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It occurs when exposure to a substance – specifically, a neurotoxin or neurotoxicant– alters the normal activity of the nervous system in such a way as to cause permanent or reversible damage to nervous tissue. [1] This can eventually disrupt or even kill neurons, which are cells that transmit and process signals in the brain and other ...
Essential fatty acids, such as omega 3s, are key to the strength and performance of the brain’s cells. Since the human body can’t produce essential fatty acids on its own, they must come from ...
This pathologic phenomenon can also occur after brain injury and spinal cord injury. Within minutes after spinal cord injury, damaged neural cells within the lesion site spill glutamate into the extracellular space where glutamate can stimulate presynaptic glutamate receptors to enhance the release of additional glutamate. [18]
Local pathology of neurotoxin exposure often includes neuron excitotoxicity or apoptosis [14] but can also include glial cell damage. [15] Macroscopic manifestations of neurotoxin exposure can include widespread central nervous system damage such as intellectual disability , [ 5 ] persistent memory impairments, [ 16 ] epilepsy , and dementia ...
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 ...
Cerebral edema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain. [1] This typically causes impaired nerve function, increased pressure within the skull, and can eventually lead to direct compression of brain tissue and blood vessels. [1]
The internal wall of the canal is very delicate and allows the fluid to filter due to the high pressure of the fluid within the eye. [7] The secondary route is the uveoscleral drainage , and is independent of the intraocular pressure, the aqueous flows through here, but to a lesser extent than through the trabecular meshwork (approx. 10% of the ...
The outcome of severe cerebral hypoxia will depend on the success of damage control, amount of brain tissue deprived of oxygen, and the speed with which oxygen was restored. [citation needed] If cerebral hypoxia was localized to a specific part of the brain, brain damage will be localized to that region. A general consequence may be epilepsy ...