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Denson G. Fujikawa 2+ within the early Nineteen Eighties it was once well-known that over the top Ca inflow, most likely via 2+ 2+ voltage-gated Ca channels, with a resultant raise in intracellular Ca, was once linked to neuronal loss of life from cerebral ischemia, hypoglycemia, and standing epilepticus (Siejo 1981). Calcium activation of phospholipases, with arachidonic acid accumulation and its oxidation, producing loose radicals, used to be considered a possible mechanism in which neuronal harm happens. In cerebral ischemia and a couple of+ hypoglycemia, power failure used to be considered the cause of over the top Ca inflow, while in prestige epilepticus it was once notion that repetitive depolarizations have been in charge (Siejo 1981). in the meantime, John Olney chanced on that monosodium glutamate, the nutrition additive, whilst given to immature rats, was once linked to neuronal degeneration within the arcuate nucleus of the hypothalamus, which lacks a blood-brain barrier (Olney 1969). He up this remark with a sequence of observations within the Seventies that management of kainic acid, which we now recognize prompts the GluR5-7 subtypes of glutamate receptor, and different glutamate analogues, brought on not just post-synaptic cytoplasmic swelling, but in addition dark-cell degeneration of neurons, whilst considered via electron microscopy (Olney 1971; Olney et al. 1974).

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Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms

Denson G. Fujikawa 2+ within the early Eighties it used to be famous that over the top Ca inflow, most likely via 2+ 2+ voltage-gated Ca channels, with a resultant bring up in intracellular Ca, was once linked to neuronal demise from cerebral ischemia, hypoglycemia, and standing epilepticus (Siejo 1981). Calcium activation of phospholipases, with arachidonic acid accumulation and its oxidation, producing unfastened radicals, used to be considered a possible mechanism during which neuronal harm happens.

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Patienten har en diabetespolyneuropati. En ascenderande symmetrisk nedsättning av muskelsträckreflexerna skulle förväntas i ett i övrigt okomplicerat fall. Livliga patellarreflexer nu tyder på förvärrad bilateral skada på corticospinala bansystem. En sådan påverkan förelåg redan för tre år sedan (sannolikt bilateralt Babinskis tecken). E. Med tanke på Lhermitte-liknande symtomatologi från höger arm/hand, progredierande stelhetskänsla i båda benen, tillkomsten av faciliterade patellarreflexer trots befintlig axonal polyneuropati, bilateralt Babinskis tecken gör att en cervikal lesion måste misstänkas.

Nästan två år senare återkom patienten till annan kollega, nu på grund av känselstörning främst i höger arm. Han upplevde domningar i höger hand samt dagligen ”elektriska stötar”, som kändes upp till axeln. De neurologiska undersökningsfynden var väsentligen oförändrade jämfört med tidigare och patienten råddes att genomgå EMG-undersökning. Denna visade måttlig neuropati av axonal typ. Vid återbesök nio månader senare angavs symtomen i stort oförändrade. Det besvär han framförallt underströk var en stelhetskänsla i benen, särskilt i underben och fötter.

EMG-ENG undersökning, som visar perifera konduktivitetsblock och förlångsammade nervledningshastigheter (kan komma något senare). k. dissociation albumino-cytologique. Proteinstegringen kan dröja 2–3 veckor efter symtomdebuten. D. Hade patienten haft någon föregående infektion, operativt ingrepp etc. innan symtomdebut? Referenser Arnason B. G. , Soliven B. Acute inflammatory demyelinating polyradikuloneuropathy. Kap. , Philadelphia, sid. 1437–1497, 1993. Ropper A. , Wijdicks E. F. , Traux B. T.

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