The administration of immunotherapy, in association with chemotherapy or tumor removal, .

Immunosuppressive therapies, encompassing corticosteroids, azathioprine, methotrexate and more recently, rituximab, are the mainstay of therapy. Other treatments include PE, IVIG, and thymectomy. Patients reportedly exhibited a heterogenous response to immunomodulation.

Antiepileptics can be used for symptomatic relief of peripheral nerve hyperexcitability. Indeed, some patients have exhibited a spontaneous remission of symptoms.

Pregnant women who are positive for Hashimoto's thyroiditis may have decreased thyroid function or the gland may fail entirely. If a woman is TPOAb-positive, clinicians can inform her of the risks for themselves and their infants if they go untreated. "Thyroid peroxidase antibodies (TPOAb) are detected in 10% of pregnant women," which presents risks to those pregnancies. Women who have low thyroid function that has not been stabilized are at greater risk of having an infant with: low birth weight, neonatal respiratory distress, hydrocephalus, hypospadias, miscarriage, and preterm delivery. The embryo transplantion rate and successful pregnancy outcomes are improved when Hashimoto's is treated. Recommendations are to only treat pregnant women who are TPOAb-positive throughout the entirety of their pregnancies and to screen all pregnant women for thyroid levels. Close cooperation between the endocrinologist and obstetrician benefits the woman and the infant. The Endocrine Society recommends screening in pregnant women who are considered high-risk for thyroid autoimmune disease.

Thyroid peroxides antibodies testing is recommended for women who have ever been pregnant regardless of pregnancy outcome. "...[P]revious pregnancy plays a major role in development of autoimmune overt hypothyroidism in premenopausal women, and the number of previous pregnancies should be taken into account when evaluating the risk of hypothyroidism in a young women ["sic"]."

The most common and helpful way to diagnose thyroiditis is first for a physician to palpate the thyroid gland during a physical examination. Laboratory tests allow doctors to evaluate the patient for elevated erythrocyte sedimentation rates, elevated thyroglobulin levels, and depressed radioactive iodine uptake (Mather, 2007). Blood tests also help to determine the kind of thyroiditis and to see how much thyroid stimulating hormone the pituitary gland is producing and what antibodies are present in the body. In some cases a biopsy may be needed to find out what is attacking the thyroid.

Diagnosis is usually made by detecting elevated levels of anti-thyroid peroxidase antibodies (TPOAb) in the serum, but seronegative (without circulating autoantibodies) thyroiditis is also possible.

Given the relatively non-specific symptoms of initial hypothyroidism, Hashimoto's thyroiditis is often misdiagnosed as depression, cyclothymia, PMS, chronic fatigue syndrome, fibromyalgia and, less frequently, as erectile dysfunction or an anxiety disorder. On gross examination, there is often presentation of a hard goiter that is not painful to the touch; other symptoms seen with hypothyroidism, such as periorbital myxedema, depend on the current state of progression of the response, especially given the usually gradual development of clinically relevant hypothyroidism. Testing for thyroid-stimulating hormone (TSH), free T3, free T4, and the anti-thyroglobulin antibodies (anti-Tg), anti-thyroid peroxidase antibodies (anti-TPO, or TPOAb) and anti-microsomal antibodies can help obtain an accurate diagnosis. Earlier assessment of the person may present with elevated levels of thyroglobulin owing to transient thyrotoxicosis, as inflammation within the thyroid causes damage to the integrity of thyroid follicle storage of thyroglobulin; TSH secretion from the anterior pituitary increases in response to a decrease in negative feedback inhibition secondary to decreased serum thyroid hormones. Typically T4 is the preferred thyroid hormone test for hypothyroidism. This exposure of the body to substantial amounts of previously isolated thyroid enzymes is thought to contribute to the exacerbation of tolerance breakdown, giving rise to the more pronounced symptoms seen later in the disease. Lymphocytic infiltration of the thyrocyte-associated tissues often leads to the histologically significant finding of germinal center development within the thyroid gland.

Hashimoto's when presenting as mania is known as Prasad's syndrome after Ashok Prasad, the psychiatrist who first described it.

The diagnosis may be made on the clinical features alone, along with tests to rule out other possible causes. An EEG will usually show the electrical features of epilepsy and slowing of brain activity in the affected hemisphere, and MRI brain scans will show gradual shrinkage of the affected hemisphere with signs of inflammation or scarring.

Brain biopsy can provide very strong confirmation of the diagnosis, but this is not always necessary.

First and foremost is high level of clinical suspicion especially in young adults showing abnormal behavior as well as autonomic instability. The person may have alteration in level of sensorium and seizures as well during early stage of the illness. Clinical examination may further reveal delusions and hallucinations

Most patients reported in the literature have been given treatments suitable for autoimmune neurological diseases, such as corticosteroids, plasmapheresis and/or intravenous immunoglobulin, and most have made a good recovery. The condition is too rare for controlled trials to have been undertaken.

Treatments for this disease depend on the type of thyroiditis that is diagnosed. For the most common type, which is known as Hashimoto's thyroiditis, the treatment is to immediately start hormone replacement. This prevents or corrects the hypothyroidism, and it also generally keeps the gland from getting bigger. However, Hashimoto's thyroiditis can initially present with excessive thyroid hormone being released from the thyroid gland (hyperthyroid). In this case the patient may only need bed rest and non-steroidal anti-inflammatory medications; however, some need steroids to reduce inflammation and to control palpitations. Also, doctors may prescribe beta blockers to lower the heart rate and reduce tremors, until the initial hyperthyroid period has resolved.

Anti-GQ1b antibodies are found in two-thirds of patients with this condition. This antibody is also found in almost all cases of Miller Fisher syndrome. The EEG is often abnormal, but shows only slow wave activity, which also occurs in many other conditions, and so is of limited value in diagnosis. Similarly, raised CSF protein levels and pleocytosis are frequent but non-specific. It was originally thought that raised CSF protein without pleocytosis ('albuminocytological dissociation') was a characteristic feature, as it is in Guillain–Barré syndrome, but this has not been supported in more recent work. In only 30% of cases is a MRI brain scan abnormal. Nerve conduction studies may show an axonal polyneuropathy.

EEG: Mostly nonspecific slowing and epileptiform activity arising from temporal lobes.

Blood tests, cerebrospinal fluid examination by lumbar puncture (also known as spinal tap), brain imaging studies, electroencephalography (EEG), and similar diagnostic studies may be used to differentiate the various causes of encephalopathy.

Diagnosis is frequently clinical. That is, no set of tests give the diagnosis, but the entire presentation of the illness with nonspecific test results informs the experienced clinician of the diagnosis.

Examination of cerebrospinal fluid (CSF) shows elevated numbers of lymphocytes (but usually < 100 cells/µl); elevated CSF protein (but usually <1.5 g/l), normal glucose, elevated IgG index and oligoclonal bands. Patients with antibodies to voltage-gated potassium channels may have a completely normal CSF examination.

The number of new cases a year is unknown. According to the California Encephalitis Project, the disease has a higher incidence than its individual viral counterparts in patients younger than 30. The largest case series to date characterized 577 patients with anti-NMDA receptor encephalitis. The epidemiological data were limited, but this study provides the best approximation of disease distribution. It found that women are disproportionally affected, with 81% of cases reported in female patients. Disease onset is skewed toward children, with a median age of diagnosis of 21 years. Over a third of cases were children, while only 5% of cases were patients over the age of 45. This same review found that 394 out of 501 patients (79%) had a good outcome by 24 months. 30 patients (6%) died, and the rest were left with mild to severe deficits. The study also confirmed that patients with the condition are more likely to be of Asian or African origin.

During the acute stage, treatment is aimed at reducing the inflammation. As in other inflammatory diseases, steroids may be used first of all, either as a short course of high-dose treatment, or in a lower dose for long-term treatment. Intravenous immunoglobulin is also effective both in the short term and in the long term, particularly in adults where it has been proposed as first-line treatment. Other similar treatments include plasmapheresis and tacrolimus, though there is less evidence for these. None of these treatments can prevent permanent disability from developing.

During the residual stage of the illness when there is no longer active inflammation, treatment is aimed at improving the remaining symptoms. Standard anti-epileptic drugs are usually ineffective in controlling seizures, and it may be necessary to surgically remove or disconnect the affected cerebral hemisphere, in an operation called hemispherectomy. This usually results in further weakness, hemianopsia and cognitive problems, but the other side of the brain may be able to take over some of the function, particularly in young children. The operation may not be advisable if the left hemisphere is affected, since this hemisphere contains most of the parts of the brain that control language. However, hemispherectomy is often very effective in reducing seizures.

The diagnosis is considered when a child with congenital rubella develops progressive spasticity, ataxia, mental deterioration, and seizures. Testing involves at least CSF examination and serology. Elevated CSF total protein and globulin and elevated rubella antibody titers in CSF and serum occur. CT may show ventricular enlargement due to cerebellar atrophy and white matter disease. Brain biopsy may be necessary to exclude other causes of encephalitis or encephalopathy. Rubella virus cannot usually be recovered by viral culture or immunohistologic testing.

Diagnostic testing in a possible paraneoplastic syndrome depends on the symptoms and the suspected underlying cancer.

Diagnosis may be difficult in patients in whom paraneoplastic antibodies cannot be detected. In the absence of these antibodies, other tests that may be helpful include MRI, PET, lumbar puncture and electrophysiology.

Treatment varies according to the type and severity of the encephalopathy. Anticonvulsants may be prescribed to reduce or halt any seizures. Changes to diet and nutritional supplements may help some patients. In severe cases, dialysis or organ replacement surgery may be needed.

Sympathomimetic drugs can increase motivation, cognition, motor performance and alertness in patients with encephalopathy caused by brain injury, chronic infections, strokes, brain tumors.

Cerebrospinal fluid (CSF) analysis shows a large number of white blood cells. Typically small mature lymphocytes are the majority of cells seen, with monocytes and neutrophils making up the rest. Definitive diagnosis is based on histopathology, either a brain biopsy or post-mortem evaluation (necropsy). A CT scan or MRI will show patchy, diffuse, or multifocal lesions. For a number of years, the basic treatment was some type of corticosteroid in combination with one or more immunosuppressive drugs, typically cytosine arabinoside and/or cyclosporine or other medications such as azathioprine, cyclophosphamide, or procarbazine, of which were usually added one at a time to the corticosteroid until a successful combination was found. There is evidence that treatment with radiation therapy for focal GME provides the longest periods of remission.

Although no specific treatment exists, the disease can be managed with anticonvulsants, physiotherapy, etc.

Treatment options include:

1. Therapies to eliminate the underlying cancer, such as chemotherapy, radiation and surgery.

2. Therapies to reduce or slow neurological degeneration. In this scenario, rapid diagnosis and treatment are critical for the patient to have the best chance of recovery. Since these disorders are relatively rare, few doctors have seen or treated paraneoplastic neurological disorders (PNDs). Therefore, PND patients should consult with a specialist with experience in diagnosing and treating paraneoplastic neurological disorders.

A specific prognosis for those afflicted with paraneoplastic syndromes links to each unique case presented. Thus, prognosis for paraneoplastic syndromes may vary greatly. For example, paraneoplastic pemphigus often included infection as a major cause of death. Paraneoplastic pemphigus is one of the three major subtypes that affects IgG autoantibodies that are characteristically raised against desmoglein 1 and desmoglein 3 (which are cell-cell adhesion molecules found in desmosomes). Underlying cancer or irreversible system impairment, seen in acute heart failure or kidney failure, may result in death as well.

Immediate treatment of drug induced OGC can be achieved with intravenous antimuscarinic benzatropine or procyclidine; which usually are effective within 5 minutes, although may take as long as 30 minutes for full effect. Further doses of procyclidine may be needed after 20 minutes. Any causative new medication should be discontinued. Also can be treated with 25 mg diphenhydramine.

The features of the MRI and the characteristics of the lesion can be correlated when a biopsy has been taken, providing a way to standarize the future MRI diagnosis

Balo concentric sclerosis lesions can be distinguished from normal lesions on MRI showing alternative hypotense and hypertense layers

Balo concentric lesions can be viewed using the myelin water imaging techniques. This is a special MRI sequence that shows the myelin's percentage of water content.

Pattern III lesions, including Balo lesions, have a specific initiation pattern under MRI (MRILIP) consisting in showing Gadolinium enhancement before FLAIR MRI appearance.

Continuous prophylactic antiepileptic drug (AED) treatment may not be needed particularly for children with only 1-2 or brief seizures. This is probably best reserved for children whose seizures are unusually frequent, prolonged, distressing, or otherwise significantly interfering with the child’s life. There is no evidence of superiority of monotherapy with any particular common AED.

Autonomic status epilepticus in the acute stage needs thorough evaluation for proper diagnosis and assessment of the neurologic/autonomic state of the child. "Rescue" benzodiazepines are commonly used to terminate it. Aggressive treatment should be avoided because of the risk of iatrogenic complications, including cardiovascular arrest. There is some concern that intravenous lorazepam and/or diazepam may precipitate cardiovascular arrest. Early parental treatment is more effective than late emergency treatment. Buccal midazolam is probably the first choice medication for out of hospital termination of autonomic status epilepticus which should be administered as soon as the child shows evidence of onset of its habitual autonomic seizures.

Parental education about Panayiotopoulos syndrome is the cornerstone of correct management. The traumatizing, sometimes long-lasting effect on parents is significant particularly because autonomic seizures may last for many hours compounded by physicians’ uncertainty regarding diagnosis, management, and prognosis.

Chorea can also be a manifestation of drug toxicity (for example, anticonvulsants, antiparkinson agents, neuroleptics, steroids, and estrogen), or a result of an infectious disease such as meningovascular syphilis, Lyme disease, viral encephalitis, and many others.