Neurological Disease is one of Health Problems

Diseases, metabolic disorders, and often even the same text can be caused by non-neurological symptoms due to congenital metabolic disease that primarily affects the nervous system, and a great challenge for correct diagnosis. Neurometabolic disease rather than a separate development delay / psychopathy, seizures, dystonia, ataxia or general signs and non-specific, begins. They, especially when the disease is organ or progressive neurological or should additional suspected of being involved in this. The main clue is the "simple" neuroanatomic not be explained by the presence of a variety of neurological symptoms.

For example, coma, ataxia, or especially at the end of the metabolic pathway - the start of the main features of inborn errors of neurological manifestations present with chronic or recurrent attacks of abnormal behavior. Many of these diseases, early diagnostic methods based on metabolic testing. During the attack of organic liquid collected in the main. If your project is the first treatment choice for the investigation, and is always considered to be impaired.

Metabolic investigations are usually separated during the middle childhood developmental delays in speech development delay was a child, such as fever, occasional seizures, or epilepsy syndrome, suggesting that there is no explicit. Outside the field of metabolism and other genetic roganidanavanne and particularly psychopathy, ataxia, dystonia, and spastic paraplegia, as a reason for that has been made.

Neurotransmitters and Neuromodulators

In some classes neuromodulation neurotransmitters regulate diverse populations of neurons central nervous system (one neuron uses different neurotransmitters to connect to multiple neurons). This is in contrast to direct synaptic transmission, in which one presynaptic neuron directly affect postsynaptic partner (one neuron reaching one other neuron), neuromodulatory transmitters secreted by a small group of neurons spread over large areas of the nervous system, the effect on some neurons. Some examples include the neuromodulators are dopamine, serotonin, acetylcholine, histamine and many others.

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Neuromodulator is a relatively new concept. It can be conceptualized as a neurotransmitter that is not absorbed by pre-synaptic neuron or broken down into metabolites. Neuromodulators like that end up spending a large amount of time in the CSF (cerebrospinal fluid), influence (or modulating) the overall level of brain activity. For this reason, several neurotransmitters are also considered as neuromodulators, such as serotonin and acetylcholine.

Neurotransmitters and Neuromodulators: Handbook of Receptors and Biological Effects

Neuromodulation is often contrasted with the classical fast synaptic transmission. In both cases the transmitter works on local postsynaptic receptors, but in neuromodulation usually 7-membrane receptor that includes the G-protein coupled receptors, while in the second case they are ligand-gated ion channel. Former type of synaptic transmission often involve effects on voltage-gated ion channels, and quite slow. The latter type is much faster. Related differences are also sometimes drawn between the modulator and the synaptic inputs to neurons driver, but here the emphasis is on ongoing modulation of neuronal spiking vs. spiking causing it.

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Neurotransmitters Disorders of Gamma Glutamyl Transpeptidase Deficiency

Five patients with gamma glutamyl transpeptidase deficiency have been reported or are under investigation. Three of them have CNS involvement, though two siblings have apparently no signs of CNS damage.

This may reflect the fact that the first three patients were identified by screening for amino acid defects in populations of mentally retarded patients.

The patients have increased glutathione concentrations in plasma and urine, butthe cellular levels are normal. In addition to glutathionuria, urinary levels of gamma glutamyl cysteine and cysteine are also increased.

The patients are often identified by urinary screening for amino acid disorders using thin layer or paper chromatography and ninhydrine detection. This reveals glutathionuria (up to 1g per day). Decreased activity of gamma glutamyl transpeptidase can be demonstrated in leukocytes or cultured skin fibroblasts, but not in erythrocytes, which lack this enzyme under normal conditions.

No specific treatment has been postulated. The prognosis must be considered as serious if the patients presents with psychiatric or neurologic symptoms. On the other hand, two siblings aged 11 and 13 years so far have no signs of CNS involvement.

Gamma glutamyl transpeptidase deficiency is transmitted by autosomal recessive inheritance.

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Disorders of the Gamma Glutamyl Cycle

The gamma glutamyl cycle involves six and zymes. The biosynthesis of glutathione is catalyzed by gamma glutamyl cysteine synthetase and glutathione synthetase. The break down of the tripeptide is mediated by four enzymes. The initial step is catalyzed by gamma glutamyl transpeptidase. The gamma glutamyl residue is then released as 5-oxoproline, which is converted to glutamic by 5-oxoprolinase. The biosythesis of glutathione is feedback regulated, i.e., glutathione acts as an inhibitor to gamma glutamyl cysteine synthetase.

Glutathione has been postulated to participate in several fundamental functions, such as free radical scavenging, redox reactions, formation of deoxyribonucleotides, xenobiotic metabolism, and amino acid transport. Patients with genetic defects in the metabolism of glutathione are therefore likely to exhibit a variety of symptoms.

In diagnostic work it is essential to remember that erythrocytes contain an incomplete gamma glutamyl cycle gamma glutamyl transpeptidase, they lack both and 5-oxoprolinase.

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