Auto immune diseases that attack the brain.

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Auto immune diseases that attack brain tissue include multiple sclerosis,  disseminated erythematic lupus,  Sydenham's chorea, Behcet's disease, encephalomyelitis,  Lambert-Eaton myasthenia syndrome.  An auto immune form of Guillain-Barré syndrome has also been found,  and this syndrome comprises polyneuritis (inflammation of several neural tissues).  Multiple sclerosis is an inflammatory attack on myelin,  primarily in the part of the brain which surrounds the central cisterns and midline channels containing cerebrospinal fluid. Heavily affected patients can be incapacitated, incontinent, and demented.   Disseminated erythematic lupus affects the brain primarily via its vascularization,  occasionally severe enough to cause psychosis (delirium, hallucination),  mental retardation or epilepsy.  Sydenham's chorea is usually the end stage of a process starting with a bacterial (streptococcal) infection, followed by rheumatism,  followed by auto immune inflammation of neurons of the basal ganglia. The basal ganglia form a large aggregate of neurons responsible for primitive motor functions.  When they are diseased or destroyed,  motor symptoms typically occur.  Chorea is one of these motor problems consisting of involuntary uncontrollable jerky spasmodic movements. These symptoms resemble those of Huntington's and Wilson's diseases which are degenerative diseases of the basal ganglia. Behcet's disease has a variant that heavily attacks the central nervous system.  This form is called neuro-Behcet syndrome.  It comprises focal lesions (hemorrhage, inflammatory necrosis) distributed throughout the encephalon, the cerebellum and the brain stem.  The meninges (membranes around the brain) are also attacked. This inflammatory destruction is detectable by magnetic resonance imaging.   As in multiple sclerosis,  the abnormalities can disappear during remissions,  but if the disease has a declining course,  permanent irreversible brain damage occurs. Many patients with auto immune disease have mild forms which produce variable symptoms difficult to diagnose.  An auto immune form of encephalomyelitis is usually termed experimental allergic encephalomyelitis because it can be virally induced in animals.  However,  it is now believed that there exists a human form distinct from,  but similar to multiple sclerosis. T cells (lymphocytes born in the thymus) invade the brain and cause excessive coagulation of blood, and consequent breakdown of the blood-brain barrier, and excretion of proteins (lymphokines) which induce inflammation and demyelination (destruction of myelin).  This is what causes the neuropsychological deficits in these patients.  Lambert-Eaton myasthenia affects principally the neuromuscular junction,  but can produce tumors in the brain and lungs.  The main brain site of predilection for tumors and degeneration is the cerebellum.   Guillain-Barré syndrome is a post-viral disease presumed to be auto immune.   It mostly affects the peripheral nerves,  but can occasionally attack the central nervous system.  Its primary target is myelin (myelin in the peripheral nerves is composed of Schwann cells as distinguished from myelin in the central nervous system which is composed of oligodendrocytes).  

Because the brain is not just composed of ordinary interneurons, but also contains glands (the choroïd plexus which secretes the cerebrospinal fluid, the hypophysis and the pineal gland which secrete hormones) as well as many non-neural tissues (vascular, glial, bony, etc.), and  also reaches out into sensory receptors such as those located in the skin, joints and eyeball,  inflammations of all of these can also seriously affect the nervous system.  Several auto immune diseases affecting the brain or non-neural tissues will no doubt be discovered in the years to come.   The most likely candidates will be,  of course, diseases with a high female prevalence.  Idiopathic dyskinesia (a motor disorder comprising involuntary movements) is such a candidate which is currently being explored for signs of an auto immune etiology.