Supplementary MaterialsAIAN-23-405-v001

Supplementary MaterialsAIAN-23-405-v001. regular use of any other medication including traditional and herbal medications. There is no recent history of vaccination or animal bite. Patient denies any intake of alcohol. Vitals initially recorded were CHIR-98014 as follows: blood pressure of 110/70 mm Hg, heart rate 82 beats per minute, temperature 37.8C, respiratory rate 20 breaths per minute, oxygen saturation 98% on room air. On examination, patient was confused with a Glasgow coma scale of E3V4M5 (E-eye opening, V-best verbal response, M-best motor response). However bradykinesia, tremors, rigidity, multifocal myoclonus were present with dystonia of all four limbs. Power was 4+ in all four limbs, with brisk deep tendon reflexes and bilateral plantar flexor response. No features of malnutrition were noted. Laboratory findings revealed a white cell count of 9,200/L, hemoglobin level of 12.7, platelet count of 250,000/L, ESR of 48 mm in 1st h, aspartate aminotransferase 22 U/L, alanine aminotransferase 11 U/L, alkaline phosphatase 74 U/L, blood urea nitrogen 14.5 mg/dl, creatinine 0.84 mg/dl, sodium 140 mEq/L, potassium 3.97 mEq/L, calcium 8.9 mg/dl, albumin 3.75 g/dL, thyroid stimulating hormone 5.81 IU/ml, free T3 2.97 pg/ml, free T4 0.64 ng/dl, antithyroid peroxidase antibody 1 IU/ml, ammonia 59 mol/L, vit B12 1500 pg/ml, creatinine kinase (NAC) 90 U/L, pyruvate 0.36. MRI brain imaging was normal. Cerebrospinal fluid analysis CHIR-98014 revealed a total white cell count of 3/L with lymphocytes 100%, protein 61.3 mg/dL, glucose 75 mg/dL. CSF for pan neuro viruses and autoimmune antibodies were negative. Electroencephalography (EEG) showed generalized theta slowing only. Positron emission tomography scan revealed fibroatelectatic lesion in lungs with multiple lung nodules and lymph nodes and global hypometabolism of brain with hypermetabolism in basal ganglia and thalami [Figure 1]. We could not assess antithyroglobulin antibody and serum/CSF levofloxacin levels in our patient. Open in a separate window Figure 1 PET scan showing global hypometabolism of FGF18 brain with hypermetabolism in bilateral basal ganglia and thalami The patient was empirically started on injection methyl prednisolone (1 gm daily for 5 days) along with intravenous immunoglobulins (IVIg) (30 gm daily CHIR-98014 for 5 days) initially suspecting autoimmune encephalitis (AE). With poor response at 8 days after administering methylrednisolone and IVIg, the diagnosis was still elusive. Suspecting levofloxacin as the culprit for the encephalopathy and myoclonus, it was stopped and in next few days patient started showing marked improvement. After full recovery, patient was discharged on 14th day. Patient’s Naranjo adverse drug reaction probability scale registered at 6 points, which indicate a probable relationship between his symptoms and levofloxacin. Patient is well at 4 months of follow-up. Though the literature suggests a definite association between levofloxacin and encephalopathy, we initially did not suspect it. AE was first suspected as it has a wide clinical spectrum that ranges from typical limbic encephalitis to syndromes with neuropsychiatric symptoms such as deficits of memory, cognition, psychosis, seizures, abnormal movements, and coma.[4] Abnormalities noted in PET scan are highly overlapping in AE and drug-induced encephalopathy as noted in our case and cannot be solely relied upon to differentiate between the two entities. All other potential causes of encephalopathy and movement disorders were ruled out as suggested by normal metabolic parameters and normal CSF study. After ruling out other causes, it was considered to be most likely as an adverse drug reaction to.