Subsequently, he developed a prominent insomnia with increasing psychological changes and then he attempted a suicide. findings included fasciculations as well as myokymia, doublets and multiplets, high rate of recurrence discharges, and afterdischarges, following engine nerve activation. No auto-antibodies were found either in his blood or cerebrospinal fluid. Magnetic resonance imaging of his mind showed small, unspecific, probably postischemic changes. A analysis of Morvans syndrome was confirmed; immunoglobulin (2g/kg body weight) was applied intravenously, and, consequently, carbamazepine 2200mg, venlafaxine 150mg, and mirtazapine each night were prescribed. His sleep improved, suicidal tendencies halted, less fasciculations occurred, and muscle mass hypertonia also improved. Hyperexcitation also partially remitted including the electromyography getting. == Conclusions == We explained here the case of a patient with Morvans syndrome; his case is definitely rare because of severe psychical changes having a suicide attempt, short admission to a psychiatric ward, prominent electromyographic changes, and because antibodies were not recognized. After therapy with immunoglobulins followed by corticosteroids with sodium channel blocker, his engine, autonomic, psychical signs and symptoms, and electromyography changes considerably improved. Keywords:Sleeping disorders, Myokymia, Neuromyotonia, Polyneuropathy, Suicidal behavior == Intro == Peripheral nerve hyperexcitability disorders are characterized IDO-IN-3 by constant muscle dietary fiber activity due to hyperexcitability in the distal engine axons [1]. Acquired neuromyotonia is characterized by continual ectopic nerve activity, which manifests clinically in cramps, fasciculations, and tightness. These symptoms are accompanied by autonomic symptoms, sensory abnormalities, and, in the case of Morvans syndrome, by mind disorders. Apart from neuromyotonia, Morvans syndrome manifests central symptoms (sleeping disorders, hallucinations, panic, agitation, misunderstandings), autonomic symptoms (hyperhidrosis, tachycardia, obstipation) [2]. On neurophysiological exam, neuromyotonia manifests prominent spontaneous activity: fibrillations, positive waves, fasciculations, myokymia, multiple discharges, neuromyotonic discharges, doublets and multiplets. After voluntary contraction, and after electric stimulation of engine fibers, multiple and long-lasting afterdischarges happen [2]. There is no obvious consensus as to the part of the peripheral engine neuron in which this ectopic activity occurs. Most authors locate the ectopic focus in distal terminal engine fibers. Both antidromic propagation of excitation and axon reflex can participate in triggering this ectopic activity. In some conditions (inflammatory changes of the central nervous system; CNS) ectopic activity sites appear in the area of the anterior horn of the spinal cord as well as with higher levels of the CNS [3]. == Case demonstration == This case statement identifies a 70-year-old Caucasian man with presented, and electrophysiologically confirmed, neuromyotonia with significant CLC autonomic and mental changes (sleeping disorders, panic, suicidal behavior), and subsequent successful treatment. In April 2014, the 70-year-old man developed crural and lower leg pain, chills, tingling, hypersensitivity to auto technician stimuli, and minor weakening of lower limbs with slight foot-drop. This disorder developed quickly and no result in was recognized. In June 2014, he developed sleeping disorders, anxiety, confusion, even auditory hallucinations, and he attempted suicide by slashing his remaining wrist. For a short period of time, he was admitted to a psychiatric ward. He was referred to our neurological medical center electromyography (EMG) laboratory because of muscle mass weakness with prominent fasciculations, myokymia, and suspected amyotrophic lateral sclerosis. An EMG confirmed fibrillations, positive waves, fasciculations, and multiple myokymic and neuromyotonic discharges, occasional high rate of recurrence fasciculations, doublets and multiplets (Number1). Contraction curve was reduced with unstable engine unit potentials with neurogenic changes. A engine nerve conduction study showed multiple afterdischarges with long-lasting repetitions, which prevented F-waves assessment (Number2). His hold strength was weakened. He could briefly stand on tiptoes but only with problems; walking on heels was only barely attempted. He also presented tactile, thermic and vibratory hypesthesia of his lower and top limbs. == Number 1. == Neuromyotonic discharge in musculus gastrocnemius medialis; right. == Number 2. == Large voltage and long-lasting afterdischarges F-wave study in tibial nerve; remaining. His blood test showed high levels of creatine kinase (CK) 12.26 (nkat/L; normal value 3.60), CK myocardial bound 0.52, but no other abnormalities. No antibodies (contactin connected protein-like 2, CASPR2; leucine-rich glioma inactivated 1 protein; contactin 2; anti-glutamic acid decarboxylase) were found in his blood or in his cerebrospinal fluid (CSF). Oligoclonal protein synthesis was not confirmed. Cancer was not recognized (oncological markers were negative; the results of chest X-ray, ultrasonography of belly, endoscopic investigation of gastrointestinal tract and urological exam were bad). His CSF showed borderline results: protein 0.40g/L and 1 mononuclear cell/1mm3. The findings were evaluated as neuromyotonia associated with central cerebral symptoms consistent with Morvans syndrome. No antibodies (including voltage-gated potassium channel, VGKC, and CASPR2) were found either in his blood or CSF. For a period of 5 days, immunoglobulin was applied intravenously at a dose of 0.4g/kg body weight. A rapid improvement in his muscle mass strength occurred, his fasciculations decreased, and his pain sensation disorders were alleviated, including hyperalgesia. Subsequently, venlafaxine 150mg, carbamazepine IDO-IN-3 2200mg, and mirtazapine 30mg each night IDO-IN-3 were prescribed. Both his sleep disorder and daytime fatigue were alleviated. A follow-up EMG showed an increased A-sensory nerve.