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- Section Writer: Dr. Om J Lakhani
- Section Editor: Dr. Om J Lakhani
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- Video lecture
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<br> - Q. What is [[Hashimoto's encephalopathy]]? <br>
- It is a form of Non-infective encephalopathy associated with Autoimmune thyroid disorder with positive [[Anti TPO antibody]]
- It has excellent response to glucocorticoids
- It is a diagnosis of exclusion
<br> - Q. Is the term "encephalopathy" same as "encephalitis"? <br>
- "Encephalopathy" means "brain disorder" and it is a broad term
- "Encephalitis" means "brain inflammation" and it deals with inflammatory disorder of the brain and it is a more specific term
<br> - Q. Who was the first to describe [[Hashimoto's encephalopathy]]? <br>
- Dr Russell Brain
<br> - Q. What is the timing in terms of presentation? <br>
- It is subacute in terms of onset
<br> - Q. What is the most typical clinical presentation of HE? <br>
- Subacute confusion with
- Seizures
- Myoclonus
- Pyschosis
- With altered consciousness
<br> - Q. What is the epidemiology of this condition? <br>
- Age of onset is on an average 51 years
- However, it has been reported via a wide age variation
- It is more common in females
<br> - Q. What are the possible etiologies of Hashimoto’s encephalopathy? <br>
- Autoimmune encephalomyelitis
- Some people think [[Hashimoto's encephalopathy]] is a subset or type of ADEM- Acute disseminated encephalomyelities
- Autoimmune cerebral vasculitis
- Some people think [[Hashimoto's encephalopathy]] is a subform of NAIM- which is [[Non-vasculitic inflammatory meningoencephalitis]]
<br> - Q. Is it because of the thyroid dysfunction? <br>
- The neurological features of this condition are INDEPENDENT of the thyroid disorder
- The symptoms are NOT due to the thyroid hormone itself and are a result of an associated autoimmune phenomenon
<br> - Q. What is the typical clinical presentation of this syndrome? <br>
- It presents as acute or subacute confusion with altered levels of consciousness
<br> - Q. How does it progress? <br>
- It progresses in two ways
- a) It may progress as stroke-like multiple episodes of recurrent focal neurological deficits with variable degree of cognitive dysfunction
- b) It may have a diffuse slow progression with deteriorating cognitive function characterized by dementia, hallucination, somnolence etc
<br> - Q. Can seizures be seen in this condition? <br>
- Yes
- 2/3rd of patients have seizures are the time of initial presentation
- it can be both focal as well as generalized seizures
<br> - Q. What are other neurological features? <br>
- 1. Psychosis and hallucinations
- 2. Hyperreflexia and pyramidal tract signs
- 3. Myoclonus, tremors etc
<br> - Q. Can pyschiatric symptoms be seen in this condition? <br>
- Yes
- In fact, 30% of patients have some form of psychosis or psychiatric symptoms
<br> - Q. Which antibody is specific against leading to [[Hashimoto's encephalopathy]] (HE)? <br>
- Anti NAE antibody (N-amino terminal of alpha enolase)
<br> - Q. Can it be associated with hypothyrodism? <br>
- Yes
<br> - Q. Is hypothyroidism always present with [[Hashimoto's encephalopathy]]? <br>
- No
- Thyroid dysfunction runs an independent course
- [[Hashimoto's encephalopathy]] may be associated with
- Hypothyroidism
- Euthyroidism
- Hyperthyroidism
- Subclinical thyroid disorders
<br> - Q. Can [[Hashimoto's encephalopathy]] be associates with [[Graves' disease]]? <br>
- Yes
- But it is very rare
- <20 cases have been reported in literature
<br> - Q. Which is key differentiating feature of HE vs neuropsychiatric manifestation due to hypothyroidism? <br>
- Symptoms of hypothyroidism improve with treatment with LT4 whereas HE they do not improve with LT4 treatment
<br> - Q. Is Anti TPO positive in HE? <br>
- It is found in 100% of cases
- Anti TPO antibody is also found in CSF and CSF anti TPO antibody may be more sensitive and specific for [[Hashimoto's encephalopathy]]
<br> - Q. What level of Anti-TPO is associated with [[Hashimoto's encephalopathy]]? <br>
- As such there is no correlation between Anti TPO antibody levels and [[Hashimoto's encephalopathy]]
- However median values reported in literature are 900 IU/ml
<br> - Q. Which test is useful for follow-up of therapy? <br>
- IgG4 level in CSF is useful for follow up of patients with HE
<br> - Q. What are other common CSF findings? <br>
- Elevated protein concentration has been reported in the CSF
<br> - Q. What are neuroimaging changes seen with [[Hashimoto's encephalopathy]]? <br>
- In many cases MRI may be normal
- However it may be associated with nonspecific focal or diffuse hyperintensities of the subcortical white matter or ischemic lesion
- These often improve with glucocorticoid therapy
<br> - Q. How common are EEG changes seen in such patients? <br>
- EEG changes are seen in 90% of the patients but they are generally non-specific
- Mainly persistent or episodic slow wave changes are seen
<br> - Q. What is the anti-NMDAR encephalitis and why is it an important differential diagnosis of this case? <br>
- Anti-NMDAR encephalitis is a form of autoimmune encephalitis which it s a paraneoplastic syndrome and it is similar in clinical presentation of this condition
- It must be ruled out in such patients
<br> - Q. What is the drug of choice for HE ? <br>
- Corticosteroids
<br> - Q. Do the level of the [[Anti TPO antibody]] change with treatment? <br>
- No
<br> - Q. What is the new name for HE? <br>
- SEAT
- Steroid responsive encephalopathy with autoimmune thyroiditis
<br> - Q. Does giving Anti-psychotic medications to such patients presenting with psychosis help? <br>
- No
- Antipsychotic medications may paradoxically worsen psychosis/psychiatricsymptoms in some cases (Tseng, 2011).
- Hence to be used cautiously.