Other
Three other treatment modalities also aim at improving LEMS symptoms, namely pyridostigmine, 3,4-diaminopyridine (amifampridine), and guanidine. They work to improve neuromuscular transmission. Tentative evidence supports 3,4-diaminopyridine] at least for a few weeks. The 3,4-diaminopyridine base or the water-soluble 3,4-diaminopyridine phosphate may be used. Both 3,4-diaminopyridine formulations delay the repolarization of nerve terminals after a discharge, thereby allowing more calcium to accumulate in the nerve terminal.Pyridostigmine decreases the degradation of acetylcholine after release into the synaptic cleft, and thereby improves muscle contraction. An older agent, guanidine, causes many side effects and is not recommended. 4-Aminopyridine (dalfampridine), an agent related to 3,4-aminopyridine, causes more side effects than 3,4-DAP and is also not recommended. History
Anderson and colleagues from St Thomas Hospital, London, were the first to mention a case with possible clinical findings of LEMS in 1953, but Edward H. Lambert, Lee Eaton, and E.D. Rooke at the Mayo Clinic were the first physicians to substantially describe the clinical and electrophysiological findings of the disease in 1956. In 1972, the clustering of LEMS with other autoimmune diseases led to the hypothesis that it was caused by autoimmunity. Studies in the 1980s confirmed the autoimmune nature, and research in the 1990s demonstrated the link with antibodies against P/Q-type voltage-gated calcium channels. References


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Binge eating habits are often associated  with changes in food preferences (cravings for more sweets, carbohydrates), eating inedible objects and snatching food from others. Recent findings from structural MRI research have indicated that eating changes in FTD are associated with atrophy (wasting) in the right ventral insula, striatum, and orbitofrontal cortex.People with FTD show marked deficiencies in executive functioning and working memory. Most become unable to perform skills that require complex planning or sequencing. In addition to the characteristic cognitive dysfunction, a number of primitive reflexes known as frontal release signs are often able to be elicited. Usually the first of these frontal release signs to appear is the palmomental reflex which appears relatively early in the disease course whereas the palmar grasp reflex and rooting reflex appear late in the disease course.In rare cases, FTD can occur in people with amyotrophic lateral sclerosis (ALS) a motor neuron disease. The prognosis for people with ALS is worse when combined with FTD, shortening survival by about a year. Genetics
A higher proportion of frontotemporal dementias seem to have a familial component than other neurodegenerative diseases such as Alzheimers disease. More and more mutations and genetic variants are being identified all the time, needing constant updating of genetic influences. Tau-positive frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) is caused by mutations in the MAPT gene on chromosome 17 that encodes the tau protein. It has been determined that there is a direct relationship between the type of tau mutation and the neuropathology of gene mutations.