AIDS Dementia Complex (ADC) is not a true opportunistic infection; it is one of the few conditions caused directly by HIV itself. However, the cause of ADC can be difficult to discern because the central nervous system can be damaged by a number of other causes related to HIV infection:

- opportunistic infections

- Primary cerebral lymphoma or metastasis of other AIDS-related cancers

- direct effects of HIV in the brain

- toxic effects of drug treatments

- malnutrition

Many researchers believe that HIV damages the vital brain cells, neurons, indirectly. According to one theory, HIV either infects or activates cells that protect the brain, known as macrophages and microglia. These cells then produce toxins that can set off a series of reactions that instruct neurons to kill themselves. The infected macrophages and microglia also appear to produce additional factors such as chemokines and cytokines that can affect neurons as well as other brain cells known as astrocytes. The affected astrocytes, which normally nurture and protect neurons, also may now end up harming neurons. HIV protein gp120 inhibits the stem cells in the brain from producing new nerve cells. In the neuronal cells, the HIV gp120 induces mitochondrial-death proteins like caspases, which may influence the upregulation of the death receptor Fas leading to apoptosis. Researchers hope that new drugs under investigation will interfere with the detrimental cycle and prevent neuron death.

HIV-associated neurocognitive disorders (HAND) are neurological disorders associated with HIV infection and AIDS. HAND may include neurological disorders of various severity. HIV-associated neurocognitive disorders are associated with a metabolic encephalopathy induced by HIV infection and fueled by immune activation of macrophages and microglia. These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of ADC are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterised by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. Histopathologically, it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS), gliosis, pallor of myelin sheaths, abnormalities of dendritic processes and neuronal loss.

ADC typically occurs after years of HIV infection and is associated with low CD4+ T cell levels and high plasma viral loads. It is sometimes seen as the first sign of the onset of AIDS. Prevalence is between 10–24% in Western countries and has only been seen in 1–2% of India-based infections. With the advent of highly active antiretroviral therapy (HAART), the incidence of ADC has declined in developed countries, although its prevalence is increasing. HAART may prevent or delay the onset of ADC in people with HIV infection, and may also improve mental function in people who already have ADC.

Dementia only exists when neurocognitive impairment in the patient is severe enough to interfere markedly with day-to-day function. That is, the patient is typically unable to work and may not be able to take care of him or herself. Before this, the patient is said to have a mild neurocognitive disorder.

PML is most common in people with HIV1 infection; prior to the advent of effective antiretroviral therapy, as many as 5% of people with AIDS eventually developed PML. It is unclear why PML occurs more frequently in AIDS than in other immunosuppressive conditions; some research suggests the effects of HIV on brain tissue, or on JCV itself, make JCV more likely to become active in the brain and increase its damaging inflammatory effects.

PML can occur in people on chronic immunosuppressive therapy like corticosteroids, for organ transplant, in people with cancer (such as Hodgkin’s disease, leukemia, or lymphoma) and individuals with autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, psoriasis, sarcoidosis, and systemic lupus erythematosus with or without biological therapies that depress the immune response and allow JC virus reactivation. These therapies include efalizumab, belatacept, rituximab, natalizumab, infliximab, cytotoxic chemotherapy, corticosteroids, and various transplant drugs such as tacrolimus.

The cause of PML is a type of polyomavirus called the JC virus (JCV), after the initials of the person from whose tissue the virus was first successfully cultured. Recent publications indicate 39% to 58% of the general population are seropositive for antibodies to JCV, indicating current or previous infection with the virus. Other publications put the percentage at 70% to 90% of the general population. JCV causes persistent asymptomatic infection in approximately one-third of the adult population, based on viral shedding into the urine from the site of asymptomatic infection in the kidney. The virus causes disease only when the immune system has been severely weakened.

Prognosis is poor, however, current analysis suggests that those associated with thymoma, benign or malignant, show a less favorable prognosis (CASPR2 Ab positive).

Most common cause of autoimmune encephalitis after acute demyelinating encephalitis in England. More than 500 cases have been reported in literature till 2013. In California Encephalitis Project it was found >4 times as frequently as herpes simplex virus type 1 (HSV-1), varicella-zoster virus (VZV), and West Nile virus (WNV). Among patients with first-onset schizophrenia incidence varies between 6–10%.

- Age – frequently 5–76 years, Median age of patients was 23 years

- Sex – 80% Female

Vascular dementia is the second-most-common form of dementia after Alzheimer's disease (AD) in older adults. The prevalence of the illness is 1.5% in Western countries and approximately 2.2% in Japan. It accounts for 50% of all dementias in Japan, 20% to 40% in Europe and 15% in Latin America. The incidence of dementia is nine times higher in patients who have had a stroke than in controls. 25% of stroke patients develop new-onset dementia within 1 year of their stroke. The relative risk of incident dementia is 5.5% within four years of suffering a stroke.

One study found that in the United States specifically, the prevalence of vascular dementia in all individuals over the age of 71 is 2.43%, and another found that the prevalence of the dementias doubles with every 5.1 years of age.

The incidence peaks between the fourth and the seventh decades of life and 80% of patients have a history of hypertension.

Many studies have been conducted to determine average survival of patients with dementia. The studies were frequently small and limited, which caused contradictory results in the connection of mortality to the type of dementia and the patient's gender. A very large study conducted in Netherlands in 2015 found that the one-year mortality was three to four times higher in patients after their first referral to a day clinic for dementia, when compared to the general population. If the patient was hospitalized for dementia, the mortality was even higher than in patients hospitalized for cardiovascular disease. Vascular dementia was found to have either comparable or worse survival rates when compared to Alzheimer's Disease, however another very large 2014 Swedish study found that prognosis was worse for male and older patients.

Unlike Alzheimer's Disease, which weakens the patient, causing them to succumb to bacterial infections like pneumonia, vascular dementia can be a direct cause of death due to the possibility of a fatal interruption in the brain's blood supply.

The onset of alcohol dementia can occur as early as age thirty, although it is far more common that the dementia will reveal itself anywhere from age fifty to age seventy. The onset and the severity of this type of dementia is directly correlated to the amount of alcohol that a person consumes over his or her lifetime.

Epidemiological studies show an association between long-term alcohol intoxication and dementia. Alcohol can damage the brain directly as a neurotoxin, or it can damage it indirectly by causing malnutrition, primarily a loss of thiamine (vitamin B1). Alcohol abuse is common in older persons, and alcohol-related dementia is under-diagnosed. A discredited French study claimed that moderate alcohol consumption (up to four glasses of wine per week) protected against dementia, whereas higher rates of consumption have conclusively been shown to increase the chances of getting it.

Individuals with MBD usually have a history of alcohol abuse, but this is not always the case. The mechanism of the disease is not completely understood, but it is believed to be caused by a Vitamin B deficiency, malnutrition, or alcohol abuse. The damage to the brain can extend into neighboring white matter and sometimes go out as far as subcortical regions.

Treatment is variable depending on individuals. Some treatments work extremely well with some patients and not at all with others. Some treatments include Therapy with thiamine and vitamin B complex. Alcohol consumption should be stopped. Some patients survive, but with residual brain damage and dementia. Others remain in comas that eventually lead to death. Nutritional counseling is also recommended. Treatment is often similar to those administered for Wenicke-Korsakoff syndrome or for alcoholism.

Type A has 21% mortality rate and an 81% long-term disability rate. Type B has a 0% mortality rate and a 19% long-term disability rate.

AIDS-related complex, or ARC, was introduced after discovery of the HIV (Human Immunodeficiency Virus) when the medical community became aware of the inherent difficulties associated with treating patients suffering from an advanced case of HIV which gave rise to the term Acquired Immune Deficiency Syndrome (AIDS). The necessity for doctors to quickly and accurately understand the special needs of unknown patients suffering from AIDS in an emergency room situation was addressed with the creation of the term ARC.

ARC is "A prodromal phase of infection with the human immunodeficiency virus (HIV). Laboratory criteria separating AIDS-related complex ( ARC) from AIDS include elevated or hyperactive B-cell humoral immune responses, compared to depressed or normal antibody reactivity in AIDS; follicular or mixed hyperplasia in ARC lymph nodes, leading to lymphocyte degeneration and depletion more typical of AIDS; evolving succession of histopathological lesions such as localization of Kaposi's sarcoma, signaling the transition to the full-blown AIDS."

Clinical use of this term was widely discontinued by the year 2000 in the United States after having been replaced by modern laboratory criteria.

Neurocognitive disorders can have numerous causes: genetics, brain trauma, stroke, and heart issues. The main causes are neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease because they affect or deteriorate brain functions. Other diseases and conditions that cause NDCs include vascular dementia, frontotemporal degeneration, Lewy body disease, prion disease, normal pressure hydrocephalus, and dementia/neurocognitive issues due to HIV infection. They may also include dementia due to substance abuse or exposure to toxins.

Neurocongnitive disorder may also be caused by brain trauma, including concussions and Traumatic Brain Injuries, as well as post-traumatic stress and alcoholism. This is referred to as amnesia, and is characterized by damage to major memory encoding parts of the brain such as the hippocampus. Difficulty creating recent term memories is called anterograde amnesia and is caused by damage to the hippocampus part of the brain, which is a major part of the memory process. Retrograde amnesia is also caused by damage to the hippocampus, but the memories that were encoded or in the process of being encoded in long term memory are erased

Incidence of demyelinating diseases vary from disorder to disorder. Some conditions, such as Tabes dorsalis appear predominantly in males and begins in mid-life. Optic neuritis on the other hand, occurs preferentially in females typically between the ages of 30 and 35. Other conditions such as multiple sclerosis vary in prevalence depending on the country and population. This condition can appear in children as well as adults.

The cause of immunodeficiency varies depending on the nature of the disorder. The cause can be either genetic or acquired by malnutrition and poor sanitary conditions. Only for some genetic causes, the exact genes are known. Although there is no true discrimination to who this disease affects, the genes are passed from mother to child, and on occasion from father to child. Women tend not to show symptoms due to their second X chromosome not having the mutation while man are symptomatic, due to having one X chromosome.

Secondary immunodeficiencies, also known as acquired immunodeficiencies, can result from various immunosuppressive agents, for example, malnutrition, aging, particular medications (e.g., chemotherapy, disease-modifying antirheumatic drugs, immunosuppressive drugs after organ transplants, glucocorticoids) and environmental toxins like mercury and other heavy metals, pesticides and petrochemicals like styrene, dichlorobenzene, xylene, and ethylphenol. For medications, the term "immunosuppression" generally refers to both beneficial and potential adverse effects of decreasing the function of the immune system, while the term "immunodeficiency" generally refers solely to the adverse effect of increased risk for infection.

Many specific diseases directly or indirectly cause immunosuppression. This includes many types of cancer, particularly those of the bone marrow and blood cells (leukemia, lymphoma, multiple myeloma), and certain chronic infections. Immunodeficiency is also the hallmark of acquired immunodeficiency syndrome (AIDS), caused by the human immunodeficiency virus (HIV). HIV directly infects a small number of T helper cells, and also impairs other immune system responses indirectly.

Various hormonal and metabolic disorders can also result in immune deficiency including anemia, hypothyroidism, diabetes and hypoglycemia.

Smoking, alcoholism and drug abuse also depress immune response.

Delirium can be caused by the worsening of previous medical conditions, substance abuse or withdrawal, mental illness, severe pain, immobilization, sleep deprivation and hypnosis.

Other common causes that may increase the risk of delirium include infections of urinary tract, skin and stomach, pneumonia, old age, and poor nutrition.

If the symptoms of alcohol dementia are caught early enough, the effects may be reversed. The person must stop drinking and start on a healthy diet, replacing the lost vitamins, including, but not limited to, thiamine. Recovery is more easily achievable for women than men, but in all cases it is necessary that they have the support of family and friends and abstain from alcohol.

Prognosis depends on the condition itself. Some conditions such as multiple sclerosis depend on the subtype of the disease and various attributes of the patient such as age, sex, initial symptoms and the degree of disability the patient experiences. Life expectancy in Multiple sclerosis patients is 5 to 10 years lower than unaffected people. MS is an inflammatory demyelinating disease of the

central nervous system (CNS) that develops in genetically susceptible individuals after exposure to unknown environmental trigger(s). The bases for MS are unknown but are strongly suspected to involve immune reactions against autoantigens, particularly myelin proteins. The most accepted hypothesis is that dialogue between T-cell receptors and myelin antigens leads to an immune attack on the myelin-oligodendrocyte complex. These interactions between active T cells and myelin antigens provoke a massive destructive inflammatory response and promotes continuing proliferation of T and B cells and macrophage activation, which sustains secretion of inflammatory mediators. Other conditions such as central pontine myelinolysis have about a third of patients recover and the other two thirds experience varying degrees of disability. There are cases, such as transverse myelitis where the patient can begin recovery as early as 2 to 12 weeks after the onset of the condition.

Fibromyalgia was found in 9% of adult patients relative to 0.03% in the general population with a link common to IBD. Concurrent IBS is found in 30% to 70%. Small intestinal bacterial overgrowth is associated is common with a transient response to antimicrobial therapy.

Chemotherapy medication, for example, fludarabine can cause a

permanent severe global encephalopathy. Ifosfamide can cause

a severe encephalopathy (but it can be reversible with stop using the drug and the use of methylene blue). Bevacizumab and other anti–vascular endothelial growth factor medication can cause posterior reversible encephalopathy syndrome.

GSE can result in high risk pregnancies and infertility. Some infertile women have GSE and iron deficiency anemia others have zinc deficiency and birth defects may be attributed to folic acid deficiencies.

It has also been found to be a rare cause of amenorrhea.

There are many types of encephalopathy. Some examples include:

- Mitochondrial encephalopathy: Metabolic disorder caused by dysfunction of mitochondrial DNA. Can affect many body systems, particularly the brain and nervous system.

- Glycine encephalopathy: A genetic metabolic disorder involving excess production of glycine.

- Hepatic encephalopathy: Arising from advanced cirrhosis of the liver.

- Hypoxic ischemic encephalopathy: Permanent or transitory encephalopathy arising from severely reduced oxygen delivery to the brain.

- Static encephalopathy: Unchanging, or permanent, brain damage.

- Uremic encephalopathy: Arising from high levels of toxins normally cleared by the kidneys—rare where dialysis is readily available.

- Wernicke's encephalopathy: Arising from thiamine (B) deficiency, usually in the setting of alcoholism.

- Hashimoto's encephalopathy: Arising from an auto-immune disorder.

- Hypertensive encephalopathy: Arising from acutely increased blood pressure.

- Chronic traumatic encephalopathy: Progressive degenerative disease associated with multiple concussions and other forms of brain injury.

- Lyme encephalopathy: Arising from Lyme disease bacteria, including "Borrelia burgdorferi".

- Toxic encephalopathy: A form of encephalopathy caused by chemicals, often resulting in permanent brain damage.

- Toxic-Metabolic encephalopathy: A catch-all for brain dysfunction caused by infection, organ failure, or intoxication.

- Transmissible spongiform encephalopathy: A collection of diseases all caused by prions, and characterized by "spongy" brain tissue (riddled with holes), impaired locomotion or coordination, and a 100% mortality rate. Includes bovine spongiform encephalopathy (mad cow disease), scrapie, and kuru among others.

- Neonatal encephalopathy (hypoxic-ischemic encephalopathy): An obstetric form, often occurring due to lack of oxygen in bloodflow to brain-tissue of the fetus during labour or delivery.

- Salmonella encephalopathy: A form of encephalopathy caused by food poisoning (especially out of peanuts and rotten meat) often resulting in permanent brain damage and nervous system disorders.

- Encephalomyopathy: A combination of encephalopathy and myopathy. Causes may include mitochondrial disease (particularly MELAS) or chronic hypophosphatemia, as may occur in cystinosis.

- Creutzfeldt–Jakob disease (CJD; transmissible spongiform encephalopathy).

- HIV encephalopathy (encephalopathy associated with HIV infection and AIDS, characterized by atrophy and ill-defined white matter hyperintensity).

- Sepsis-associated encephalopathy (this type can occur in the setting of apparent sepsis, trauma, severe burns, or trauma, even without clear identification of an infection).

- Epileptic encephalopathies:

- Early infantile epileptic encephalopathy (acquired or congenital abnormal cortical development).

- Early myoclonic epileptic encephalopathy (possibly due to metabolic disorders).

The Huntington's disease-like syndromes (often abbreviated as HD-like or "HDL" syndromes) are a family of inherited neurodegenerative diseases that closely resemble Huntington's disease (HD) in that they typically produce a combination of chorea, cognitive decline or dementia and behavioural or psychiatric problems.

In one case, a patient was diagnosed with both Morvan's syndrome and pulmonary hyalinizing granulomas (PHG). PHG are rare fibrosing lesions of the lung, which have central whorled deposits of lamellar collagen. How these two diseases relate to one another is still unclear.

Thymoma, prostate adenoma, and in situ carcinoma of the sigmoid colon have also been found in patients with Morvan’s Syndrome.