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There are several different forms of glycine encephalopathy, which can be distinguished by the age of onset, as well as the types and severity of symptoms. All forms of glycine encephalopathy present with only neurological symptoms, including intellectual disability (IQ scores below 20 are common [5]), hypotonia, apneic seizures, and brain ...
Treatment is administered during the acute stages of excitotoxic shock along with glutamate antagonists. Dehydration should be avoided as this also contributes to the concentrations of glutamate in the inter-synaptic cleft [ 7 ] and "status epilepticus can also be triggered by a build up of glutamate around inter-synaptic neurons."
The three main signs of hyperekplexia are generalized stiffness, excessive startle response beginning at birth, and nocturnal myoclonus. [5] Affected individuals are fully conscious during episodes of stiffness, which consist of forced closure of the eyes and an extension of the extremities followed by a period of generalised stiffness and uncontrolled falling at times. [6]
Although no treatment options have been proven to help manage 3-Methylcrotonyl-CoA carboxylase deficiency [9] proposed treatments include L-carnitine supplements, [10] glycine administration, [11] biotin supplements [4] and dietary restriction of leucine.
In mature adults, glycine is a inhibitory neurotransmitter found in the spinal cord and regions of the brain. [15] As it binds to a glycine receptor, a conformational change is induced, and the channel created by the receptor opens. [17] As the channel opens, chloride ions are able to flow into the cell which results in hyperpolarization.
Symptom severity appears to be dose-dependent (higher doses cause more severe symptoms) [24] and the duration of supplementation with vitamin B 6 before the onset of systems appears to be inversely proportional to the amount taken daily (the smaller the daily dosage, the longer it will take for symptoms to develop).
The onset of symptoms is 10 to 120 minutes after ingestion. [26] Symptoms include seizures, a "sawhorse" stance, and opisthotonus (rigid extension of all four limbs). Death is usually secondary to respiratory paralysis. Treatment is by detoxification using activated charcoal, pentobarbital for the symptoms, and artificial respiration for apnea.
Protein toxicity is the effect of the buildup of protein metabolic waste compounds, like urea, uric acid, ammonia, and creatinine.Protein toxicity has many causes, including urea cycle disorders, genetic mutations, excessive protein intake, and insufficient kidney function, such as chronic kidney disease and acute kidney injury.