Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Fasciculation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 919 records · Page 51Linked to original sources
PubMed1989

Growth cone-growth cone interactions in cultures of rat sympathetic neurons.

Growth cones of sympathetic neurons from the superior cervical ganglia of neonatal rats were studied using video-microscopy to determine events following contact between growth cones and other cell surfaces, including other growth cones and neurites. A variety of behaviors were observed to occur upon contact between growth cones. Most commonly, one growth cone would collapse and subsequently retract upon establishing filopodial contact with the growth cone of another sympathetic neuron. Contacts resulting in collapse and retraction were often accompanied by a rapid and transient burst of lamellipodial activity along the neurite 30-50 microns proximal to the retracting growth cone. In no instances did interactions between growth cones and either fibroblasts or red blood cells result in the growth cone collapsing, suggesting that a specific recognition event was involved. On several occasions, growth cones were seen to track other growth cones, although fasciculation was rare. In some cases, there was no obvious response between contacting growth cones. Growth cone-growth cone contact was almost four times more likely to result in collapse and retraction than was growth cone-neurite contact (45% vs 12%, respectively). These observations suggest that the superior cervical ganglion may be composed of neurons with different cell surface determinants and that these determinants are more concentrated on the surface of growth cones than on neurites. These results further suggest that contact-mediated inhibition of growth cone locomotion may play an important role in growth cone guidance.

Animals↗
PubMed1989

Selective recognition between embryonic afferent neurons of grasshopper appendages in vitro.

Selective affinity between afferent neurons has been proposed as a major mechanism underlying the assembly of the insect peripheral nervous system during development. Afferent insect neurons establish adhesive interactions in vivo that are resistant to proteolytic degradation by elastase and independent of the basal lamina. We have tested whether afferent neurons express selective affinity for one another under more simplified and controlled conditions in vitro. We report here that (1) afferent neurons from dissociated embryonic tissue selectively aggregate within 80 min when incubated with rotation, (2) afferent axons establish and maintain fasciculation in vitro, and (3) afferent neuronal processes in vitro preferentially contact the somata of other afferent neurons in a mixed field of cells.

Afferent Pathways↗
PubMed1989

Expression of L1 and N-CAM cell adhesion molecules during development of the mouse olfactory system.

The expression of the neural adhesion molecules L1 and N-CAM has been studied in the embryonic and early postnatal olfactory system of the mouse in order to gain insight into the function of these molecules during development of a neural structure which retains neuronal turnover capacities throughout adulthood. N-CAM was slightly expressed and L1 was not significantly expressed in the olfactory placode on Embryonic Day 9, the earliest stage tested. Rather, N-CAM was strongly expressed in the mesenchyme underlying the olfactory placode. In the developing nasal pit, L1 and N-CAM were detectable in the developing olfactory epithelium, but not in regions developing into the respiratory epithelium. At early developmental stages, expression of the so-called embryonic form of N-CAM (E-N-CAM) coincides with the expression of N-CAM, whereas at later developmental stages and in the adult it is restricted to a smaller number of sensory cell bodies and axons, suggesting that the less adhesive embryonic form is characteristic of morphogenetically dynamic neuronal structures. Moreover, E-N-CAM is highly expressed at contact sites between olfactory axons and their target cells in the glomeruli of the olfactory bulb. L1 and N-CAM 180, the component of N-CAM that accumulates at cell contacts by interaction with the cytoskeleton are detectable as early as the first axons extend toward the primordial olfactory bulb. L1 remains prominent throughout development on axonal processes, both at contacts with other axons and with ensheathing cells. Contrary to N-CAM 180 which remains detectable on differentiating sensory neuronal cell bodies, L1 is only transiently expressed on these and is no longer detectable on primary olfactory neuronal cell bodies in the adult. Furthermore, whereas throughout development L1 has a molecular form similar to that seen in other parts of the developing and adult central nervous systems, N-CAM and, in particular, N-CAM 180 retain their highly sialylated form at least partially throughout all ages studied. These observations suggest that E-N-CAM and N-CAM 180 are characteristic of developmentally active structures and L1 may not only be involved in neurite outgrowth, but also in stabilization of contacts among fasciculating axons and between axons and ensheathing cells, as it has previously been found in the developing peripheral nervous system.

Animals↗
PubMed1990

The role of cell adhesion molecules in neurite outgrowth on Müller cells.

The roles of neural cell adhesion molecule (NCAM), L1, N-cadherin, and integrin in neurite outgrowth on various substrates were studied. Antibodies against these cell surface molecules were added to explants of chick retina and the neurites from retinal ganglion cells were examined for effects of the antibodies on neurite length and fasciculation. On laminin, an anti-integrin antibody completely inhibited neurite outgrowth. The same antibody did not inhibit neurite outgrowth on polylysine or Müller cells. Antibodies to NCAM, L1, and N-cadherin did not significantly inhibit neurite outgrowth on laminin but produced significant inhibition on Müller cells. The inhibition of neurite outgrowth on glia by anti-L1 antibodies supports the hypothesis that L1 is capable of acting in a heterophilic binding mechanism. On laminin, both anti-N-cadherin and anti-L1 caused defasciculation of neurites from retinal ganglion cells, while anti-NCAM did not. None of these antibodies produced defasciculation on Müller cells. The results indicate that these three cell adhesion molecules may be very important in interactions with glia as axons grow from the retina to the tectum and may be less important in axon-axon interactions along this pathway. No evidence was found supporting the role of integrins in axon growth on Müller cells.

Animals↗
PubMed1990

Genetic dissection of a complex neurological mutant, polyhomeotic, in Drosophila.

Null mutations at the polyhomeotic locus of Drosophila produce a complex phenotype during embryogenesis, which includes death of the ventral epidermis, misregulation of homeotic and segmentation gene expression, and global misrouting of CNS axons. It is shown here, through the use of mosaic analyses, double mutant combinations, and in vitro culture experiments, that all aspects of the phenotype with the exception of the axonal phenotype are cell autonomous. The changes in homeotic and segmentation gene expression in the CNS are not caused by death of the ventral epidermis, but are cell autonomous effects which most likely cause changes in neuronal cell identity. The axonal phenotype associated with ph mutations is also independent of epidermal cell death, but may be due to the nonautonomous effects of altered neuronal identities or to death or transformation of some as yet unidentified cell type. Despite the apparent autonomy of the ph mutation, mutant neurons can influence the development of adjacent wild-type neurons, presumably by depriving them of their normal fasciculation partners.

Animals↗
PubMed1992

Cholinergic differentiation of rat sympathetic neurons in culture: effects of factors applied to distal neurites.

Cholinergic properties are induced in sympathetic neurons by several factors applied to entire neurons in culture. Evidence from work with the rat sweat gland model indicates that factors located in target tissues can induce cholinergic differentiation in vivo. We now report that when leukemia inhibitory factor (LIF), heart cell-conditioned medium (HCCM), or dermal fibroblast-conditioned medium (DFCM) is applied to only distal neurites in compartmented cultures of rat sympathetic neurons, the neurons exhibit an increase in specific choline acetyltransferase activity and a concomitant decrease in levels of tyrosine hydroxylase. LIF, HCCM, and DFCM also induce neurite fasciculation, thus suggesting an additional role of cholinergic switching factors in regulating axon-axon and/or axon-substrate adhesion. These results demonstrate that rat sympathetic neurons have the cellular machinery to respond to cholinergic differentiation cues located in peripheral targets, analogous to the response to nerve growth factor.

Animals↗
PubMed1992

Cytotactin is involved in synaptogenesis during regeneration of the frog neuromuscular system.

The expression of cytotactin, an extracellular matrix glycoprotein involved in morphogenesis and regeneration, was determined in the normal and regenerating neuromuscular system of the frog Rana temporaria. Cytotactin was expressed in adult brain and gut as two major components of Mr 190,000 and 200,000 and a minor form of higher molecular weight, but was almost undetectable in skeletal muscle extract. However, cytotactin was concentrated at the neuromuscular junctions as well as at the nodes of Ranvier. After nerve transection, cytotactin staining increased in the distal stump along the endoneurial tubes. In preparations of basal lamina sheaths of frog cutaneous pectoris muscle obtained by inducing the degeneration of both nerve and muscle fibers, cytotactin was found in dense accumulations at original synaptic sites. In order to define the role of cytotactin in axonal regeneration and muscle reinnervation, the effect of anti-cytotactin antibodies on the reinnervation of the basal lamina sheaths preparations was examined in vivo. In control preparations, regenerating nerve terminals preferentially reinnervate the original synaptic sites. In the presence of anti-cytotactin antibodies, axon regeneration occurred with normal fasciculation and branching but with altered preterminal nerve fibers pathways. Ultrastructural observations showed that synaptic basal laminae reinnervation was greatly delayed or inhibited. These results suggest that cytotactin plays a primordial role in synaptogenesis, at least during nerve regeneration and reinnervation in the adult neuromuscular system.

Animals↗
PubMed1988

Physiological hypnic myoclonus.

Physiological hypnic myoclonus (PHM) was quantified during wakefulness and sleep in 7 normal subjects. PHM was evident during relaxed wakefulness and increased during stage 1 and especially REM sleep. In some muscles, however, (e.g., soleus) it showed no increase during sleep. PHM resembled simple fasciculation potentials, or, when repeated or in clusters, the fragmentary myoclonus in NREM sleep. Both 'hypnic' and 'myoclonus' are terms inappropriate to the description of this physiological spontaneous motor activity.

Adult↗
PubMed1992

Antagonism by beta-eudesmol of neostigmine-induced neuromuscular failure in mouse diaphragms.

beta-Eudesmol, a sesquiterpenol extracted from a Chinese herb, Atractylodes lancea, at 10-80 microM, did not affect muscle action potentials, miniature and evoked endplate potentials and acetylcholine-induced depolarization in the presence or absence of neostigmine in mouse phrenic nerve-diaphragms. However, the tetanic fade, muscle fasciculation and twitch potentiation induced by neostigmine were effectively antagonized by 20 microM beta-eudesmol. When trains of pulses were applied to the nerve in the presence of neostigmine, beta-eudesmol reduced the incidence of explosive depolarization of the endplate from 95% to 35-67% of junctions, and shortened the duration when it occurred. Moreover, both the maximal and steady-state depolarizations during repetitive stimulation were reduced while the amplitudes of steady-state endplate potentials were increased. The results suggest that beta-eudesmol antagonized neostigmine-induced neuromuscular failure mainly by a presynaptic action to depress the regenerative release of acetylcholine during repetitive stimulation. The mechanism of antagonism is obviously not tubocurarine-like and it is unrelated to desensitization of acetylcholine channels.

Acetylcholine↗
PubMed1995

Effect of MDL 73,745 on acetylcholine and biogenic amine levels in rat cortex.

We postulate that the effect of cholinesterase inhibitors to ameliorate the cholinergic deficit in Alzheimer's disease is related to their ability to maintain long-lasting, non-toxic steady-state levels of acetylcholine in cortex. We investigated the effect of the cholinesterase inhibitor, MDL 73,745 (2,2,2-trifluoro-1-(3-trimethylsilylphenyl)ethanone), on the extracellular levels of acetylcholine, norepinephrine, dopamine and 5-hydroxytryptamine in the cerebral cortex of the rat by high-performance liquid chromatography coupled with electrochemical detection. The drug significantly increased acetylcholine levels above the baseline at 2 and 10 mg/kg s.c., but not at the 1 mg/kg dose. At both 2 and 10 mg/kg there was a good correlation between cholinesterase inhibition and acetylcholine increase in cortex. At the 2 and 10 mg/kg doses, the maximal cholinesterase inhibition was 64% and 77%, respectively, and the increase in acetylcholine release was 481% and 1016%, respectively. Norepinephrine and dopamine, but not 5-hydroxytryptamine levels, were also significantly increased by the 10 mg/kg dose. The increases of norepinephrine and dopamine levels reached a maximum of 124% and 370%, respectively, and continued for a period of at least 8 h. Cholinergic side-effects were most marked at the 10 mg/kg dose but were also noticeable at the 2 mg/kg dose in the form of fasciculations, tremor and splay.

Acetophenones↗
PubMed1996

The effect of Phoneutria nigriventer (armed spider) venom on arterial blood pressure of anaesthetised rats.

The changes induced in the mean arterial blood pressure of anaesthetised rats following the administration of armed spider (Phoneutria nigriventer) venom have been investigated. The intravenous injection of Phoneutria nigriventer venom (0.1 mg/kg) evoked a brief and reversible decrease in the mean arterial blood pressure whereas a higher dose of venom (0.3 mg/kg) caused a biphasic response characterized by a short-lasting hypotension followed by a sustained and prolonged hypertension (40-50 min). These changes were accompanied by tachycardia, salivation, fasciculations, defecation and respiratory disturbances. Pretreatment of the animals with atropine (10 mg/kg), propranolol (100 mg/kg), phenoxybenzamine (100 mg/kg) and indomethacin (4 mg/kg) did not significantly affect the mean arterial blood pressure changes induced by Phoneutria nigriventer venom. Similarly, the bradykinin B2 receptor antagonist Hoe 140 (D-Arg-[Hyp3,Thi5,DTic7,Oic8]-bradykinin) (0.6 mg/kg), the PAF receptor antagonist WEB 2086 (3-(4-(2-chlorophenyl)-9-methyl-6H-thieno-(3,2f) (1,2,4)-triazolo-(4,3-a) (1,4)-diazepine-2-yl)-(4-morpholinyl)-1-propanone) (20 mg/kg), the tachykinin NK1 receptor antagonist SR 140333 ((S)1-(2-[3-(3,4-dichlorophenyl)-1-(3-iso-propoxyphenyl acetyl) piperidin-3-yl] ethyl)-4-phenyl-1-azoniabicyclo[2.2.2] octane, chloride) (0.5 mg/kg), the tachykinin NK2 receptor antagonist SR 48968 ((S)-N-methyl-N[4-(4-acetylamino-4-phenylpiperidino)-2-(3,4-dichlorophen yl) butyl]benzamide) (0.5 mg/kg) and the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (10 mg/kg) had no significant effect on the mean arterial blood pressure changes induced by Phoneutria nigriventer venom. The increase in the blood pressure induced by Phoneutria nigriventer venom was also not significantly affected by either the angiotensin II receptor antagonist losartan (10 mg/kg) or the endothelin ETA receptor antagonist FR 139317 ((R)2-[(R)-2-[[1-(hexahydro-1H-azepinyl]carbonyl]amino-4-methyl- pentanoyl]amino-3-[3-(1-methyl-1H-indoyl)]propionyl] amino-3-(2-pyridyl) propionic acid) (30 mg/kg). The ATP-dependent K+ channel antagonist glibenclamide (50 mg/kg) reduced by 40% the hypotension induced by Phoneutria nigriventer venom without affecting the hypertensive response. Pretreatment of the animals with L-type Ca2+ channel antagonists such as verapamil (10-100 micrograms/kg/min), diltiazem (40-120 micrograms/kg/min) and nifedipine (0.3-10 mg/kg) markedly attenuated the hypertension induced by Phoneutria nigriventer venom. Verapamil (30 micrograms/kg/min) and diltiazem (120 micrograms/kg/min) also promptly reversed the established hypertension induced by Phoneutria nigriventer venom when infused 8 min after venom injection. Our results indicate that the brief decrease of blood pressure induced by Phoneutria nigriventer venom is partially due to ATP-dependent K+ channel activation. The prolonged hypertension seems to result from direct Ca2+ entry into vascular and/or cardiac muscles.

Acetylcholine↗
PubMed1985

Regeneration of central nervous system axons into an acellular tube in the absence of distal tissue.

To differentiate between local and distant influences on central nerve regeneration, an impervious, stainless-steel cannula, 12 mm long, was placed in the path of severed axons within the corpus callosum of adult rats. The cannula was occluded for 1 week after implantation to prevent herniation of tissue into its lumen. The extracranial end of the tube was plugged with Gelfoam rather than tissue. Inflammatory cells within the tube decreased in number with time and all animals survived for the experiment's duration of 4 to 16 weeks. Some callosal axons grew into the cannula and eventually extended about 1.3 mm. After 8 to 16 weeks, the lumen of the cannula contained many unmyelinated axons, some of which formed fascicles, myelinated axons, demyelinating axons, a few oligodendrocytes, and many astrocytic processes, macrophages, and blood vessels. A striking feature was the linear orientation of cells and their processes. The distal tip of the core resembled a central nervous system explant: it included an appreciable number of growth cones, synaptic terminals embedded in a generous extracellular space, and occasional remyelinating axons. Thus, within an impervious, acellular conduit and in the absence of distal tissue, intrinsic, neuronal processes can be redirected, fasciculate, myelinate, and can regrow alongside glia and endothelium. An indwelling tube, isolating the growth from surrounding brain fluid, may permit assessment of glial, neuronal, and extracellular contributions to the directed regeneration of adult, central axons.

Animals↗
PubMed1987

Influence of substratum on the retrograde response of the rat superior cervical ganglion in vitro.

To study the role of the substratum on the retrograde response of injured peripheral noradrenergic neurons, embryonic rat superior cervical ganglia were grown in vitro on four different substrata: collagen, poly-D-lysine, fibronectin, or tissue culture plastic. The rate and pattern of neurite outgrowth were determined for a 2-week period following injury with explantation. In addition, changes in the activity of tyrosine hydroxylase, the neurotransmitter enzyme that has been shown to be altered during the retrograde response, was measured. The pattern and rate of neurite outgrowth varied directly with the ability of the neuronal growth cone to adhere to the underlying substratum. On poly-D-lysine and collagen, neurites grew as individual processes with extensive branching, whereas on plastic and fibronectin there was little branching and marked neurite fasciculation. The rate of neurite elongation on poly-D-lysine (0.75 mm/day) was faster than on collagen (.53 mm/day), fibronectin (0.33 mm/day), or plastic (0.15 mm/day). On plastic, neurons of the superior cervical ganglion showed a severe and prolonged retrograde response as characterized by a reversible decrease in tyrosine hydroxylase activity to 28% of control which persisted until the 10th day in culture. In contrast, on collagen, there was a smaller, but still significant, decrease in tyrosine hydroxylase activity to 73% of control which lasted only 5 to 6 days. On poly-D-lysine, there was no measureable change in the activity of that enzyme after injury. These studies provide quantitative evidence showing an important role of the microenvironment, and in particular the extracellular matrix, in determining the ability of neurons to respond successfully to injury.

Adrenergic Fibers↗
PubMed1988

A two-compartment modification of the silicone chamber model for nerve regeneration.

In the nerve regeneration silicone chamber model, the regenerate which forms across a 10-mm gap between proximal and distal nerve stumps is a monofascicular structure with an outer perineurial-like cell sheath. Recent work has provided indications that the geometry of the regenerate within a silicone chamber can be altered by experimental modifications of the chamber matrix. In the present study we modified the standard silicone chamber into a two-compartment chamber by inserting a 6- or 10-mm-long siliconized nitrocellulose strip in order to obtain two separate regenerates. Light microscopy 16 days after implantation revealed that two separate nerve structures had formed, one on each side of the nitrocellulose partition and adjacent to it, and each with its own perineurial-like cell sheath. In chambers with 6-mm-long strips a monofascicular regenerate started from the proximal stump and divided into two separate structures as it approached the proximal end of the strip: the two fascicles joined again into a monofascicular structure in the distal portion of the chambers. The new two-compartment silicone chamber model appears suitable for future examinations of experimental fasciculation. In addition, the nitrocellulose partition should allow one to study specific effects of growth factors on axonal regeneration in vivo, as growth factors bind strongly to untreated nitrocellulose while retaining their biological activity.

Animals↗
PubMed1992

Receptor cell regeneration and connectivity in olfaction and taste.

The capacity of adult mammalian gustatory and olfactory receptor cells to regenerate and make synaptic reconnections provides examples that may be useful in initiating replacement of other kinds of sensory receptor cells. The sensory code for taste quality may not be degraded by taste receptor cell turnover because axons probably recouple to the appropriate type of new receptor cell by axon-receptor cell affinity. Experiments on the development and regeneration of taste receptor cells suggest that they regenerate and turn over by recapitulating the late but not the early steps in taste bud development. To evaluate the replacement of vertebrate olfactory receptors, we began by characterizing the spatial pattern of primary olfactory projections in rainbow trout. Contiguous clusters of HRP-labeled olfactory receptor neurons (ORN) make highly divergent projections to the olfactory bulb. Retrograde transport of fluorescent latex beads revealed that a given restricted site in the glomerular layer received axons from ORNs widely scattered in the epithelium. Hence, ORN axons do not form point-to-point or regional topographic maps. Rather, the olfactory epithelial sheet makes a plane-to-point or holographic-like projection, since any given point in the glomerular layer receives information from the entire olfactory epithelial plane. Receptor cells that reacted with the lectin pokeweed agglutinin were highly dispersed in the olfactory epithelium with axons widely scattered in the olfactory nerve. Yet, as a consequence of the extensive reaggregation of axons at the nerve-bulb interface, the lectin-positive axons fasciculated and converged into a subregion of the glomerular layer.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Alternate strategies in lesion-induced reactive synaptogenesis: differential expression of L1 in two populations of sprouting axons.

In the CNS the cell adhesion molecule L1 plays a role in axonal growth and fasciculation. Since its roles in synapse formation and CNS regeneration are unknown, we followed the staining of L1 through the sequence of degeneration and reactive axon sprouting in the denervated outer molecular layer (ML) of the hippocampal dentate gyrus following ipsilateral entorhinal cortex (ERC) lesion. We compared immunohistological and ultrastructural localization of L1 and employed image analysis to evaluate lamina-specific changes over time. L1 staining was uniformly distributed over the ML in unlesioned animals. Following ERC lesion, L1 staining markedly declined in the outer ML; L1 staining in the inner ML remained constant. Over 30 days postlesion, commissural and associational (C/A) afferents from inner ML sprouted partway into the denervated zone, and L1 was expressed on these sprouting afferents. L1 staining exactly corresponded to fiber outgrowth as assessed by Holmes fiber stain. As the L1-bearing axons of the C/A projection expanded, staining for embryonic N-CAM (reexpressed on the dendrites of the denervated zone) appeared to recede. There was never overlap of L1 and embryonic N-CAM staining; the difference always marked the boundary between inner and outer ML. Ultrastructural analysis confirmed localization of L1 staining to axonal profiles, indicating that the new pattern of L1 staining reflected distinct types of axonal growth. These changes in cell adhesion molecule expression closely paralleled the known sequence of reactive synaptogenesis and axonal sprouting and demonstrate a link between cell adhesion molecule expression and axonal sprouting during self-repair by the CNS.

Afferent Pathways↗
PubMedDate not supplied

Adult onset of stuttering as a presenting sign in a parkinsonian-like syndrome: a case report.

Stuttering onset in adulthood is rare. With no prior history of stuttering or demonstrable neurological insult, diagnosis is often that of a conversion reaction. Stuttering as the first sign of a parkinsonian-like syndrome in extrapyramidal disease has only been reported once in the previous 30 years (Koller, 1983). The present case study differs from and builds upon the case reports in the literature, and describes a 29-year-old white male who began stuttering purportedly secondary to psychological stress. The fluency evaluation revealed severe stuttering characterized by multiple repetitions and/or blocks, with 20 or more repetitions per word routinely noted during both conversational speech and oral reading. No starters or secondary stuttering characteristics, no specific word fears or avoidances, and no situational fears were exhibited. The subsequent neurological examination found resting tremor in hands and legs, lingual fasciculations, gait imbalance, and numbness and tingling of the hands and feet, all of which were progressive in nature. Rehabilitation initially focused on fluency therapy, but then included psychiatric therapy, and finally medical intervention. Fluency and psychiatric therapies were unsuccessful in eliminating stuttering. Following a diagnosis of parkinsonian-like syndrome, medical intervention with carbidopa-levodopa resulted in dramatic improvement of motor, sensory, and fluency symptoms. It is important to consider extrapyramidal disease as an etiological factor in patients with adult onset of stuttering.

Adult↗
PubMed1975

X-linked spinal and bulbar muscular atrophy of late onset. A separate type of motor neuron disease?

The clinical, electrophysiological and muscle biopsy findings of 7 cases with a peculiar form of X-linked hereditary degenerative motor neuron disease are presented. It is suggested that the disease might be a separate clinical entity with the following characteristics: (1) sex-linked recessive inheritance, (2) unusual but not invariable late onset, (3) slow progression, (4) facial-bulbar and proximal spinal muscle involvement, (5) consistent fasciculations, sometimes massive and more pronounced about the lips, chin and tongue, (6) fine tremor of the hands, (7) muscle cramps usually preceding the other symptoms, and (8) gynaecomastia as a frequent but not a constant feature.

Action Potentials↗