Can Hashimoto's encephalopathy cause parkinsonism?

Can Hashimoto's Encephalopathy Cause Parkinsonism?

Yes, Hashimoto's encephalopathy (also called steroid-responsive encephalopathy associated with autoimmune thyroiditis, or SREAT) can present with parkinsonism as one of its diverse neurological manifestations, though this is not the most common presentation. 1, 2

Clinical Presentation of Parkinsonism in Hashimoto's Encephalopathy

The neurological manifestations of Hashimoto's encephalopathy are highly variable and include:

• Extrapyramidal features such as parkinsonism have been documented in case reports, presenting with bradykinesia, rigidity, and other parkinsonian features 1, 2
• The most common presentations are consciousness disturbance, psychosis, cognitive dysfunction, involuntary movements, seizures, and ataxia—with parkinsonism being a less frequent but recognized manifestation 3
• One documented case showed a 52-year-old woman with parkinsonism associated with Hashimoto's thyroiditis who responded well to corticosteroids 1
• Another case demonstrated a 41-year-old woman with gradually worsening parkinsonism and MRI findings mimicking a brain tumor at the left caudate nucleus, which improved with glucocorticoid treatment 2

Critical Diagnostic Considerations

The presence of thyroid antibodies alone does NOT establish the diagnosis of autoimmune encephalopathy, as thyroid antibodies are highly prevalent in the general population and are often incidental findings. 4, 5

Key diagnostic features that support true autoimmune CNS involvement:

• Subacute symptom onset (not insidious, chronic progression) 5
• Objective neurological findings: seizures, stroke-like episodes, aphasia, or ataxia 5
• Inflammatory CSF findings (elevated protein, pleocytosis) 5
• Abnormal EEG showing diffuse slowing or epileptiform activity 5, 3
• Response to immunotherapy (corticosteroids) 5, 1

Important pitfall to avoid:

In a large retrospective study of 144 patients referred with suspected Hashimoto's encephalopathy, 73% had alternative non-immune-mediated diagnoses, including functional neurological disorder, neurodegenerative conditions, primary psychiatric disorders, and chronic pain syndromes. 5 The thyroid antibody titers were not different between those with true autoimmune CNS disorders and those with alternative diagnoses. 5

Distinguishing Hashimoto's Encephalopathy from Neurodegenerative Parkinsonism

When evaluating parkinsonism in the context of elevated thyroid antibodies, you must distinguish between:

Features suggesting Hashimoto's encephalopathy (potentially reversible):

• Subacute onset over days to weeks 5
• Fluctuating symptoms 6
• Associated encephalopathy (altered consciousness, confusion) 3
• Seizures or myoclonus 5, 3
• Inflammatory CSF (elevated protein >45 mg/dL, mild pleocytosis) 5
• Abnormal EEG with diffuse slowing 3
• Response to corticosteroids within days to weeks 1, 6

Features suggesting primary neurodegenerative parkinsonism (irreversible):

• Insidious, chronic progression over months to years 4
• Classic asymmetric resting tremor, bradykinesia, rigidity 4
• No encephalopathy or consciousness changes 4
• Normal or non-inflammatory CSF 5
• Normal EEG 5
• No response to immunotherapy 4

Diagnostic Algorithm

When encountering parkinsonism with positive thyroid antibodies:

1. Assess the tempo of symptom onset: Subacute (days-weeks) suggests autoimmune; insidious (months-years) suggests neurodegenerative 5

2. Look for encephalopathic features: Altered consciousness, confusion, seizures, or cognitive fluctuations strongly suggest Hashimoto's encephalopathy 5, 3

3. Obtain inflammatory markers:

   • CSF analysis (protein, cell count) 5
   • EEG (diffuse slowing supports autoimmune) 3
   • Brain MRI (usually normal or nonspecific in Hashimoto's encephalopathy, but may show rare tumor-like lesions) 2

4. Screen for neural-specific antibodies: NMDAR, VGKC-complex, GAD65, and other neuronal surface antibodies, as these may coexist with thyroid antibodies and represent the true pathogenic mechanism 4, 5

5. Consider therapeutic trial: If clinical features suggest autoimmune etiology (subacute onset, encephalopathy, inflammatory CSF), a trial of corticosteroids is warranted, with objective reassessment after 2-4 weeks 5, 1

Treatment Implications

Corticosteroids are the cornerstone of treatment for true Hashimoto's encephalopathy, with most patients showing significant improvement. 1, 6 However, the parkinsonism associated with advanced liver disease (cirrhosis-associated parkinsonism) is unresponsive to ammonia-lowering therapy and represents a distinct entity. 4

In elderly patients presenting with parkinsonism, SREAT should be considered as a potentially treatable cause, particularly when accompanied by subacute onset and encephalopathic features, as simple corticosteroid treatment can lead to significant neurological improvement. 1

The key is recognizing that thyroid antibodies are a marker of general autoimmunity, not necessarily the cause of neurological symptoms—the diagnosis requires objective neurological abnormalities, inflammatory markers, and ideally, response to immunotherapy. 5