Acute disseminated encephalitis is an autoimmune condition where the body’s immune cells attack the myelin sheath of nerves in the brain and spinal cord, resulting in neurological symptoms. It can be caused by infections or immunizations and is treated with anti-inflammatory agents. Recovery usually occurs within one to six months, but complications may occur.
Acute disseminated encephalitis, also called acute disseminated encephalomyelitis (ADEM), is an inflammatory autoimmune condition involving the white matter of the brain and spinal cord. This means that the body’s immune cells attack and destroy the myelin sheath of the nerves, resulting in neurological symptoms similar to those of multiple sclerosis. Unlike other types of encephalitis, such as disseminated multiphasic or recurrent encephalomyelitis which has multiple demyelinating episodes, demyelination in ADEM occurs only once. Acute disseminated encephalitis can have viral, parasitic or bacterial causes, but it can also occur spontaneously. Treatment of the condition generally involves the use of anti-inflammatory agents and the provision of symptomatic relief.
The different causes of acute disseminated encephalitis include various infections or immunizations. Some of the most commonly suspected viral causes are Epstein-Barr virus, herpes simplex virus, and cytomegalovirus. Other implicated viruses include influenza, enteroviruses, chicken pox, mumps, rubella, hepatitis A and coxsackieviruses. Bacterial infections include beta-haemolytic streptococci, Leptospira, Mycoplasma pneumoniae and Borrelia burgdorferi. Semple’s rabies vaccine has been shown to induce ADEM, but vaccination with hepatitis B, polio, whooping cough, diphtheria, pneumococcus, measles, chicken pox, mumps, rubella, influenza, and Japanese encephalitis can also lead to ADEM.
Symptoms of acute disseminated encephalitis usually occur one to three weeks after the initial viral gastrointestinal or respiratory symptoms. The most prominent symptoms of ADEM include fever, headache, and neurological abnormalities such as irritability, drowsiness, seizures, weakness, or paresis, and sometimes coma. Other symptoms include cranial nerve palsies, hallucinations, slurred speech, blindness, vomiting, and psychiatric abnormalities. These symptoms occur suddenly, but can also develop over a few days. The median time from onset to peak symptom severity is approximately five days.
Treatment involves the aggressive use of anti-inflammatory agents, such as corticosteroids, to reduce central nervous system inflammation and improve symptoms. Doctors usually gave high doses of intravenous methylprednisolone or dexamethasone, followed by oral prednisolone over the next three to six weeks. When these drugs are not effective or when the patient cannot take them, high-dose intravenous immunoglobulin (IVIG) is given instead. Other alternative treatments include plasmapheresis, cyclophosphamide and mitoxantrone.
Cases of ADEM usually recover within one to six months after onset, and affected children tend to recover spontaneously. Poorer outcomes are seen in ADEM patients who are unresponsive to corticosteroids, have severe neurologic abnormalities, or have sudden onset of symptoms. About 5% of affected patients die of this condition. Complications of acute disseminated encephalitis may occur among survivors. Complications are usually impairments of motor function including mild clumsiness, hemiparesis or weakness on one side of the body, and ataxia or uncontrolled body movements.
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