By Michael J. Strong
During the last ten years, there was an expanding popularity that syndromes of frontotemporal disorder (FTD) are a standard incidence in sufferers with amyotrophic lateral sclerosis (ALS). Such syndromes can be found in as many as 60% of sufferers with ALS. Conversely, the incidence of motor neuron disorder in sufferers with clinically natural frontotemporal dementia is more and more well-known. this means that to some degree there are overlapping syndromes during which either ALS and FTD take place in the similar person.
This quantity summarizes the advances in our figuring out of those problems, in addition to the aptitude courting among the 2. Key themes contain advances in our skill to clinically describe the frontotemporal syndromes, preclinical detection, neuroimaging, and genetics. The exploding box of latest markers in neuropathology is tested, as is the function of latest genetic mutations in DNA/RNA delivery structures. This booklet is the fundamental reference textual content for this subject, and may be of curiosity to neurologists and neurological trainees with a scientific or study curiosity within the FTDs or ALS, neuropsychologists, neuropathologists, and researchers.
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Additional resources for Amyotrophic Lateral Sclerosis and the Frontotemporal Dementias
In 1874, Charcot and Cuveilheir described a syndrome of corticospinal tract pathology and anterior horn cell degeneration. The concept of generalized motor neurone involvement was thus introduced as ALS (10). Shortly after this report, a syndrome of isolated UMN pathology was introduced as primary lateral sclerosis (PLS) (Erb), not associated with atrophy or weakness (23). Currently, there remains significant controversy whether ALS, progressive bulbar palsy, bulbar ALS, PLS, and PMA are all variations along a continuum of a single disease entity.
Pure LMN disease (PMA) can be quite benign, particularly when the disease is limited to few extremities, sparing bulbar function. By contrast, some patients with PMA experience a very virulent course with rapid progression of both bulbar and extremity involvement despite aggressive supportive care (15,30,31,41). There are, as yet, no clinical markers that will crisply differentiate between those with a more benign versus aggressive course of PMA. Specific phenotypes of LMN disease (PMA variants) have been identified affecting primarily the upper extremities (23,42,43) or the lower extremities (23,44).
2004). Neurofibrillary tangles in ALS and Parkinsonism-dementia complex focus in Kii, Japan. Neurology, 53, 2399–2401. 27. Garruto RM. (1985). Elemental insults provoking neuronal degeneration: the suspected etiology of high incidence amyotrophic lateral sclerosis and parkinsonism-dementia of Guam. In: Hutton JT, Kenny AD (eds), Senile Dementia of the Alzheimer Type (Neurology and Neurobiology Series), 18, pp. 319–336. Alan R. Liss. 28. Hirano A, Kurland LT, Krooth RS, Lessel S. (1961). Parkinsonism-dementia complex, and endemic disease on the island of Guam.