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Neurotoxicity is a form of toxicity in which a biological, chemical, or physical agent produces an adverse effect on the structure or function of the central and/or peripheral nervous system. [1] It occurs when exposure to a substance – specifically, a neurotoxin or neurotoxicant – alters the normal activity of the nervous system in such a ...
The magnitude of ethanol neurotoxicity in fetuses leading to fetal alcohol syndrome has been shown to be dependent on antioxidant levels in the brain such as vitamin E. [108] As the fetal brain is relatively fragile and susceptible to induced stresses, severe deleterious effects of alcohol exposure can be seen in important areas such as the ...
Excitotoxicity can occur from substances produced within the body (endogenous excitotoxins).Glutamate is a prime example of an excitotoxin in the brain, and it is also the major excitatory neurotransmitter in the central nervous system of mammals. [14]
Olney's lesions, also known as NMDA receptor antagonist neurotoxicity (NAT), is a form of brain damage consisting of selective death of neurons but not glia, observed in restricted brain regions of rats and certain other animal models exposed to large quantities of psychoactive drugs that inhibit the normal operation of the neuronal NMDA receptor.
Toxic encephalopathy is a neurologic disorder caused by exposure to neurotoxic organic solvents such as toluene, following exposure to heavy metals such as manganese, as a side effect of melarsoprol treatment for African trypanosomiasis, adverse effects to prescription drugs, or exposure to extreme concentrations of any natural toxin such as cyanotoxins found in shellfish or freshwater ...
Neuroinflammation is widely regarded as chronic, as opposed to acute, inflammation of the central nervous system. [5] Acute inflammation usually follows injury to the central nervous system immediately, and is characterized by inflammatory molecules, endothelial cell activation, platelet deposition, and tissue edema. [6]
A potential cause of chronic alcoholic cerebellar dysfunction is an alteration of GABA-A receptor. This dysfunction causes an increase in the neurotransmitter GABA in cerebellar Purkinje cells, granule cells, and interneurons leading to a disruption in normal cell signaling. [8] GABA-A receptor embedded in cell membrane
Blood tests are performed to rule out other causes and to confirm an elevated level of vitamin B 6 with an absence of hypophosphatasia. [ 14 ] [ 11 ] [ 12 ] [ 57 ] [ 58 ] Examination does not typically show signs of a motor deficit , dysfunction of the autonomic nervous system or impairment of the central nervous system , [ 4 ] [ 3 ] although ...