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PubMed1995

Fasciculation of granule cell neurites is responsible for the perpendicular orientation of small inhibitory interneurons in mouse cerebellar microexplant cultures in vitro.

To study the cellular and molecular mechanisms involved in the perpendicular orientation of stellate and/or basket cells to the direction of fasciculating granule cell neurites, we have used cultures of microexplants from early postnatal mouse cerebellum that show this cellular behaviour in vitro. When these cultures were maintained in the presence of antibodies to the neural cell adhesion molecules L1 and N-CAM or immunoglobulin-like domains I, II and IV of N-CAM, the resulting decrease or increase in the fasciculation of granule cell neurites changed the perpendicular orientation and morphology of the small inhibitory interneurons. Additives which did not perturb fasciculation did not affect the perpendicular orientation and morphology of stellate and/or basket cells. Furthermore, when perturbation of fasciculation was prevented, neither L1 nor N-CAM antibodies modified the positioning or morphology of interneurons. These observations indicate that ordered fasciculation of granule cell neurites is an important parameter in the perpendicular orientation and elaboration of the typical morphology of the small cerebellar inhibitory interneurons.

Animals↗

PubMed1999

Ultrastructural observations on the expression of axonin-1: implications for the fasciculation of sensory axons during axonal outgrowth into the chick hindlimb.

To help understand how axons interact as they grow into the developing chick hindlimb, we used electron microscopy in conjunction with immunoperoxidase staining for the cell adhesion molecule axonin-1 to label sensory axons. The results showed that sensory axons travel together in bundles, tightly apposed to one another. In contrast, motoneuron axons are more widely spaced, although motoneuron axons situated at the perimeter of sensory axon bundles are found in close contact with neighboring sensory axons. Sensory growth cones and lamellipodia tend to be located centrally within the bundles, with several lamellipodia typically being found stacked together. Strikingly, regions of close axonal apposition are accompanied by axonin-1 expression, suggesting that such contacts are indeed adhesive. Taken together, these observations suggest that groups of sensory axons of a similar age grow together, with some of the older sensory axons fasciculating along motoneuron axons and younger sensory axons later fasciculating along older sensory axons. Axons situated at the periphery of sensory bundles are typically partly labelled, such that axonin-1 is expressed on membranes apposing other labelled axons but not on those facing unlabelled axons or unlabelled Schwann cells. Thus, axonin-1 appears to become redistributed within the membranes of axons growing into the limb, as it does on cultured neurons. In contrast, the neuron-glia cell adhesion molecule (NgCAM), which binds heterophilically to axonin-1, appears uniformly distributed on even those axons that would have an asymmetric distribution of axonin-1. Thus, the localization of axonin-1 strongly suggests that it plays an important role in sensory axon fasciculation, but the relative contributions of its interactions with various potential ligands are unclear. Finally, we found that some sensory growth cones have lamellipodia that are spread over considerable expanses. This suggests that although fasciculation is important in sensory axon guidance, sensory axons may also explore the local environment.

Animals↗

PubMed1993

Long-term follow-up of 121 patients with benign fasciculations.

Using the case records of Mayo Clinic patients, 121 patients with a diagnosis of benign fasciculations were identified. All had a normal neurological examination and normal electrophysiological studies, except for fasciculation potentials. Interviews by telephone were conducted 2 to 32 years after diagnosis. None of the patients developed symptomatic motor neuron disease. Forty individuals were in health care careers. A subset of 19 patients described acute onset of fasciculations following a viral infection. Benign fasciculations are not a preclude to progressive motor neuron disease.

Adult↗

PubMed1981

The influence of thiopentone and alfathesin on succinylcholine-induced fasciculations and myalgias.

Thiopentone doses corresponding to 5.238 mg x kg-1, that is 2UD95 (UD95:unconsciousness dose 95) inhibit the intensity of succinylcholine-induced fasciculations compared with UD95. Alfathesin doses corresponding to 0.570 mg x kg-1, also 2UD95 (calculated as alphaxalone at a concentration of 9 mg/ml in alfathesin), do not have any greater effect on the degree of fasciculations compared to UD95. Furthermore, neither induction agent influences the incidence, distribution and duration of succinylcholine-induced myalgias. The inhibition of the degree of fasciculations caused by thiopentone is believed to be a consequence of a postsynaptic depressant effect of thiopentone at the neuromuscular junction. The evaluation of the degree of succinylcholine-induced fasciculations must take into consideration the dose of thiopentone administered at induction of anaesthesia.

Adult↗

PubMed1998

Rocuronium is the best non-depolarizing relaxant to prevent succinylcholine fasciculations and myalgia.

PURPOSE: To determine which non-depolarizing relaxant among d-tubocurarine, vecuronium, atracurium, mivacurium and rocuronium prevented muscular fasciculations and myalgia following succinylcholine. METHODS: In this double blind randomized study, 120 female patients scheduled for laparoscopic procedures were studied. They were divided into six groups of 20 according to the non-depolarizing pretreatment used: NaCl 0.9% (control), 0.05 mg.kg-1 d-tubocurarine, 0.01 mg.kg-1 vecuronium, 0.05 mg.kg-1 atracurium, 0.02 mg.kg-1 mivacurium and 0.06 mg.kg-1 rocuronium. Four minutes after the pretreatment, 1.5 mg.kg-1 succinylcholine was injected. Side effects of the pretreatment, the presence and magnitude of fasciculations, the ease of tracheal intubation, myalgia 1, 24 and 48 hr after surgery were observed. A Puritan Bennett Datex 221 NMT Relaxograph monitor was used to evaluate the neuromuscular block. RESULTS: Muscle fasciculations were observed in 19 of the 20 patients in the control group and in 3 of the 20 patients in the rocuronium group, the best of the pretreatments in that aspect. Four patients in the mivacurium group were unable to sustain more than four seconds head-lift after pretreatment (P < 0.05). Tracheal intubation conditions were better and the onset of block was faster and longer after succinylcholine in the control group (P < 0.05). Myalgias were present in 71% of the patients 24 hr postoperatively and the frequency was not different among the groups. CONCLUSION: Among the pretreatments tested, 0.06 mg.kg-1 rocuronium was the best to prevent muscular fasciculations following succinylcholine injection. In the population studied, pretreatment did not prevent postoperative myalgia. Succinylcholine 1.5 mg.kg-1 was more effective without a non-depolarizing pretreatment.

Adult↗

PubMed1997

Comparison of rocuronium and d-tubocurarine for prevention of succinylcholine-induced fasciculations and myalgia.

PURPOSE: We compared d-tubocurarine and rocuronium for the prevention of succinylcholine-induced fasciculations and postoperative myalgia (POM) and evaluated the influence of both drugs on the speed of onset and recovery of succinylcholine. METHODS: Seventy-five women undergoing surgery of short duration were studied. They were randomized to one of three groups: group SAL received normal saline followed three minutes later by 1.0 mg.kg-1 succinylcholine; group ROC received 0.05 mg.kg-1 rocuronium + 1.5 mg.kg-1 succinylcholine; group DTC received 0.05 mg.kg-1 d-tubocurarine + 1.5 mg.kg-1 succinylcholine. Single-twitch stimulation was applied to the ulnar nerve every 10 sec and the EMG response of the adductor pollicis was recorded. Fasciculations were assessed by a blinded observer on a scale of 0-3. Patients were asked 24 and 48 hr later to rate POM using a scale of 0-10. RESULTS: The interval needed for twitch height to decrease to 10% of initial value after succinylcholine was longer in group ROC (58 +/- 20 sec) (mean +/- SD) compared with group SAL (44 +/- 13 sec) (P < 0.05). Recovery to 20% occurred faster in group ROC (324 +/- 83 sec) than in groups SAL (456 +/- 103 sec) and DTC (450 +/-132 sec) (P < 0.05). Fasciculations were more intense in groups SAL than in groups ROC and DTC (P < 0.001). Patients rated POM as less intense 24hr postoperatively only in group ROC (1.2 +/- 2.4) compared with group SAL (3.3 +/- 3.5) (P < 0.05). CONCLUSION: Rocuronium prevents succinylcholine-induced fasciculations and POM. Rocuronium also delays the onset of succinylcholine and shortens its duration compared with d-tubocurarine.

Adolescent↗

PubMed2000

Neurophysiological features of fasciculation potentials evoked by transcranial magnetic stimulation in amyotrophic lateral sclerosis.

We report 13 patients with amyotrophic lateral sclerosis in whom fasciculation potentials (FPs) driven by transcranial magnetic stimulation (TMS) were recorded. A total of 18 different FPs were analyzed. TMS-driven fasciculations had a simple morphology and were stable. Complex potentials were never cortically driven. Recruitment by a slight voluntary contraction was verified in 7 of 13 tested FPs. FPs were driven by threshold stimuli in 7 of 10 patients and by stimuli 5% below threshold in 3 of 6. Mapping demonstrated that FPs were driven in an area close to the center of gravity of the muscle cortical area. In one case FPs were evoked from most of the cortical representation area of a very weak muscle. Three other patients with profuse fasciculations associated with other clinical conditions were also studied. No TMS evoked fasciculation was observed in this group. The results of this systematic study suggest that cortically evoked FPs arise centrally, at spinal cord or even more proximally, and can represent a marker of increased corticomotor excitability, which is predominant at an earlier phase but can persist as the disease progresses.

Adult↗

PubMed1983

Neostigmine-induced fasciculations--a useful diagnostic test?

Previous studies have concluded that provocation of fasciculations by neostigmine indicates a lesion of lower motor neurones. We performed 20 control experiments in 18 healthy volunteers. Ten subjects received an intramuscular injection of 1.0 mg neostigmine per 60 kg body weight. All showed fasciculations, most profusely after 30-60 minutes, on average in 6-7 muscle groups. Ten other tests with half the dosage provoked fasciculations in eight cases (2-3 muscle groups on average). Neostigmine-induced fasciculations should therefore not be interpreted as a sign of disease.

Adult↗

PubMed2006

Retroviral misexpression of cVax disturbs retinal ganglion cell axon fasciculation and intraretinal pathfinding in vivo and guidance of nasal ganglion cell axons in vivo.

The transcription factor cVax (Vax2) is expressed in the ventral neural retina and restricted expression is a prerequisite for at least three prominent aspects of retinal dorsal-ventral patterning: polarized expression of EphB/B-ephrin molecules, the retinotectal projection and the distribution of rod photoreceptors across the retina. In the chick retina, the fasciculation pattern of ganglion cell axons also differs between the dorsal and ventral eye. To investigate the molecular mechanisms involved, the nerve fiber layer was analyzed after retroviral misexpression of several factors known to regulate the positional specification of retinal ganglion cells. Forced cVax expression ventralized the fasciculation pattern and caused axon pathfinding errors near the optic disc. Ectopic expression of different ephrin molecules indicated that axon fasciculation is, at least in part, mediated by the EphB system. Finally, we report that retroviral misexpression of cVax increased the pool of EphA4 receptors phosphorylated on tyrosine residues and altered the guidance preference of nasal axons in vitro. These results identify novel functions for cVax in intraretinal axon fasciculation and pathfinding as well as suggest a mechanism to explain how restricted cVax expression may influence map formation along the dorso-ventral and antero-posterior axes of the optic tectum.

Animals↗

PubMed2006

BMP signaling regulates murine enteric nervous system precursor migration, neurite fasciculation, and patterning via altered Ncam1 polysialic acid addition.

The enteric nervous system (ENS) forms from migrating neural crest-derived precursors that differentiate into neurons and glia, aggregate into ganglion cell clusters, and extend neuronal processes to form a complex interacting network that controls many aspects of intestinal function. Bone morphogenetic proteins (BMPs) have diverse roles in development and influence the differentiation, proliferation, and survival of ENS precursors. We hypothesized that BMP signaling might also be important for the ENS precursor migration, ganglion cell aggregation, and neurite fasciculation necessary to form the enteric nervous system. We now demonstrate that BMP signaling restricts murine ENS precursors to the outer bowel wall during migration. In addition, blocking BMP signaling causes faster colonization of the murine colon, reduces ganglion cell aggregation, and reduces neurite fasciculation. BMP signaling also influences patterns of neurite extension within the developing bowel wall. These effects on ENS precursor migration and neurite fasciculation appear to be mediated at least in part by increased polysialic acid addition to neural cell adhesion molecule (Ncam1) in response to BMP. Removing PSA enzymatically reverses the BMP effects on ENS precursor migration and neurite fasciculation. These studies demonstrate several novel roles for BMP signaling and highlight new functions for sialyltransferases in the developing ENS.

Animals↗

PubMed1984

[Prevention of hyperkalemia and muscular fasciculations induced by suxamethonium].

Suxamethonium has not yet been replaced to ease endotracheal intubation despite its many undesirable side effects. Hyperkalemia and muscle pain are two such side effects; they are not reliably prevented by giving, before suxamethonium, a small dose of a non depolarizing muscle relaxant, although it does decrease muscle fasciculations. The purpose of this study was to compare with a control group three different pretreatments of these undesirable effects of suxamethonium: 1) hyperventilation, 2) calcium chloride which are accepted means of lowering the serum potassium, and 3) magnesium sulfate which has been reported in a non-controlled study to decrease muscle fasciculations. The study was performed in 40 patients (10 per group) in whom changes of plasma potassium and calcium levels were determined and muscle fasciculations measured by an objective method. Serum electrolyte variations and the quantity and duration of muscle fasciculations were similar in all groups. None of the pretreatments administered had any adverse effect on the neuromuscular block induced by suxamethonium.

Adolescent↗

PubMed2001

A congenital dermal sinus presenting the muscle fasciculation and hypertrophy.

OBJECTIVE: To report unique and unknown clinical features of muscle fasciculation and muscle hypertrophy in a case of congenital dermal sinus. PATIENTS: A 16-year-old girl presented with continuous fasciculation, often cramp, and hypertrophy of the left calf muscle. The radiography showed spina bifida of L4, L5 and S1. MRI revealed dermal sinus tract from the skin dimple of the back to the dura mater, and connected to the intradural inclusion tumor. At surgery the inclusion tumor contained many short hairs, and the cauda equina were severely adherent. Microdissection of the tumor and the adhesion was performed. At 2 years after surgery fasciculation decreased but continued; however, painful cramps of the calf muscle do not occur. CONCLUSIONS: Short hairs of dermoid and the adherence might be irritative to the cauda equina. The hyperactivity of the stimulated motor neuron may cause the muscle fasciculation leading to hypertrophy of the calf muscle.

Adolescent↗

PubMed2000

Pathophysiological significance of fasciculations in the early diagnosis of ALS.

In amyotrophic lateral sclerosis (ALS), muscles with preserved strength can have fasciculation potentials (FPs) as the only abnormality. The FPs in strong muscles are predominantly simple and stable, and can often be recruited by a slight voluntary contraction. In weak and atrophic muscles, the FPs are generally complex and unstable, tend to have a slower firing rate and are not recruited by voluntary contraction. Macro-electromyography studies suggest that these FPs are part of a more complex motor unit, as opposed to simple FPs which can represent all the motor unit. FPs driven by transcranial magnetic stimulation (TMS) were observed in 13 ALS patients. TMS-driven fasciculations had a simple morphology and were stable. Complex potentials were never cortically driven. These observations strengthen the conviction that fasciculations in ALS can have different origins. Simple, stable FPs arise proximally and are probably related to excitotoxicity phenomena, while complex, unstable FPs are most likely to originate in distal axonal sprouts that are associated with the reinnervation process. Some ALS patients with fatigue and mild weakness can have profuse fasciculations at an early phase in the evolution of the disease. Patients with denervation localized in one region and diffuse FPs should be strongly suspected of having ALS. With this strategy it should be possible to shorten the diagnosis time.

Aged↗

PubMed1987

Drug actions at mammalian motor nerve endings: the suppression of neostigmine-induced fasciculations by vecuronium and isoflurane.

The occurrence of fasciculations following administration of agents is a well-known pharmacologic phenomenon. Using the cat soleus nerve-muscle preparation, intravenous neostigmine doses between 20-200 micrograms/kg evoked fasciculations in a dose-related manner. The data demonstrate that the fasciculations were the result of the direct effect of neostigmine acting at the motor nerve endings. Vecuronium in a dose-related manner (3 and 5 micrograms/kg iv) suppressed this prejunctional activity of neostigmine. The prejunctional effect of vecuronium explains its effectiveness in preventing succinylcholine-induced fasciculations. In the presence of isoflurane (end-tidal concentration 0.20-0.25%), the suppressant effect of vecuronium on motor nerve endings was enhanced. The prejunctional action of isoflurane may be a major contribution to the additive effects of non-depolarizing muscle relaxants and potent inhalation agents.

Animals↗

PubMed1993

Isoflurane inhibits muscle fasciculations caused by succinylcholine in children.

The incidence and intensity of muscle fasciculations as well as the occurrence of cardiac arrhythmias following succinylcholine were evaluated in 36 premedicated children (1.0-5.7 years) after intravenous induction with thiopentone or after inhalation induction with isoflurane (3.75 vol-% in 70% nitrous oxide in oxygen). The study was randomized. In the thiopentone group, fasciculations were seen in all children and in the isoflurane group in 5 of 18 children (P < 0.001). The median of the duration of fasciculations was 15 s with a minimum of 5 s and maximum of 36 s (1st quartile 9 s and 3rd quartile 20 s) in the thiopentone group and 0 (0-15) s with a 1st quartile of 0 and a 3rd quartile of 3 s in the isoflurane group (P < 0.001). No cardiac arrhythmias were noted in either group. In conclusion, isoflurane in nitrous oxide inhibits succinylcholine-induced muscle fasciculations in children.

Anesthesia, Inhalation↗

PubMed1980

Suxamethonium fasciculations: a topographical study.

It has been found in a group of 455 gynaecological patients that not all the voluntary muscles of the body respond to suxamethonium in the same way. One group of muscles (e.g. biceps) which is sensitive to suxamethonium, responds by fasciculating in almost every individual. A second, resistant, group of muscles (e.g. pectoralis major) is almost totally unresponsive to suxamethonium. A third muscle group (e.g. triceps) shows fasciculations in about 60% of cases and appears intimately associated with the development of suxamethonium pains, for if fasciculations do occur then suxamethonium pains are likely to ensure, but not necessarily involving all the fasciculating muscles. A theory to account for these different groups has been proposed involving the known variation in distribution of red and white muscle fibres throughout the body.

Adolescent↗

PubMed1986

From benign fasciculations and cramps to motor neuron disease.

Fasciculations and cramps may occur in motor neuron disease or as part of a more benign syndrome. A man with apparently benign fasciculations and cramps for 4 years developed progressive muscle weakness and wasting. Such a previously undocumented evolution of benign fasciculations and cramps to motor neuron disease may further implicate anterior horn cell dysfunction in the pathogenesis of muscle fasciculation-cramp syndromes.

Atrophy↗

PubMed1991

Cramp-fasciculation syndrome: a treatable hyperexcitable peripheral nerve disorder.

We report nine patients with muscle aching, cramps, stiffness, exercise intolerance, and peripheral nerve hyperexcitability. Neurologic examination showed calf fasciculations in seven, quadriceps myokymia in two, and deltoid myokymia in one patient. Two patients had mild increase in serum creatine kinase. Muscle biopsy showed either no abnormality (three patients) or mild neurogenic changes (four patients). Fasciculations were the only abnormality on routine electrodiagnostic studies. Supramaximal stimulation of the median, ulnar, peroneal, and posterior tibial nerves at frequencies of 0.5, 1, 2, and 5 Hz produced showers of electrical potentials following the M response in at least one nerve. In three patients, the fasciculations and evoked electrical potentials were abolished by regional application of curare but not nerve block. Carbamazepine therapy caused moderate-to-marked reduction of symptoms and nerve hyperexcitability. We designate this hyperexcitable peripheral nerve disorder as the "cramp-fasciculation syndrome."

Carbamazepine↗