O/T Hashimoto's encephalopathy

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Hashimoto's encephalopathy

A Treatable Form of Dementia

Jul 1, 2006

Elaine

laboratory worker - national institutes of healthHashimoto's encephalopathy is

an autoimmune neuroendocrine disorder caused when the thyroid antibodies seen in

Hashimoto's thyroiditis affect brain tissue.

Hashimoto's encephalopathy (HE), which has recently been designated

steroid-responsive encephalopathy associated with autoimmune thyroiditis

(SREAT), is an autoimmune disorder that can cause memory impairment, cognitive

changes, dementia and associated neurological symptoms. HE can occur in patients

with hypothyroidism related to Hashimoto's thyroiditis and in patients with

normal thyroid function. In some cases, particularly when HE occurs in

association with non-thyroid related disorders such as Sjogren's syndrome or

systemic lupus erythematosus (SLE), it's called nonvasculitic autoimmune

meningoencephalitis (NAIM).

The first cases of Hashimoto's encephalopathy were reported in 1966 when the

existence of thyroid antibodies in the blood of patients with the autoimmune

hypothyroid disorder Hashimoto's thyroiditis was first demonstrated. SREAT is

caused by the same thyroid antibodies that cause Hashimoto's thyroiditis

although in SREAT, rather than destroying thyroid tissue, these antibodies

attack and destroy brain cells known as neurons. Most experts believe that SREAT

is under-diagnosed and that many patients thought to have Alzheimer's disease

actually have SREAT, which is a treatable disorder. Hashimoto's encephalopathy

has been reported worldwide, and cases have been documented in patients ranging

from 12-82 years with women more likely to be affected than men.

Encephalopathy is a general term referring to an inflammatory brain disease that

alters the brain's structure or function. Encephalopathy is suspected in

patients showing signs of an altered mental state. Common symptoms of

encephalopathy include stroke-like symptoms of memory loss, difficulty

concentrating, hallucinations, irritability, restlessness, amnesia, diminished

cognitive ability, myoclonus (involuntary muscle twitching), tremors, nystagmus

(rapid, involuntary eye movement), muscle weakness, dementia, seizures,

convulsions, difficulty swallowing, impaired speech, confusion, disorientation,

psychosis, headache, right-sided hemiparesis or partial paralysis, and fine

motor problems, including incoordination of arms, hands and fingers.

HE is diagnosed in patients with high titers of thyroid peroxidase (TPO)

antibodies who show signs of cognitive impairment responsive to corticosteroids.

Lymphocytic vasculitis of the veins and venules of the brain stem in HE supports

the notion that HE may be an autoimmune vascular disorder. Vasculitis as a

contributing factor to HE is also supported by the presence of

anti-alpha-enolase antibodies in HE. These antibodies are also seen in other

conditions of vasculitis including systemic lupus erythematosus (SLE) and

ANCA-associated vasculitis. Other diagnostic changes seen in HE include an

elevated cerebrospinal fluid protein, EEG abnormalities (diffusely slowed), and

perfusion deficits in the presence of normal structural neuroimaging.

Although hypothyroidism may be present, most patients have normal levels of

circulating thyroid hormone, suggesting that inflammation rather than myxedema

is responsible for the cognitive defects. CT scans may be normal or show

cerebral swelling (patchy edema) secondary to diffuse white-matter edema

appearing as diminished attenuation with increased signal intensity on

T2-weighted matter MRI images. The variation in imaging test results may

represent different stages or subtypes of HE.

Read on

Thyroid and Systemic Autoimmune Diseases

Autoimmune Endocrine Diseases

Autoimmune Diseases

HE may, like multiple sclerosis, also cause a relapsing form of encephalopathy

with imaging test results varying depending if the disease is an active or

relapsing mode. Relapsing white-matter edema is the usual presentation. Most

patients have elevated titers of TPO antibodies and some patients have

thyroglobulin antibodies. However, because 20 percent of the older population,

especially women, may have these antibodies, antibody test results must be

interpreted with caution. Patients with HE are also reported to occasionally

have antinuclear antibodies (ANA) and anti-parietal cell antibodies. Fine needle

aspiration (FNA) studies in patients with HE show lymphocytic thyroiditis.

Patients with SREAT show a good response to corticosteroids such as prednisone

and related immunosuppressants because of the ability of these medications to

reduce thyroid antibody production and reduce inflammation. Researchers in India

report a case of SREAT that did not respond to corticosteroids but showed a very

favorable response to plasma exchange, a technique used to remove circulating

antibodies,

Resource: Pablo Castillo, Steroid-Responsive Encephalopathy Associated with

Autoimmune Thyroiditis, Archives of Neurology, February 2006.

Read more at Suite101: Hashimoto's encephalopathy: A Treatable Form of Dementia

http://www.suite101.com/content/hashimoto-s-encephalopathy-a3823#ixzz11unlNqOl

http://www.suite101.com/content/hashimoto-s-encephalopathy-a3823