What is Acute disseminated encephalopathy?
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Acute disseminated encephalomyelitis (ADEM) is a nonvasculitic inflammatory demyelinating condition that bears a striking clinical and pathological resemblance to multiple sclerosis (MS). However, in most instances, ADEM and MS cases occurring in children are readily distinguishable on the basis of clinical features and findings on laboratory investigations. MS is typically a chronic relapsing and remitting disease of young adults, while ADEM is typically a monophasic disease of prepubertal children. Abnormalities of findings on cerebrospinal fluid immunoglobulin studies are likely in MS but are much less common in ADEM. The onset of ADEM usually occurs in the wake of a clearly identifiable febrile prodromal illness or immunization and in association with prominent constitutional signs and encephalopathy of varied degree, features that are uncommon in MS. \n\nHowever, the division between these processes is indistinct, which is suggestive of a clinical continuum. Moreover, other conditions along the suggested continuum include optic neuritis, transverse myelitis, and Devic syndrome, clinical entities that may occur as manifestations of either MS or ADEM. Other boundaries of ADEM merge indistinctly with a wide variety of inflammatory encephalitic and vasculitic illnesses as well as monosymptomatic postinfectious illnesses that should remain distinct from ADEM, such as acute cerebellar ataxia (ACA). A further indistinct boundary is shared by ADEM and Guillain-Barré syndrome and is manifested in cases of Miller-Fisher syndrome and encephalomyeloradiculoneuropathy (EMRN). \n\nSusceptibility to either condition is likely the product of multiple factors, including a complex interrelationship of genetics and exposure to infectious agents and possibly other environmental factors. Of particular interest are the indications that susceptibility to either condition is in part age related. Most cases of either MS or of ADEM possibly occur as the result of an inflammatory response provoked by prepubertal infection with a virus, viral vaccine, or other infectious agent. Typically, the manifestations of ADEM occur quickly after this prepubertal febrile systemic illness and are monophasic. In a minority of cases, patients with ADEM experience 1 or 2 prepubertal recurrences followed by remission. \n\nMS, on the other hand, typically manifests as a relapsing-remitting illness in ensuing adolescence or young adulthood, a significant and unexplained latency of effect with apparent permanency of immunodysregulation. Bouts of MS occur without febrile prodrome. Uncommonly, MS develops in prepubertal individuals and ADEM develops in postpubertal individuals, and some cases of adolescent-onset MS may go into remission. In very rare instances, individuals manifest prepubertal ADEM and, after long latency, MS in adolescence.\n\nHope this helps!
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Meningitis is an inflammation of the leptomeninges and underlying subarachnoid cerebrospinal fluid (CSF). It can be useful to divide symptom onset into acute, subacute, and chronic categories. Unlike subacute (1-7 d) or chronic (>7 d) meningitis, which have myriad infectious and noninfectious etiologies, acute meningitis (<24 h) is almost always a bacterial infection caused by one of several organisms. Depending on age and general condition, these gravely ill patients present acutely with signs and symptoms of meningeal inflammation and systemic infection of less than 1 day's duration. Patients may decompensate quickly and require emergency care, including antimicrobial therapy, within 30 minutes of emergency department (ED) presentation. \n\nNot all bacterial meningitis is acute. Approximately 75% of patients with bacterial meningitis present subacutely. These ill patients still require urgent ED diagnosis and care. \n\nThe emergence of resistant strains has prompted changes in antibiotic protocols in some countries, including the US. Apart from dexamethasone, neuronal cell protectants still hold only future promise as adjunctive therapy. \n\nThe challenges for emergency physicians when treating meningitis are to (1) identify and treat patients with acute bacterial meningitis, (2) assess whether a central nervous system (CNS) infection is present in those with suspected subacute or chronic meningitis, and (3) identify the causative organism. Bacterial meningitis must be excluded. Emergency physicians should be aware that future therapies will be based on improved understanding of the pathogenesis of acute bacterial meningitis and may include caspase inhibitors, antioxidants, poly (ADP-ribose) polymerase inhibitors, inhibitors of lipid peroxidation, and metalloproteinase inhibitors, in addition to antibiotics and steroids.\n\n\nPathophysiology: A number of factors influence the development of bacterial meningitis, including virulence of the strain, host defenses, and bacteria-host interactions. \n\nBacterial seeding usually occurs by hematogenous spread. In those without an identifiable source of infection, local tissue and bloodstream invasion by bacteria colonized in the nasopharynx may be a common source. Rarely, infected contiguous structures invade via septic thrombi or osteomyelitic erosion; meningeal seeding also may occur with a direct bacterial inoculate during trauma, neurosurgery, or instrumentation. Meningitis in the newborn is transmitted vertically from colonized pathogens in the maternal intestinal or genital tract or horizontally from nursery personnel or caregivers at home. \n\nOnce in the CSF, the paucity of antibodies, complement components, and white blood cells (WBCs) allows the bacterial infection to flourish. Bacterial cell wall components initiate a cascade of complement- and cytokine-mediated events that result in at least 3 critical events: increased permeability of the blood-brain barrier, cerebral edema, and presence of toxic mediators in the CSF. Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions in membrane transport, and increased vascular and membrane permeability perpetuate the infectious process and account for the characteristic changes in CSF cell count, pH, lactate, protein, and glucose. Exudates extend throughout the CSF, particularly to the basal cisterns, damaging cranial nerves (eg, cranial nerve VIII, with resultant hearing loss), obliterating CSF pathways (causing obstructive hydrocephalus), and inducing vasculitis and thrombophlebitis (causing local brain ischemia). \n\nAs intracranial pressure (ICP) continues to rise and brain edema progresses, CNS autoregulatory processes begin to fail. This pivotal event may occur when the transient increase in cerebral blood flow (CBF) reverses and begins to decrease. CBF reduction correlates with the patient's decreasing alertness and changes in mental status. \n\nWithout medical interventi
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Encephalitis?  This is an infection of the brain and is a serious illness.  Viruses like measles, mumps, chicken pox may cause encephalitis shortly after you become ill.  You can also get encephalitis from a virus that you have had for many years - an example would be herpes simplex which is the same virus that causes cold sores.  It may lie dormant in your body for years.  Another way to get encephalitis is from insect or animal bites that are carrying a certain virus.  To sum this up and give you an answer to your question......cold sores do not cause encephalitis, the virus causes the disease just as it caused the cold sore.  Hope this helps.
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Alzheimer's disease (AD), a neurodegenerative disease, is the most common cause of dementia and characterized clinically by progressive cognitive deterioration together with declining activities of daily living and neuropsychiatric symptoms or behavioral changes. The most striking early symptom is memory loss (amnesia), usually manifests as minor forgetfulness that becomes steadily more pronounced with illness progression, with relative preservation of older memories. As the disorder progresses, cognitive (intellectual) impairment extends to the domains of language (aphasia), skilled movements (apraxia), recognition (agnosia) and those functions (such as decision-making and planning) closely related to the frontal and temporal lobes of the brain as they become disconnected from the limbic system, reflecting extension of the underlying pathological process. This consists principally of neuronal (cell) loss (or atrophy), together with an inflammatory response to the deposition of amyloid plaques and neurofibrillary tangles.
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Intravenous immunoglobulin therapy (IVIg) for Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIPD), a rare syndrome that consists of weakness and paralysis of many body parts, along with abnormal sensations.  It is very difficult to diagnose in its early stages.  Cause is thought to be from an autoimmune reaction.  If I understand it correctly, this is not like HIV or AIDS where the immune system slowly shuts down; with this the nerves of an affected person are attacked by the body's own defense system.  This damages myelin (the insulation around nerves) and sometimes that axons (the part of the nerve that conducts or transmits messages) which causes either a delay or change in the message that is being sent through the nerve, usually from the brain, cortex, or spinal column, and the intended receiver such as a muscle or a percepter that senses hot/cold, sharp/dull, etc.
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Any disease that would restrict oxygen flow to the brain would inhibit movement and hinder walking without falling down.  Pneumonia is probably the most common.
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Progressive multifocal leukoencephalopathy - this is a very rare condition caused by a virus & it usually only occurs in people with AIDs or who received organ transplants. If you don't have AIDs & have never received a transplant - I'd get a 2nd opinion.\n\nPML is like another disease, multiple sclerosis, but it progresses faster. Do some research on MS to learn about it.
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You will find a good explanation on this site.\nhttp://en.wikipedia.org/wiki/Brain_death
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I'm guessing no.\n\nAbdominal distension; agranulocytosis; amblyopia, toxic, or retinal or macular disturbances; anaphylaxis or anaphylactoid reactions; anemia, hemolytic; angioedema; blood in urine; blurred vision or double vision; bronchospastic allergic reaction; change in hearing; cholestatic hepatitis or jaundice; colitis or regional enteritis; congestive heart failure or exacerbation of; constipation; crystalluria, renal calculi, or ureteral obstruction; dermatitis, allergic; dermatitis, exfoliative; diarrhea; dizziness; drowsiness; dry irritated or swollen eyes; erythema multiforme; erythema nodosum; esophagitis; fever; gastritis; gastrointestinal hemorrhage or ulceration; glomerulonephritis; headache; hepatitis; increased blood pressure; muscle cramps or pain; nephritis, interstitial; nephrotic syndrome; nervousness or irritability; neuropathy, peripheral; neutropenia; oliguria/anuria; pancreatitis, acute; pancytopenia; pericarditis; petechiae; proteinuria; regional enteritis or exacerbation of; renal impairment or failure; renal papillary or tubular necrosis; retinal hemorrhage; ringing or buzzing in ears; scotomata; serum sickness–like reaction; Stevens-Johnson syndrome; stomatitis, aphthous; systemic lupus erythematosus [SLE]–like syndrome; thrombocytopenia with or without purpura; toxic epidermal necrolysis; trembling; troubled breathing; unusual weakness; vasculitis; vomiting\n\nPage 7 of\nhttp://www.usp.org/pdf/EN/veterinary/phenylbutazone.pdf
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The basic mechanism of a concussion is the brain banging up against the inside of the skull. Think of coffee in a cup in your lap in the car. You hit the brakes hard and the coffee tries to keep going, sloshing out of your cup. When the head under goes a rapid change in direction, the brain continues to travel in the direction it was already going. If it is a sudden stop, it continues to move forward in the cerebral spinal fluid that surrounds it, striking the inside of the skull. \nOversimplifying slightly, this kills a bunch of brain cells. The death of brain cells (and other interruptions in brain function caused by the same basic mechanism) causes the symptoms of loss of consciousness, dizziness, memory loss, "stars in front of the eyes."
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You mean "Transient Ischemic Attacks".  These are sometimes called "mini-strokes" by some people.  They are short lasting episodes where small parts of the brain do not receive enough oxygen.  I will find a good article for you and re-post it.\n\nHere we go - you can learn more here:\nhttp://www.healthcomm.com/resources/imc/OneMedicineCons/ConsConditions/StrokeTransientcc.html
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Causes\nThe cause of encephalitis is most often a viral infection. Some examples include herpes viruses; arboviruses transmitted by mosquitoes, ticks and other insects; and rabies and monkeypox viruses transmitted through animal bites.\n\nEncephalitis takes two forms, categorized by the two ways that viruses can infect your brain:\n\nPrimary encephalitis. This occurs when a virus directly invades your brain and spinal cord. It can happen to people at any time of the year (sporadic encephalitis), or it can be part of an outbreak (epidemic encephalitis). \nSecondary (post-infectious) encephalitis. This form occurs when a virus first infects another part of your body and secondarily enters your brain. \n\n\n\nchildhood viral infections, including:\n\nMeasles (rubeola) \nMumps \nRubella (German measles)
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meningitis\nmononucleosis\ndoctor asap
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Read about MS and it's exacerbation's here:\n\nhttp://www.nationalmssociety.org/What%20is%20MS.asp
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A stroke, or CVA [cerebral vascular accident], is a medical term for an event where the brain does not get enough blood flow (whether is due to a leak or a blockage).  The nervous tissue in the brain requires a constant supply of blood (because it carries oxygen).  If this supply is insufficient, the nervous tissue will die, and therefore parts of the brain tissue dies.  The brain is the center of the nervous system.
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Toxic shock syndrome (TSS) is an uncommon but potentially serious illness that occurs when poisonous substances (toxins) produced by certain bacteria enter the bloodstream. The toxins cause a type of blood poisoning caused by staphylococcal, or less commonly streptococcal, infections in the lungs, throat, skin or bone, or from injuries. Women using super-absorbent tampons during menstruation were found to be most likely to get toxic shock syndrome.
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Septicemia is the presence of bacteria in the blood (bacteremia) and is often associated with severe disease. Septicemia is a serious, life-threatening infection that gets worse very quickly. It can arise from infections throughout the body, including infections in the lungs, abdomen, and urinary tract. It may come before or at the same time as infections of the bone (osteomyelitis ), central nervous system (meningitis ), or other tissues. Septicemia can rapidly lead to septic shock and death. Septicemia associated with some organisms (germs) such as meningococci can lead to shock, adrenal collapse, and disseminated intravascular coagulopathy, a condition called Waterhouse-Friderichsen syndrome. Septicemia can begin with spiking fevers and chills, rapid breathing and heart rate, the outward appearance of being seriously ill (toxic) and a feeling of impending doom. These symptoms rapidly progress to shock with decreased body temperature (hypothermia), falling blood pressure, confusion or other changes in mental status, and blood-clotting abnormalities evidenced by a specific type of red spots on the skin (petechiae and ecchymosis).