Causes and clinical manifestations of Hashimoto's encephalopathy

Causes and clinical manifestations of Hashimoto's encephalopathy

Hashimoto's encephalopathy, also known as thyrotoxic encephalopathy and hormone-responsive encephalopathy associated with autoimmune thyroiditis (i.e. Hashimoto's disease), is an autoimmune disease related to Hashimoto's disease and characterized by neurological dysfunction. It is easy to misdiagnose, and early hormone treatment can achieve significant results.

1. The etiology and pathogenesis of HE have not yet been fully elucidated

(1) Vasculitis mediated by autoimmune mechanisms causes microvascular damage, leading to cerebral edema or cerebral blood flow hypoperfusion, which may affect the brainstem and cortex, resulting in clinical symptoms such as focal neurological deficits or coma; --- stroke-like attacks

(2) Autoimmune reactions between autoantibodies against nerve cells or anti-α-enolase (NAE) antibodies and antigens common to the thyroid tissue and central nervous system cause disease. NAEs are ubiquitous in the brain, so the damage lacks specific sites.

(3) The toxic effect of thyrotropin-releasing hormone (TRH) causes the disease; this mechanism is high and low

2. Two distinct clinical types:

1. One is the vascular type with repeated stroke-like attacks and mild cognitive impairment (stroke-like attacks, in addition to MELAS, we should also pay attention to HE)

2. One is a continuously progressive type characterized by dementia and mental symptoms. (There are many diseases of acute and subacute dementia, such as poisoning, infection, paraneoplasm, etc., so please be careful to distinguish them.)

3. Both types may present with epileptic seizures, myoclonus, tremor, coma, extrapyramidal symptoms and cerebellar ataxia. May be accompanied by fever (easily confused with encephalitis).

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