was observed which was clearly more pronounced than the amplitude reduction to ElStim. This discrepancy occurred very early during the disease, the mean amplitude (expressed in percent of the amplitude on the unaffected side) being 82% (S.D. 9.1) for ElStim and 1% (2.7) for MagStim at days 0-4. It persisted for several months, often when facial nerve function had recovered to normal, as assessed by clinical observation, ElStim, and CxStim. This amplitude decrease to MagStim, which appears to be related to a locally enhanced stimulation threshold of the facial nerve, is a very sensitive and reproducible finding in Bell's palsy. It may prove specific of the disorder, of diagnostic value, and of interest in the follow-up of patients during treatment trials.

Action Potentials↗
PubMed1994

Conduction block in vasculitic neuropathy.

We describe a 28-year-old man who developed a mononeuropathy with a conduction block of the median nerve in the forearm, during the acute stage of a polyarteritis nodosa. Sequential studies show progressive disappearance of the conduction block (together with the clinical symptoms), without signs of axonotmesis.

Adult↗
PubMed1994

Neuromuscular disorder in intensive care unit patients treated with pancuronium bromide. Occurrence in a cluster group of seven patients and two sporadic cases, with electrophysiologic and histologic examination.

During six consecutive months, seven patients admitted to our ICU (15 beds, general ICU, approximately 300 intubated patients per year) for acute respiratory failure requiring intubation and mechanical ventilation presented with a peculiar neuromuscular disorder. After the occurrence of this cluster group of patients, we detected two more similar but isolated cases in the following 18 months, ie, altogether 9 patients in 2 years of observation, or 1.55 percent of all intubated patients in our ICU. Sedation was achieved using midazolam, curarization was effected with the neuromuscular non-depolarizing agent pancuronium bromide (PB), and corticosteroids were administered to eight patients. Shortly after discontinuation of sedation and curarization, we observed a persistent tetraparetic syndrome and/or peroneal palsy with a concomitant increase of serum creatine kinase (CK). None of the patients was septic or had the multisystem organ failure. A strong association between CK increase and PB administration was found, whereas no patient suffered severe liver or kidney failure. The duration of the neurologic deficit ranged from 4 to 52 weeks, with only partial recovery for some patients; the duration of dysfunction was apparently related to the total dose of corticosteroids received. Two patients had difficulty being weaned from the respirator and required tracheostomy. Electrophysiologic studies showed signs of axonal neuropathy and myopathic changes, ie, motor units of brief duration, small amplitude, overly abundant for the voluntary effort being exerted. Muscle biopsies showed significant myopathic alterations, with foci of muscle necrosis in most patients and minimal lymphocytic inflammation in one patient. The neurologic complication described differs from the polyneuropathy in critically ill patients. Furthermore, PB or corticosteroids or both appear to be the causal agents. The duration of the neuromuscular dysfunction may be related to concomitant steroid therapy. The CK enzyme seems to be a marker of the disorder. This disorder is associated with myopathic alterations and axonal degeneration in some patients. Pancuronium bromide should be used with caution, particularly when associated with steroids therapy, and it may cause difficulty in weaning patients from the respirator.

Adult↗
PubMed1992

Motor axon reflex and indirect double discharge: ephaptic transmission? A reappraisal.

Causal mechanisms of the motor axon reflex (MAR) and indirect double discharge (IDD) are re-examined. The hypothesis that these indirect intermediate latency responses result from an axono-axonal ephaptic transmission mechanism has recently been suggested. The various conceivable responses of models of axonal cross-talk are compared with actual observations made from the limbs. We conclude that the ephaptic hypothesis does not explain MAR and IDD, and that the earlier understanding that MAR results from axonal branching and IDD from proximal re-excitation on the axon holds true.

Aged↗
PubMed1991

Predictive value of anti-GM1 ganglioside antibodies in neuromuscular diseases: a study of 180 sera.

The incidence of anti-GM1 antibodies in the serum of 104 patients with neurological diseases, 35 patients with non-neurological diseases (NND) and 41 normal controls was determined by enzyme-linked immunosorbent assay (ELISA). Anti-GM1 antibodies were found in 90% of patients presenting with a motor neuropathy (all except one had multifocal conduction blocks). A large proportion (60%) of these patients displayed high antibody titer ranging from 101 to 788. A low incidence of anti-GM1 antibodies was found in the other groups of patients, i.e. 21% of amyotrophic lateral sclerosis (ALS), 26% of other neurological diseases (OND) and 23% of NND. High antibody titers ranging from 106 to 260 were found in two (5%) ALS patients, one (2%) OND patient (myasthenia gravis), and one (3%) NND patient (Waldenström's disease). This study shows that high titers of anti-GM1 antibodies are found in a large proportion of patients with motor neuropathy with multifocal conduction blocks. This argues for a possible autoimmune origin of this neuropathy. We suggest that anti-GM1 antibody determination should be included systematically in the evaluation of all patients with motor neuron diseases and predominantly motor neuropathies.

Adult↗
PubMed1990

Positive giant potentials: an electromyographic investigation.

Positive giant potentials (PGPs) consist of a peculiar EMG activity which is observed mostly in the large lower limb muscles, and mainly in men, either during the insertion of the needle electrode or during muscle contraction. PGPs have a shape similar to that of positive sharp waves, but with a larger amplitude (up to 25 mV). Their firing rate may reach 200 c/s. PGPs probably have no diagnostic significance since they are frequently observed in healthy individuals. They correspond to an insertional activity and should be recognized as such because they may be mistaken for giant motor unit potentials and thus be the source of diagnostic errors. The mechanism involved in the genesis of PGPs remains a matter of speculation.

Action Potentials↗
PubMed1990

Cryptogenic hemifacial spasm. A neurophysiological study.

Whether hemifacial spasm (HFS) is due to axono-axonal ephaptic transmission or to facial nucleus abnormal hyperexcitability remains controversial. The neurophysiological hallmark of HFS is the delayed response (DR). This response has an indirect pathway and thus a long latency. It is evoked A) as a distant response in muscles innervated by a facial branch other than the one stimulated, and B) in muscles innervated by the branch stimulated. In this work, 99 single all-or-none DRs of 24 cases of cryptogenic HFS were studied by threshold stimulation of a branch, or of the trunk, of the facial nerve. A) Eighty-eight distant DRs were studied. Fifty-four of them were frequently evoked as double discharges (DDs), or sometimes as multiple discharges, with a 3 to 7 ms interval. A collision technique, using paired stimuli, showed that the second discharge of 12 out of 20 DDs was accompanied by a back-wave due to a proximal ectopic re-excitation on the axon, or to the back-firing of an alpha cell (F-response), or to both. F-waves in HFS were more frequent than in normals or in other facial pathologies. B) Eleven DRs were recorded in muscles innervated by the facial branch stimulated. Some of them persisted when, using a stronger stimulus, the same all-or-none potential was also evoked as a direct response. In other cases both the direct response and the DR were evoked with identical stimulation threshold. The direct-indirect response interval of these 11 DRs was shorter than the normal M-F interval. These findings suggest that, in the case of HFS, axons are interconnected by uni- and bidirectional ephapses. Self-sustained repetitive firing in such a group of axons apparently results from re-excitations occurring both at the ephapse site and at the cellular level (F-responses). Spasm develops when several groups fire together. The changing excitability of the alpha cells modulates the importance of the phenomenon.

Adult↗
PubMed1988

[Post-radiation brachial plexopathy. Persistent conduction block. Myokymic discharges and cramps].

The distinction between radiation and tumor brachial plexopathy may be difficult. The electrophysiological recording of myokymic discharges, frequently present in the former but rare in the latter type of plexopathy, can be helpful for the diagnosis. However, the pathophysiology and the site of origin of these discharges remain unclear. We describe a patient presenting with radiation brachial plexopathy, clinical myokymia, cramps and pain. In this patient, the myokymia--due to abundant myokymic discharges--and the cramps, were related to the existence of persistent conduction block of several years duration. Several findings suggest that the myokymic discharges were generated on blocked axons: voluntary activity did not influence their occurrence nor modify their course; the motor unit potentials involved in the discharges were not evoked by stimulation proximal to the site of the conduction block, whereas the stimulation distal to this site could evoke, modify the rhythm, or interrupt the course of the discharges; the latency of these evoked responses indicated that the site of reflection was proximal on the axon, and likely coincided with that of the conduction block. Recent observations (Roth and Magistris, 1987b) indicated that myokymia, produced by numerous single or grouped fasciculations generated on axon terminals, may be related to persistent conduction blocks of various etiologies. The present case demonstrates that myokymia provoked by myokymic discharges may as well be related to persistent conduction block. The reason why these blocks are accompanied by fasciculations in some situations and by myokymic discharges in others remains an unsolved question. The cramps observed in this patient were also of interest as they occurred in the muscle territory of blocked axons and were provoked by passive muscle shortening. Their origin, distal to the conduction block, is unknown. Finally, a neurolysis did not prevent the progressive transformation of conduction block into axonotmesis.

Brachial Plexus↗
PubMed1987

Neuropathies with prolonged conduction block, single and grouped fasciculations, localized limb myokymia.

Fourteen patients presented prolonged conduction block (CB) related to hereditary neuropathy with liability to pressure palsies (n = 7), neuropathy with proximal multifocal persistent CB (n = 2), radiation plexopathy (n = 3) and chronic acquired polyneuropathy (n = 2). All subjects presented both single and grouped fasciculation potentials that resulted in visible limb myokymia in 9 patients. This ectopic activity was recorded only in muscles affected by the CB, was more important in severe or complete CB, and often arose from terminal branches of blocked axons. These fasciculations and grouped fasciculations therefore appear to be causally related to the CB. In the presence of localized myokymia, a prolonged CB should be suspected.

Chronic Disease↗
PubMed1986

Motor neuropathy with proximal multifocal persistent conduction block, fasciculations and myokymia. Evolution to tetraplegia.

We describe a patient with chronic asymmetric motor neuropathy, which began in the upper extremity. The paretic muscles showed abundant fasciculations and myokymia but only little amyotrophy. Electrophysiologic examination revealed proximal multifocal persistent conduction block (CB) not located at the usual entrapment sites, and arrhythmic isolated or grouped fasciculation potentials originating distally on blocked axons. Over the years, new CBs developed, which led to tetraplegia, and amyotrophy slowly increased with progressive denervation. This patient differs from the cases of chronic acquired demyelinating polyneuropathy described in the literature by the absence of sensory deficit and the proximal location of CB.

Demyelinating Diseases↗
PubMed1985

[Muscle-nerve ephapse in chronic denervation? Axonal localization].

Muscle-to-nerve ephaptic responses, taking place between a reinnervated motor unit and a motor axon, have been reported in the case of chronic denervation (Roth and Magistris, 1985). One of these responses is described here. Its main features are that it manifests itself as a motor unit potential, which, when present, is evoked either as a direct tardive response (RE), or as an indirect F response, the two potentials never being observed together on any recording. The characteristics of these potentials show that two distinct competitive pathways lead to the same muscular fiber group which suggests the existence of an ephaptic connection. Furthermore, a slight difference in the shape of the RE and F potentials suggests an axon terminal branch localisation of this ephapse.

Carpal Tunnel Syndrome↗
PubMed1985

Long-lasting conduction block in hereditary neuropathy with liability to pressure palsies.

We detected 29 conduction blocks in 12 patients with hereditary neuropathy and liability to pressure palsies. The blocks occurred at entrapment sites, most often the ulnar nerve at the elbow. Some had lasted for several years. This kind of block seems to be characteristic of the neuropathy, and may be related to the localized thickening of myelin ("tomacula"). In one patient with two permanent and severe blocks, neurolysis was beneficial.

Humans↗
PubMedDate not supplied

Generalized convulsions induced by pentylenetetrazol in the cat: participation of forebrain, brainstem, and spinal cord.

The respective capabilities of forebrain, brainstem, and spinal cord to generate seizures in response to intravenous pentylenetetrazol (PTZ) were determined in intact, precollicular, and spinal cord transected (C2-C3) cats. Threshold doses for the induction of generalized EEG seizures were similar, approximately 26 mg/kg, in all groups, but only in intact cats was this associated with generalized clonic convulsions. In cats with precollicular transection, in spite of an unchanged EEG seizure threshold, induction of convulsions required on average 63 mg/kg of PTZ. They consisted of generalized tonic contractions. In cats with spinal cord transection, convulsions began with a mean dose of 167 mg/kg of PTZ. They consisted of bilateral, frequently asynchronous jerks, although tonic contractions were also observed. These experiments show widespread central nervous system (CNS) sensitivity to PTZ, and demonstrate that (a) ictal EEG activity in the forebrain, normally associated with clonic convulsions, may occur independently from brainstem influence; (b) clonic convulsions in intact cats likely originate from the forebrain with little contribution from the brainstem; and (c) the brainstem and spinal cord can induce tonic and predominantly clonic seizures, respectively, at PTZ levels exceeding those required to induce seizures in intact cats.

Animals↗
PubMedDate not supplied

Identification of motor conduction block despite desynchronisation. A method.

Identification of incomplete motor conduction block (CB) by the usual single stimulation method is problematic when impaired conduction velocity of the axons spared by the block exists at the site of the presumed CB, leading to desynchronisation. Indeed, the area of the compound muscle action potential (MAP) evoked by stimulation applied above this site may be reduced by the phase cancellation related to desynchronisation. A triple stimulation method with double collisions allows virtual displacement of the CB distally to the site where desynchronisation occurs. A first stimulus applied on the nerve above the site of the CB is followed--after a delay--by a stimulation applied distally on the nerve where a collision occurs. This collision, however, does not concern the antidromic wave of the blocked axons which travels towards the block. A third stimulus is then applied--after a second delay--below the site of the CB, where a second collision occurs in the blocked axons. Thus, the third stimulus evokes a MAP that concerns only the unblocked axons, as would the stimulus applied above the site of the CB. In this manner, desynchronisation occurring at the CB site is avoided. The method was developed on simulated CBs of the ulnar nerve at the elbow of 33 normal subjects and compared with the usual single stimulation method. Subsequently, it was evaluated on 8 pathological CBs of the ulnar nerve at the elbow and of the peroneal nerve at the fibular head. The method detects CBs of 5% or more despite the occurrence of desynchronisation.

Action Potentials↗
PubMedDate not supplied

[Conduction blocks and peripheral neuropathies].

The conduction block (CB) of the nerve impulses in the peripheral nervous system induces a partial or complete loss of the nerve function, usually more marked on the motor fibers. The CB is due to a focal loss of the electrical properties of the nerve fibers. The underlying mechanisms include paranodal and segmental demyelination, and physical or chemical dysfunction of the ionic channels. The electrophysiological study allows distinction of axonal lesion from dysfunction due to CB. Recognition and quantification of the CB requires criteria that are not yet widely accepted. The different modalities of the examination are detailed and the criteria are discussed. The peripheral neuropathies with CB have different aetiologies; physical (electrical, thermal, percussion, compression or constriction injuries, radiation-induced), toxic (acting either on the axon or the myelin), more rarely ischaemic (arteriopathy or vasculitis), but frequently inflammatory (acute or chronic, primary or secondary) or related to dysimmune states (multifocal sensory-motor and motor neuropathies with persistent CB). Their review allows a discussion of their differential diagnosis in relation to the underlying mechanisms, site and duration (transient to persistent) of the CB.

Animals↗