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Morvan's syndrome associated with antibodies to multiple components of the voltage-gated potassium channel complex.

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We describe a patient presenting with a combination of muscle fasciculations, paresthesias, hyperhidrosis, as well as insomnia, agitation and confusion. He went on to develop psychosis and respiratory failure requiring intensive care. Electromyography confirmed the presence of neuromyotonia and CSF

[From Morvan's disease to potassium channelopathies].

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The term Morvan's disease, first coined in 1890, is still in use, although the generic term neuromyotonia--which is not exempt from criticism--has largely superseded it. Symptoms and signs are variable, ranging from benign painful fasciculations, pseudomyotonic cases, rigid forms, cases in which

Management of voltage-gated potassium channel antibody disorders.

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Syndromes from antibodies to voltage-gated potassium channels include neuromyotonia (NMT), limbic encephalitis (LE) and Morvan syndrome (MVS). There are distinct clinical features for NMT (cramps, stiffness, fasciculations, myokymia, hyperhidrosis; afterdischarges and continuous motor activity on

Potassium channel antibody-associated encephalitis with hypothalamic lesions and intestinal pseudo-obstruction.

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A subgroup of limbic encephalitis is associated with antibodies against voltage-gated potassium channels (VGKC), and responds well to immuno-modulating therapies. Anti-VGKC antibodies are also found in Isaacs' syndrome and Morvan's syndrome, both of which are sometimes complicated by thymoma. We

Development of Isaacs' syndrome following complete recovery of voltage-gated potassium channel antibody-associated limbic encephalitis.

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Autoantibodies against voltage-gated potassium channels (VGKC-Abs) are associated with acquired neuromyotonia (Isaacs' syndrome) and related disorders such as Morvan's syndrome and some cases of limbic encephalitis. The mechanisms underlying the various phenotypes induced by VGKC-Abs are not fully

Involvement of activin a receptor type 1 (ACVR1) in the pathogenesis of primary focal hyperhidrosis

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The pathogenesis of primary focal hyperhidrosis (PFH) is still not clear. PFH is thought to be a genetic disease. Whether activin A receptor type 1 (ACVR1) is involved in the pathogenesis of PFH is unknown. In this study, the expression of ACVR1 in sweat glands of patients with PAH was detected by

Chronic pain as a manifestation of potassium channel-complex autoimmunity.

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OBJECTIVE Autoantibodies targeting voltage-gated potassium channel (VGKC) complexes cause a spectrum of neuronal hyperexcitability disorders. We investigated pain as a manifestation of VGKC-complex autoimmunity. METHODS We reviewed the prevalence and characteristics of pain in

Tatami Mats: A Source of Pitted Keratolysis in a Martial Arts Athlete?

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Dear Editor, Pitted keratolysis (PK), also known as keratosis plantaris sulcatum, is a non-inflammatory, bacterial, superficial cutaneous infection, characterized by many discrete superficial crateriform ''pits'' and erosions in the thickly keratinized skin of the weight-bearing regions of the soles

Ecstasy induces reactive oxygen species, kidney water absorption and rhabdomyolysis in normal rats. Effect of N-acetylcysteine and Allopurinol in oxidative stress and muscle fiber damage.

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BACKGROUND Ecstasy (Ec) use produces hyperthermia, excessive sweating, intense thirst, an inappropriate antidiuretic hormone secretion (SIADH) and a multisystemic toxicity due to oxidative stress (OS). Intense thirst induces high intake of pure water, which associated with SIADH, usually develops

Morvan Syndrome (Morvan Fibrillary Chorea, MFC)

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Morvan syndrome or Morvan’s fibrillary chorea (MFC) is a rare constellation of neurological symptoms, consisting of peripheral nerve hyperexcitability, autonomic instability, and encephalopathy often associated with autoantibodies to voltage-gated potassium channel complexes (VGKCs). On 12

Peripheral nerve hyperexcitability syndromes.

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Peripheral nerve hyperexcitability (PNH) syndromes can be subclassified as primary and secondary. The main primary PNH syndromes are neuromyotonia, cramp-fasciculation syndrome (CFS), and Morvan's syndrome, which cause widespread symptoms and signs without the association of an evident peripheral

[A case of Isaacs' syndrome causing various central nervous symptoms successfully treated with high-dose intravenous methylprednisolone therapy].

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A 44-year-old man with a bilateral hand tremor suffered from a decline in concentration and abnormal vision for several months. He also complained of easily falling down because of muscle stiffness and cramps in his lower limbs. On admission, he demonstrated lower limb stiffness, muscle cramps,

Models of glycerol-induced acute renal failure in rats.

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Acute renal failure (ARF) following rhabdomyolysis is not uncommon in man. The popular model for ARF formation following rhabdomyolysis in experimental animals is glycerol injection into the leg muscle following a 24 hour period of water deprivation. A large percentage of patients developing ARF

Hereditary palmoplantar keratoderma (four cases in three generations).

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A 39-year-old man reported with progressive thickening of the skin of the hands and feet and an inability to flex his hand. It was largely asymptomatic; however, brisk walking caused excessive sweating, pain, and widening of the fissures on the soles of the feet. He was unable to walk barefooted.

Morvan's syndrome and myasthenia gravis related to familial Mediterranean fever gene mutations.

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BACKGROUND We present the first case of Morvan's syndrome (MoS) and myasthenia gravis (MG) related to familial Mediterranean fever (FMF) gene mutations. METHODS A 40-year-old woman with a 1-year history of bilateral ptosis and limb muscle weakness presented to our hospital. She also had memory

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