Neurology International 2014; volume 6:5208

Another perspective Introduction Correspondence: Marco Antonio Araujo Leite, on fasciculations: Fluminense Federal University – UFF Niterói, Rio when is it not caused The fasciculations can be defined as visible de Janeiro, Brazil. by the classic form fast, fine, spontaneous and intermittent con- E-mail: [email protected] tractions of muscle fibers. Some neurologists of amyotrophic lateral sclerosis call them verminosis, because they look like Key words: fasciculations, neurological diseases, electromyography treatment. or progressive spinal atrophy? worms moving below the dermis.¹,² Undoubtedly, this finding in a neurological Contributions: the authors contributed equally. Marco Antonio Araujo Leite, examination is of concern, given its close rela- ¹ Marco Orsini,1 Marcos R.G. de Freitas, tionship with amyotrophic lateral sclerosis Conflict of interests: the authors declare no João Santos Pereira,1,2 ¹ (ALS), a disease that leads to a depletion of neu- potential conflict of interests. Fábio Henrique Porto Gobbi,3 rons in the fore tip and the pyramidal bundle. Received for publication: 29 November 2013. Victor Hugo Bastos,4 The presence of fasciculations, however, is not a sign of ALS when no other symptoms or signs Accepted for publication: 28 March 2014. Dionis de Castro Machado,4 of involvement of the fore tip and the pyramidal Sergio Machado,5 Oscar Arrias-Carrion,6 This work is licensed under a Creative Commons bundle are identified.³ No one knows whether Jano Alves de Souza, Acary Bulle Attribution NonCommercial 3.0 License (CC BY- the origin of ALS is central, in the first or sec- NC 3.0). Oliveira7 ¹ ond motor neurons, in the peripheral, or even in Neurology Service, Movement Disorders the terminal motor nerve − which is an even ©Copyright M.A.A. Leite et al., 2014 Unit,¹ Fluminense Federal University, more intriguing aspect for experts. In short, it is Licensee PAGEPress, Italy incorrect to associate fasciculations directly to Neurology International 2014; 6:5208 Niterói, Rio de Janeiro, Brazil; doi:10.4081/ni.2014.5208 Neurology Service, Rio de Janeiro the injury of fore tip of the spinal cord, because the skeletal pathophysiological involvement can University,² Brazil; 3Neurology be quite broad.3,4 Department, São Paulo University, Brazil; Potential fasciculations may also persist after only 4 Methods Departament of Physiotherapy, Piaui a distal nerve block. This suggests that fascicu- Federal University, Parnaíba, Brazil; lation potentials may originate anywhere in the We reviewed several articles using the fol- 5Physical Activity Neuroscience, Physical axon, probably within the distal axonal arboriza- lowing databases: Lilacs, Scielo, Medline and Activity Sciences Postgraduate Program, tion. However they are known to be associateduse Pubmed. In our search we used the following Salgado de Oliveira University, Niterói, with a hypersensitivity of denervated muscles. It keywords: fasciculations, epidemiology, etiolo- Brazil; 6Movement Disorders and Sleep is also important to consider that several condi- gy, benign fasciculations syndrome, exercises, tions may trigger them, such as other diseases Unit, General Hospital Dr. Manuel Gea amyotrophic lateral sclerosis, motor neuron of the fore tip of the spinal cord (benign González, Secretaria de México D.F., diseases, neuromuscular diseases, movement monomelic amyotrophy, progressive spinal México; 7Neurology Service, São Paulo disorders, drugs, poisoning, physical activity muscular atrophies, Hirayama disease and oth- Federal University, São Paulo, Brazil and their correspondents in Portuguese, ers), neuromuscular junction disorders, elec- Spanish, Japanese in the period between 1940 trolyte disorders, systemic diseases and use of and 2013. certain medications.5 Also healthy individuals Abstract can have fasciculations, although they are gen- erally located in well-defined sites, such as the brachial distal third, the crural area and the eye- Fasciculations are visible, fine and fast, Fasciculations in healthy lids.¹ With regard to fasciculations potentials sometimes vermicular contractions of fine induced by drugs, Masland and Wigiton,6 in a subjects muscle fibers that occur spontaneously and pioneering experimental study, concluded that intermittently. The aim of this article is to dis- neostigmine can cause fasciculation potentials Fasciculations can also be found in individ- cuss the main causes for fasciculations and Non-commercialby increasing the concentration of acetylcholine uals with no neurological disease. In 1963, their pathophysiology in different sites of the at the neuromuscular junction in felines. Reed and Kurland warned that the presence of central/peripheral injury and in particular to Discharges are caused by the direct effect of fasciculations was not necessarily a prelude to disprove that the presence of this finding in acetylcholine in the motor nerve terminals. A the onset of a progressive and lethal disease, the neurological examination is indicative of similar mechanism also occurs during induc- due to the involvement of the lower motor neu- amyotrophic lateral sclerosis. Undoubtedly, tion of anesthesia with succinylcholine endotra- ron.8 Since then, several authors have most fasciculations have a distal origin in the cheally.7 Orsini et al.5 reported the case of a explored this topic, defining a benign fascicu- motor nerve both in normal subjects and in young man with benign fasciculations, trig- lation syndrome (BFS), that most frequently patients with motor neuron disease. Most of gered by the use of oral corticosteroids adminis- affects young healthcare professionals,9,10 them spread to other dendritic spines often tered in immunosuppressive doses in patients who, in some cases, have already developed producing an antidromic impulse in the main with immune-mediated kidney disease, which dyspnea.11 An interesting Australian prospec- axon. The clinical and neurophysiological subside completely after medication tapering. tive study published recently examined the diagnosis must be thorough. It may often take The objective of this study based on the cur- cases of 20 physicians (20 consecutive cases) long to record fasciculations with electroneu- rent literature is to describe various causes of complaining of fasciculations.9 Fourteen of romyography. In other cases, temporal moni- fasciculations and to discuss the pathophysio- them were very concerned about being diag- toring is necessary before the diagnosis. The logical skeletal involvement, when present nosed with ALS. The fasciculations were main- treatment, which may be adequate in some (Table 1). ly in the lower limbs, which had normal muscle cases, is not always necessary. strength. In the electrophysiological study, fas-

[Neurology International 2014; 6:5208] [page 47] Review ciculations potentials were of the simple type, al.18 observed fasciculations in half of patients, Montagna et al.²4 reported fasciculations motor conduction was normal and no signs of most commonly in the facial region. Potential and amyotrophy in five cases of Shy-Drager denervation or neurogenic changes of motor fasciculations were noticed in conventional syndrome. Clinical, electrophysiological, and units were apparent. electromyography in 41 cases. The authors anatomopathological examinations indicated These authors, in agreement with others, reported the involvement of the peripheral the degenerative involvement of spinal previ- concluded that physical exercise, stress, nerves. ous ends. fatigue and caffeine abuse can precipitate or Kanai and Kuwabara posited that in SCA 3 In 2008, Luo et al.25 described the case of a aggravate this picture. Among the other six the severity of cramps/fasciculations correlates 68-year-old man, whose manifestations were individuals in the sample, five patients mani- with peripheral axonal excitability,19 suggest- muscle weakness, amyotrophy, fasciculations, fested a cramp-fasciculation syndrome ing that the appearance of potentials is associ- tremor and cerebellar syndrome. The ENMG (Denny-Brown syndrome) and only one suf- ated with subjacent axonal peripheral deple- was consistent with spinal muscular atrophy fered from ALS. tion and attempted sprouting of the remaining (SMA) and olivopontocerebellar atrophy Some authors have stated that, in order to motor neurons for reinnervation of partially (OPCA), a type of MSA, which was confirmed establish the clinical diagnosis of BFS, a mini- denervated muscles. Another cerebellar degen- by the MRI results. As there were no other mum of five years is necessary, due to the evo- eration in which the ataxia is associated with cases in the family of the patient, the authors lution, in some cases, of the motor neuron dis- fasciculations is SCA 36. Recently described in reported this to be the first case of SMA with ease.12-14 Japanese families by Kobayashi et al., it is sporadic OPCA. Unlike fasciculations, these A work by Fermont et al.15 reported the characterized by an increasing expansion of are more frequent in patients with MAS, prevalence and distribution of fasciculations the hexanucleotide GGCCTG repeat in the first myoclonus, myokymia, and involved particular- in healthy adults. The potentials were studied intron of the NOP56 gene.20 ly the face.26 by ultrasound in 58 individuals from different Ikeda et al.21 found that amyotrophy and fas- Machida et al.²7 reported a case of sporadic age groups. The subjects were also interviewed ciculations affected the tongue of most of the amyotrophic lateral sclerosis with multiple sys- using questionnaires about the exacerbation 18 SCA36 patients, and in more than half of tem degeneration found at necropsy. A 48-year- of caffeine consumption and physical activity. them, trunk and limbs were also affected. They old man who died one year after the onset of Of the total sample, 43% had fasciculations, detected the involvement of the lower motor the diseaseonly had muscular atrophy, weakness especially in the hallucis longus abductor mus- neuron using electroneuromyography and fasciculations in various body segments, cle. In the lower limbs, fasciculations were (ENMG). In the same period, García-Murias et ataxia and an increase of deep tendon reflexes rarely found and reported. Older individuals al.²² described SCA 36 in two families from the in all four limbs in addition to rigidity and showed more fasciculations than young adults. region of Galicia in Spain. However, the tremor. The necropsy showed a degeneration The authors have noted that certain physical observed phenotype differed from use the of the upper and lower motor neurons, the sub- activities, when very intense, may exacerbate Japanese one, since it occurred in association stantia nigra, the dentate nucleus and the symptoms in the lower limbs. with a cerebellar syndrome, a condition of sen- locus coeruleus. sorineural hearing loss and restriction of Under certain situations, fasciculations are movement like fasciculation or myokymia, in associated with parkinsonisms. However, this addition to (small) amyotrophy in the tongue. link cannot be considered in the presence of at Fasciculations associated with According to the previous description of Arias least two aspects. The distinction between motor disorders et al., SCA has been present in Spain since the hypertonia is not always an easy task in clini- 17th century, when such cases were discovered cal practice. Spasticity and rigidity can occur at Although fasciculations are not classified as in the Galician village of Death Coast. the same time in a patient. a motor disorder, they are conceptually abnor- In certain situations, fasciculation poten- The pyramidal damage can be so intense mal movements. Despite they are not rare, only tials are associated with parkinsonisms. There that it is not possible to verify a plastic hyper- a few studies investigate the association are few reports of cases where such correlation tonicity, even when this results from a severe between fasciculations and motor disorders.¹6 is highlighted in the context of an atypical impairment of the substantia nigra.28 The In the cerebellum medullary degeneration form of parkinsonism called multiple system other aspect is the bureaucratic interpretation type 3 (Machado-Joseph disease, SCA 3), a atrophy (MSA). In an original article describ- of an excellent consensus for the diagnosis of dominant autosomal disease relatedNon-commercial to an ing the Shy-Drager syndrome,²³ a type of MSA, amyotrophic lateral sclerosis, as the El Escorial unstable and increased expansion of the CAG the authors reported the coexistence, in the revised, and diseases that are similar to trinucleotide, is often associated with cramps, two cases described, of fasciculations with parkinsonism, as can be seen in the Brain fasciculations and amyotrophy.¹7 dysautonomia, parkinsonism, cerebellar syn- Bank of the Parkinson’s Disease Society of the In a series of 50 cases of SCA 3 France et drome and other manifestations. United Kingdom.29,30

Table 1. Causes of fasciculations. Fasciculationss in healthy subjects Coffee; exhaustive physical activity/fatigue; stress; cramp syndrome and benign fasciculations Fasciculations associated with movement disorders Espino-cerebell,ar degeneration-type 3; espino-cerebellar degeneration-type 36; parkinsonisms (multiple system atrophy, ALS-plus syndromes) Motor neuron diseases Amyotrophic lateral sclerosis; progressive spinal muscular atrophies; benign monomelic amyotrophy; Post-polio syndrome; Kennedy disease Systemic diseases Hipertiteoidism; syndrome of inappropriate secretion of thyrotropin (Ohba); hypophosphatemia, calcium disorders secondary to hyperparathyroidism Drugs and/or intoxications by heavy metals pollutants Neostigmine; corticosteroids; succinylcholine; elemental mercury intoxication; association of lithium and nortriptyline; flunarizine; isoniazid ALS, amyotrophic lateral sclerosis.

[page 48] [Neurology International 2014; 6:5208] Review

Inaccurate reading of guidelines such as between gene variations in the gene for angio- ance of motor neuron disease and parkinson- these can cause the elimination of different genin in patients with ALS and signs of PD and ism varied in both patients. The authors cases, due to their lack of consistency with increased risk of developing PD in relatives of named these cases as Early Onset Parkinson these criteria. As a result there is a lack of patients with ALS and these variations. The disease (EOPD)/ALS. Under the heading of studies and reports of non-classical cases. The authors suggest that these variations should neuromyotonias, there are reports of the coex- first references concerning the coexistence of be linked between the neurodegenerative istence of involuntary movements with fascic- signs of involvement of both the upper and the process of ALS and PD. Brait, Fahn and ulations. This group is characterized by the lower motor neurons and the parkinsonian Shwartz described three patients who showed occurrence of a failure of muscle relaxation syndromes date back to almost a century ago. an uncommon disease.³4 It was observed in and continuous muscle fiber activity. The most In 1923, van Bertrand and van Bogaert report- them the occurrence of symptoms and signs well-knonwn is the Isaacs Syndrome. This rare ed the pathological involvement of the basal consistent with PD persistent to levodopa and syndrome has several causes, such as neoplas- ganglia in patients with ALS. In 1926, the subsequent development (a few months to tic diseases, immune-mediated diseases, Alajouanine described the existence of motion two years later) of ALS, in the absence of any including para-neoplastic, hereditary and disorders in rare cases of Charcot disease. other neurological signs or symptoms. Gilbert, degenerative diseases. Furthermore, it is Subsequently, in 1959, van Bondelle and col- Fahn, Mitsumoto and Rowland reviewed data referred to as canulopatia due to loss of the leagues presented a case of a woman who suf- from 5500 cases of parkinsonism documented voltage-dependent potassium channels func- fered from Parkinson’s disease associated with by the Columbia University Division of tion (VGKCs) damaged by antibodies. The fail- ALS.³¹ More recent studies confirm the rela- Movement Disorders database and compared ure of VGKCs results in hyperexcitability of tionship between these disorders in experi- with data from Columbia University’s peripheral nerves and consequent continuous mental animals (transgenic mouse with super- MDA/ALS Research Center.³ As search words muscle fiber activity. Clinically, cramps are oxide dismutase - GH1) based on brain scintig- parkinsonism and upper motor neuron observed with fasciculations, continuous invol- raphy with an assessment of the dopaminergic (UMN), lower motor neuron (LMN) dysfunc- untary muscle activity (clinical myokymia), transmission.²8 Several syndromes, be them tion, or both were used. Twenty-five patients stiffness, delayed muscle relaxation and hyper- sporadic or hereditary, with the most diverse were identified. Two patients treated by Prof. hidrosis. names have been described in relation to over- Lewis P. Rowald were added. Out of these 27 In the electroneuromyography, spontaneous lapping signs of parkinsonism, fasciculations cases in total, 7 had a form of ALS-p called by dischargesonly of motor unit potentials are detect- and amyotrophy. Symptoms and signs of the authors Brait-Fahn disease, though with ed during the needle test, which appear as parkinsonism, usually bradykinesia and axial minor differences compared to the initial generalized myokymia or neuromiotonic dis- rigidity, occur in 5 to 17% of ALS patients and description, whereas in 3 cases there was a charges. often respond badly to the use of levodopa. In cognitive disorder and in 1 there wereuse cerebel- In Morvan Syndrome (Morvan’s fibrillary these patients, brain scintigraphy shows a lar changes. There were also 4 cases of chorea), another neuromyotonia even more decreased striatal dopaminergic function, Frontotemporal Dementia whith ALS, 6 cases unusual in which an hyperactivity in the cen- while neuropathological studies reveal a neu- of multiple system atrophy with ALS and 3 with tral nervous systems (mental confusion, dis- ronal loss in the substantia nigra and in the a potential hereditary spastic paraplegia in turbances mnésticos, hallucinations, insomnia globus pallidus.³² On the basis of El Escorial which parkinsonism occurred with signs of and myoclonus) coexist with peripheral symp- criteria they are classified as ALS-Plus involvement of LMN with or without a UMN toms (neuromyokymias), the combination of Syndromes and ALS Mimic Syndromes in the disorder. The authors did not specify in how fasciculations and movement disorder is con- presence of a parallel development of ALS and many of these patients fasciculations were troversial. There are few reports. Deymeer et extrapyramidal signs.²9 However, besides the assessed, given the fact that they are consid- al.³6 describe fasciculations and tremor in a fortuitous presence of extrapyramidal signs in ered a sign of malfunction of the lower motor case of Morvan Syndrome associated with thy- the clinical course of some patients with ALS, neuron, amyotrophy and/or fasciculation. Of moma, whereas Irani et al.³7 do not mention it is likely that, in some conditions, PD and ALS the 23 cases with both parkinsonism and LMN fasciculation in any of the patients in a series develop in the same individual from the same signs, 11 showed an improvement with the use of 29 cases with Morvan (11 manifested thy- pathogenic pathway. of levodopa. Manno et al.,³² described 2 cases of moma). Park and colleagues found a decrease in the Brait-Fahn-Schwartz disease in which progres- transportation of dopamine in the putamen of sive parkinsonian symptoms and signs preced- two patients who showed parkinsonianNon-commercial signs ed the appearance of ALS. and diffuse and progressive involvement in the In these patients, SPECT with 123I- Fasciculations in motor neuron upper and lower motor neurons.³³ In both, Ioflupane analysis revealed a bilateral reduced diseases bradykinesia, rigidity and tremor were asym- striatal uptake and genetic screening for metrical and responsive to levodopa and SOD1, TDP-43, C9orf 72, FUS, angiogenin, Numerous motor neuron diseases occur dopamine agonist. Both manifested bilateral Park-1, Park-2-Park and Park-6 7 (DJ-1) muta- with fasciculations,38 such as Progressive pyramidal signs and amyotrophy with diffuse tions were negative. In both the dopaminergic Spinal Muscular Atrophies, Amyotrophic fasciculations. In one, the signs of ALS preced- therapy (pramipexole and levodopa) was effec- Lateral Sclerosis, Benign Monomelic ed the PD ones, while in the other the opposite tive and long lasting in the treatment of Amyotrophy, Post-Polio Syndrome, Kennedy’s occurred. The authors also noticed that the Parkinsonian syndrome. disease, among others. With respect to ALS, decrease in dopamine transportation, deter- Annesi et al.³5 described a family from there are few studies that describe the early mined by a pre-synaptic dysfunction of the Southern Italy with a double homozygous changes in the motor unit and the pathophysi- nigrostriatal pathway was more pronounced in mutation in the DJ-1 gene and a rather com- ological aspects both in the initial stage and the contralateral striatum than the parkinson- plex phenotype. In two of the patients along the natural course of disease.³9 For this ian signs and reported such cases as ALS with described, amyotrophy and diffuse myofascicu- purpose De Carvalho and Swash studied the parkinsonism (ALS-D). A recent multicentric lations coexisted with bilateral piramidalism, neurophysiological aspects of the anterior tib- study,³¹ which evaluated 6,471 with ALS, 7668 bradykinesia, tremor at rest, rigidity. Some of ialis muscle (TA) in 73 ALS patients during the controls and 3146 with PD, found a correlation them also had dementia. The order of appear- disease progression.40 Of these, 61 had a nor-

[Neurology International 2014; 6:5208] [page 49] Review mal muscle strength (Medical Research and inappropriate secretion of thyrotropin syn- a new approach to treat the Cramps Syndrome Council: 5) in TA and 12 a moderate paresis drome (Ohba) can also trigger fasciculations. and Benign Fasciculations through the identi- (Medical Research Council: 4). We also evalu- Similarly, hypophosphatemia and calcium dis- fication and correction of sleep apnea, which ated the potential presence of fasciculations orders secondary to hyperparathyroidism can in most cases can be one of the triggers.50 and fibrillations/sharp-waves (fibs-sw), and sometimes cause the same.43 With regard to Meanwhile, one should be aware of the diagno- quantified MU potentials (MUPs) and jitter. pharmacological treatments, in a pioneering sis, rule out the possibility of other neurologi- ALS patients with a normal strength in the TA experimental study Wigiton and Masland con- cal diseases and look for less obvious causes or muscle were investigated in serial studies. cluded that neostigmine may cause fascicula- the presence of systemic diseases, sometimes Fasciculation potentials were recorded in the tions potentials by increasing the concentra- decompensated, for example, thyroid disorders anterior tibialis muscle (MRC=5) in 21 tion of acetylcholine in the neuromuscular and electrolyte abnormalities. Also one should patients with ALS and normal motor unit junction in felines.6 Discharges are caused by watch for adverse effects to drugs, whose cor- potentials. Longitudinal studies confirmed that the direct effect of acetylcholine on motor rection and control will allow an adequate ther- the patients presenting fasciculation poten- nerve terminals. Moreover, due to a similar apeutic response. Since no specific drug has tials as the only abnormality progressed to mechanism, the same occurs during the induc- yet been identified to treat these disorders, a MUP instability before large motor unit poten- tion of anesthesia with succinylcholine by regular clinical monitoring should be per- tials associated with fibs-sw were detected. endotracheal tube.7 formed for some time before formulating the The complexity of FPs in patients with weak TA Finelli described an interesting case under diagnosis. Considering the wide pathophysio- muscle was greater than in the latter group. the title of Drug-Induced Creutzfeldt-Jakob- logical skeletal involvement in the genesis of The authors consider the potential of an early like Syndrome.44 An elderly manifested rapidly fasciculations, first it is necessary to identify marker in fasciculations (ALS), which progressive dementia, postural tremor, gait their origin and then the therapeutic target. undoubtedly anticipates instability of motor instability, myoclonus and fasciculations unit potentials or the re-innervation process. caused by a combination of lithium and nor- This finding can be seen in the early stages of triptyline. Postural tremor, multifocal the disease, in which axonal excitability is myoclonus, amyotrophy and fasciculations References increased. With disease progression neuronal were also reported in a woman treated with dysfunction occurs with loss of motor unit topiramate for migraine without aura. Orsini 1. Buainainonly RP, Souza Moura L, Oliveira ASB. potentials and a transitional process of com- et al.5 also presented a case of fasciculations Fasciculations. Rev Neurocienc 2000;8:31- pensatory re-innervation. caused by oral corticosteroids at immunosup- 4. Deficits in neuromuscular transmission are pressive doses in patients with immune-medi- 2. Masland RL, Wigiton RS. Nerve activity considered one of the most important signs in ated kidney disease. use accompanying fasciculations produced by the pathophysiology of ALS. Among them fascic- Adams et al. described the case of a 54-year- prostigmin. J Neurophysiol 1940;3:269-75. ulation potentials are almost always identified old man who presented a ALS-like condition 3. Mills KR. Characteristics of fasciculation- during the clinical and neurophysiological exam- after a brief, but intense exposure to elemental ss in amyotrophic lateral sclerosis and the ination, since, according to some authors, they mercury. After the fall of mercury serum levels, benign fasciculations syndrome. Brain originate in peripheral axons. It is postulated the clinic signs ceased completely. The toxicity 2010;133:3458-69. that the dysfunction of potassium channels in of mercury should be considered not only in 4. Kleine BU, Stegeman DF, Schelhaas HJ, axons of ALS patients evokes hyperexcitability of subjects with recent dysfunction of cells of the Zwarts MJ. Firing pattern of fasciculation- the membrane (axonal), which show potential anterior horn of the spinal cord, but also with ss in ALS: evidence for axonal and neu- fasciculations. An important fact is that the mag- conditions like peripheral neuropathies of ronal origin. Neurology 2008;70:353-9. netic cortical stimulation can evoke the same unknown origin, tremor, ataxia, and a range of 5. Orsini M, Sztajnbok FR, Oliveira AB, et al. potential fasciculations, corroborating the idea psychiatric symptoms including confusion and Benign fasciculationss and corticosteroid that such hyperexcitability may be present in depression.46 use: possible association? An update. both with the depletion of spinal motor neurons Shinkeigaku et al.47 presented a Neurol Int 2011;3:e11. as cortical (pyramidal tract). After analyzing 2681 case (21-year-old man) of anti VGKC-complex 6. Masland RL, Wigiton RS. Nerve activity fasciculation potentials in 17 patients with ALS, antibody associated with a disorder presenting accompanying fasciculations produced by Hirota et al.41 also supports the theoryNon-commercial that the severe pain and fasciculations that predomi- prostigmin. J Neurophysiol 1940;3:269-75. origin of fasciculations is combined. According to nantly in a single upper extremity. Recently 7. Muravchick S, Burkett L, Gold MI. the authors, supraspinal segments have con- also isoniazid and flunarizine have been con- Succinycholine-induced fasciculationss tributed to the onset of the process. All these sidered a potential source of fascicula- and intragastric pressure during induction findings suggest that involvement affects both tions.48,49 of anesthesia. Anesthesiology 1981;55: the central and the peripheral system in ALS42. 180-3. Such considerations may explain in part why 8. Reed DM, Kurland LT. Muscle fascicula- patients with peripheral nerve injuries and\or tions in a healthy population. Arch Neurol first motor neuron lesions may present potential Treatment 1963;9:363-7. fasciculations, although not very frequently. 9. Simon NG, Kiernan MC. Fasciculations It is noteworthy that there is no specific anxiety syndrome in clinicians. J Neurol treatment for fasciculations, as it is sympto- 2013;260:1743-7. matic. The use of antiepileptic drugs such as 10. Forcelini CM, Rotta FT, Posenato N. Fasciculations induced by carbamazepine and phenytoin has shown a Benign fasciculationss responsive to systemic diseases, drugs and/ partial therapeutic response. Gabapentin can gabapentin. Arq Neuropsiquiatr 2007;65: also be used generally at low doses from 300 to 1015-7. or intoxication by heavy metals 600 mg.¹ However, due to their benign and 11. Rigby J, Holton A, Partridge J, transitional nature, it is not always necessary Satchithananda D. Dyspnoea fascicula- Thyroid disorders such as hyperthyroidism to treat fasciculations. A recent study proposed tions syndrome: the clue is in the title.

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