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More Encephalopathy Causes
Metabolic encephalopathy (toxic metabolic encephalopathy) is a broad category that describes abnormalities of the water, electrolytes, vitamins, and other chemicals that adversely affect brain function. In addition to liver and kidney waste products, it may include abnormally high or low blood sugar (hyperglycemia, hypoglycemia), thyroid problems, and sodium levels in the blood (hyponatremia=low sodium, hypernatremia=high sodium).
Toxic metabolic encephalopathy can also include medication side effects or drug ingestions affecting the chemical transmitters in the brain. Called neurotransmitters, dopamine, GABA, serotonin, acetylcholine, and glutamine help nerve endings pass electrical signals between brain cells. Alterations in these transmitters can decrease brain function. Concentrations of neurotransmitters and abnormal function can be seen in seizure disorders and Alzheimer's disease.
Head trauma can cause brain damage due to bleeding in and around the brain. This can cause increased pressure within the skull that presses on brain tissue and cause abnormal brain function. Shear injuries to brain tissue can disrupt the neurons that connect brain cells together. Aside from the direct brain tissue injury, increased pressure buildup within the skull can decrease the amount of blood flow to the brain causing anoxic or hypoxic damage.
Blood supply to the brain may be compromised because of stroke, where one of the arteries to the brain becomes blocked and that part of the brain is replaced with scar tissue. If enough cells are injured, there can be permanent damage. Alternatively, hemorrhagic stroke occurs when bleeding occurs into the brain itself causing damage.
Chronic Traumatic Encephalopathy (CTE) describes a brain that has gradual degeneration in function because of repeated head injuries causing both concussions with symptoms and those that are asymptomatic. The symptoms of concussion usually fade, but months or years later, new symptoms can occur. CTE symptoms gradually progress. Initially, there may be concentration and memory issues with episodes of disorientation and confusion, dizziness, and headache. Emotions can be labile and the patient can develop aggressive and psychotic behavior. As CTE progresses, the behavior can become erratic and Parkinson's-like symptoms may be seen. Finally, thought processes decrease even further into dementia with more Parkinson's symptoms including speech and walking abnormalities. These symptoms are progressive and cannot be stopped.
The diagnosis of CTE is made clinically. Neither bleeding nor major abnormalities are seen on CT scan and it appears to act like other diseases that attack brain function. It can be confirmed in retrospect on autopsy and dissection of the brain. An abnormal protein called tau builds up in the brain and causes abnormal nerve fiber and cell tangles in the brain. At autopsy, the brain has a different appearance than that seen in Alzheimer's disease.
Acute or chronic kidney failure can lead to uremic encephalopathy. When the kidneys fail to adequately cleanse the bloodstream, a variety of toxins can gradually build and cause brain function to decrease. If kidney function is not restored or if dialysis is not instituted, permanent brain tissue damage can occur, ultimately leading to death.
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