A 46-year-old female patient with no previous complaints applied with weakness and numbness in arms, legs and face with a sudden onset. Her medical history had no remarkable condition. In neurological examination her time orientation was lost and she had a side changing hemiparesis. Cranial MRI showed hyperintensity in left temporal cortex. The patient started to get treatment with pre-diagnosis of ischemic cerebral disease.
Serum TSH level was 8.788 μIU/mL (0.63-4.82); fT3, 2.84 pg/mL (2.3-4.2); fT4, 1.07 ng/dL (0.88-1.72). EEG revealed significant bioelectric disruption in both frontotemporal areas (Figure-1a).The patient was monitored in the intensive care unit due to progressive worsening of consciousness and developing respiratory deficiency. A lumbar puncture was performed with a pre-diagnosis of encephalitis. In CSF examination there was no cell, protein level was 76.7 mg/dL (15-40) and the rest of biochemistry was normal. The patient received Acyclovir 30 mg/kg/day with a pre-diagnosis of atypical viral encephalitis, but did not respond. Mycobacterium tuberculosis, Brucella, Borrelia, HSV types 1-2, CMV, VZV, EBV PCR, VDRL-RPR and ARB were negative.
Click Here to Zoom
|Figure 1: a. EEG of the first patient. Bioelectric disruption in both frontotemporal areas.b. EEG of the second patient. Mild and diffuse bioelectric disruption more apparent in left hemisphere.
Case 2. A 52-year-old female patient applied to our hospital with generalized tonic clonic seizure. She had a seizure and got well without treatment one month before admission to our hospital. She had a known hypothyroidism and was using l-thyroxin treatment. Impaired consciousness was found in neurological examination after controlling seizures. Cranial MRI was normal. Serum TSH level was 17.04 μIU/mL (0.63-4.82); fT3, 1.93 pg/mL (2.0-4.4); fT4, 0.865 ng/dL (0.93-1.70). EEG revealed mild and diffuse bioelectric disruption in left hemisphere (Figure-1b). Similar to the first patient, there was no cell, protein level was 64.7 mg/dL (15-40) and the rest of biochemistry was normal in CSF and bacteriological and viral markers were negative. The patients history of hypothyroidism and repetitive process caused us to think Hashimotos encephalopathy rapidly.
For the differential diagnosis of limbic encephalitis, malignancy, metabolic encephalopathy and vasculitis NMDA-R, AMPA-R1 Ab, AMPA-R2 Ab, CASPER, Abu LGI1, GAD Ab, CEA, CA 125, CA 19-9, CA 15-3, CA 72-4, lactate, pyruvate, ammonia, lupus anticoagulant, protein C, protein S, ANA, ANCA, p-ANCA, anti-cardiolipin antibodies, anti-Ro, anti-La, anti-dsDNA were examined for both patients and were negative.
For both patients taking the abnormality in the thyroid function tests into consideration, anti-thyroid antibodies were checked with pre-diagnosis of Hashimotos encephalopathy. The results were, in orderly, anti-TPO Ab: >600 IU/mL (0-35) anti-thyroglobulin Ab: 540.1 IU/mL (0-115) and anti-TPO Ab: >600 IU/mL, anti-thyroglobulin Ab: 475.7 IU/mL. These results supported the diagnosis, so patients started taking methyl-prednisolon 1mg/kg/day. Their clinical conditions started to improve after the first week of treatment and at 15th day of treatment both were conscious and oriented.
Written informed consent was obtained from the two patients for publishing the individual medical records.