Diagnosis is difficult because of the diversity of phenotypes seen in people with CVID. For example, serum immunoglobulin levels in people with CVID vary greatly. Generally, people can be grouped as follows: no immunoglobulin production, immunoglobulin (Ig) M production only, or both normal IgM and IgG production. Additionally, B cell numbers are also highly variable. 12% of people have no detectable B cells, 12% have reduced B cells, and 54% are within the normal range. In general, people with CVID display higher frequencies of naive B cells and lower frequencies of class-switched memory B cells. Frequencies of other B cell populations, such as IgD memory B cells, transitional B cells, and CD21 B cells, are also affected, and are associated with specific disease features. Although CVID is often thought of as a serum immunoglobulin and B cell-mediated disease, T cells can display abnormal behavior. Affected individuals typically present with low frequencies of CD4+, a T-cell marker, and decreased circulation of regulatory T cells and iNKT cell. Notably, approximately 10% of people display CD4+ T cell counts lower than 200 cells/mm3; this particular phenotype of CVID has been named LOCID (Late Onset Combined Immunodeficiency), and has a poorer prognosis than classical CVID. Types
The following types of CVID have been identified, and correspond to mutations in different gene segments. Treatment
Treatment options are limited, and usually include lifelong immunoglobulin replacement therapy. This therapy is thought to help reduce bacterial infections.
It can cause paranoid and grandiose delusions, agitation, hallucinations (visual and auditory), bizarre behavior, fear, short-term memory loss, and confusion.HIV encephalopathy can lead to dementia. Types
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, usually caused by prenatal exposure to ethanol. Uremic encephalopathy: Arising from high levels of toxins normally cleared by the kidneys—rare where dialysis is readily available. Wernickes encephalopathy: Arising from thiamine (B1) deficiency, usually in the setting of alcoholism. Hashimotos encephalopathy: Arising from an auto-immune disorder. Anti-NMDA receptor encephalitis: An auto-immune encephalitis. Hyperammonemia: a condition caused by high levels of ammonia, which is due to inborn errors of metabolism (including urea cycle disorder or multiple carboxylase deficiency), a diet with excessive levels of protein, deficiencies of specific nutrients such as  arginine or biotin, or organ failure. Hypertensive encephalopathy: Arising from acutely increased blood pressure. Chronic traumatic encephalopathy: a 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 and prescription drugs, often resulting in permanent brain damage.