Effects of Ferulic Acid and Angelica archangelica Extract (Feru-guard ®) on Mild Cognitive Impairment: A Multicenter, Randomized, Double-Blind, Placebo-Controlled Prospective Trial.

We conducted a multicenter, randomized, double-blind, placebo-controlled prospective trial examining a supplement containing ferulic acid and Angelica archangelica extract (Feru-guard ®) for mild cognitive impairment (MCI). In the intention-to-treat population, Mini-Mental State Examination (MMSE) scores were significantly better at 24 weeks (p = 0.041) in the active group. In the per protocol population, MMSE was significantly better in the active group at 24 weeks (p = 0.008), and mixed effect models for repeated measures (MMRM) showed significant difference (p = 0.016). ADAS-Jcog was significantly better at 24 (p = 0.035) and 48 weeks (p = 0.015) in the active group, and MMRM was significant (p = 0.031). Thus, Feru-guard ® may be useful for MCI.

[Two Cases of Parkinson's Disease Accompanied with Nasogastric Tube Syndrome].

We report 2 cases of patients with Parkinson's disease who exhibited bilateral vocal cord paralysis induced by an indwelling nasogastric tube (N-G tube). Both patients showed abrupt inspiratory stridor after N-G tube placement. A fiberoptic laryngeal examination revealed bilateral vocal cord abductor paralysis (VCAP). After N-G tube removal, patient symptoms improved. Nasogastric tube syndrome (NGTS) is an uncommon but life-threatening syndrome that causes sore throat and bilateral VCAP following N-G tube insertion. Throat pain is considered an important early manifestation of NGTS. However, in cases of advanced Parkinson's disease, subjective symptoms of NGTS, such as throat pain, may be difficult to recognize. We here report 2 patients with parkinson's disease accompanied by NGTS with literature review and proposed that inspiratory strider is a useful objective symptom in early diagnosing of NGTS. (Received March 25, 2020; Accepted May 18, 2020; Published September 1, 2020).

Atypical type of familial Mediterranean fever: An underdiagnosed cause of chronic aseptic meningitis.

We report an atypical case of familial Mediterranean fever (FMF) concomitant with chronic aseptic meningitis. The patient experienced fever, abdominal and back pain because of serositis, and headache because of aseptic meningitis for 4 weeks. Blood examinations revealed increased white blood cells and serum amyloid A level. Medications, including steroids, did not improve his symptoms. However, the patient experienced immediate relief after the administration of colchicine. We diagnosed him as having atypical FMF based on the symptoms, especially positive response to colchicine, and heterozygous mutations on exon2 and 5 (E148Q/S503C) in MEFV gene. Unlike typical FMF, a cause of recurrent aseptic meningitis, atypical FMF might be an underdiagnosed cause of chronic aseptic meningitis.

[A case of cerebral venous angioma with paresis of the left arm and face].

A 75-year-old woman was admitted to our hospital because of sudden onset of paresis in her left arm and face. She had untreated hypertension and hyperlipidemia. When she came back home after playing with children in the park, she felt weakness in her left hand. On admission, physical examination revealed that her blood pressure was very high (200/102 mmHg). Only slight weakness in her left arm and left facial palsy were recognized neurologically. An electroencephalogram showed normal findings. Brain CT and MRI revealed a venous angioma near the right central sulcus. Gadolinium-DTPA enhanced MRI showed a group of small radiating veins (so called "the caput medusae sign") connected to the venous angioma. The remaining symptoms decreased with the normalization of blood pressure. It is suggested the intracranial motor tracts of the face and arm in the precentral gyrus are adjacent to the location of this venous angioma. The dilation of venous angioma due to high blood pressure was thought to cause the paresis of face and arm in this patient.

[Late-onset leukoencephalopathy induced by long-term chemotherapy with capecitabine and cyclophosphamide for liver metastasis from breast cancer].

A 55-year-old woman with a 3-year and 4-month history of liver metastasis from breast cancer underwent chemotherapy with capecitabine and cyclophosphamide for following 10-months. She did not have hypertension and was not pregnant. She showed dysarthria and mild somnolence, and her conscious level developed to semicoma after 6 days. She had pyrexia. Cerebrospinal fluid (CSF) demonstrated increased cell-count and elevated protein but no evidence of positive cytological finding and cultivation of bacteria was found in the CSF. Brain magnetic resonance imaging (MRI) revealed multiple lesions with hyperintensity in the brain stem, bilateral middle cerebellar peduncles, left splenium of corpus callosum, bilateral basal ganglia, bilateral thalami, bilateral corona radiata, and bilateral subcortical white matters of parietal lobes on the T(2) weighted and fluid attenuated inversion recovery (FLAIR) images. These lesions demonstrated mild hyperintensity on the diffusion weighted images but did not demonstrate hypointensity on the T(1) weighted images. Capecitabine and cyclophosphamide were discontinued at 4th day after onset of symptoms, and her conscious disturbance showed improvement slowly since day 12 after cessation of these drugs and hyperintensity areas detected on FLAIR image of MRI showed decreasing intensity after three weeks of onset. Capecitabine is an oral prodrug converted to 5-fluorouracil (5-FU). 5-FU and cyclophosphamide are known to induce leukoencephalopathy. Reversible multiple lesions with leukoencephalopathy on brain MRI which is called as a posterior reversible encephalopathy syndrome (PRES). Capecitabine is also reported to induce PRES in rare cases. Combination of these drugs was considered for the possible cause to induce leukoencephalopathy like PRES. Usually leukoencephalopathy occurs in relatively early time after start of chemotherapy with capecitabine or cyclophosphamide, but we consider that late-onset leukoencephalopathy can be induced by long-term chemotherapy with these drugs. It is necessary to observe leukoencephalopathy by brain MRI regularly when these drugs are used.