Neurological damage/deficits

Hyponatremia/Hypochloremia - A chloride deficit is generally mild and usually does not require specific treatment, except in extraordinary circumstances (as in liver or renal disease). Thiazide-induced hyponatremia has been associated with death and neurologic damage in elderly patients. 

Previous observations have shown that most patients who develop aseptic meningitis or encephalitis due to LCMV recover completely. No chronic infection has been described in humans, and after the acute phase the virus is cleared. However, as in all infections of the central nervous system, particularly encephalitLs, temporary or permanent neurological damage is possible. Nerve deafness and arthritis have been reported. Infection of the human fetus during the early states of pregnancy may lead to developmental deficits that are permanent. 

With modest impairment of blood flow, this mechanism allows for preservation of oxidative metabolism without alteration in electrical function. However, when CPP and therefore CBF are sufficiently low, OEF reaches a maximum and cannot increase further. Brain tissue ceases to function electrically, resulting in a neurologic deficit. Microvascular collapse occurs, and CBV falls. If the oxygen supply falls low enough, the tissue dies. Of critical clinical importance is the observation that the amount of time it takes for tissue to suffer irreversible damage is inversely related to the severity of the ischemic insult. Tissue that is completely deprived of blood will die within a few minutes, but less severely hypoperfused tissue may survive for many hours, and may be saved by timely thrombolysis that restores perfusion, or perhaps by another therapeutic intervention. 

Cellular therapy is the replacement of unhealthy or damaged cells or tissues with new ones. Because neurodegenerative diseases, cerebral strokes and traumatic injuries to the CNS produce neurological deficits that result from neuronal loss, cell therapy is a major area of investigation for the treatment of neurological diseases and injuries. 

Taghavy A, Hamer H. Parenchymal damage in transient ischemic attacks (TIAs) and prolonged reversible ischemic neurologic deficits (PRINDs) the role of cranial CT and EEG. Int J Neurosci 1992 Oct 66(3-4) 251-61. 

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