We report a 71-year-old man with legionellosis, who presented with abducens nerve palsy, singultus, confusion, memory impairment, ataxia, and hyporeflexia. Legionella pneumonia was diagnosed on the basis of detection of Legionella pneumophila antigen in the urine. The cerebrospinal fluid was negative for the antigen and antibody, but an oligoclonal band was detected, and the IgG index was elevated. It was speculated that an undetermined immune-mediated mechanism had contributed to the development of the neurological manifestations.
A 51-year-old man was admitted with left lateral medullary infarction due to vertebral artery dissection (figure 1). Neurologic examination revealed nystagmus, dissociated sensory disturbance, and no evidence of paralysis. Miosis and ptosis were observed on the ipsilateral side, but hypohidrosis was not apparent. Thermography revealed a bilateral discrepancy in body temperature, as if the patient were split down the middle (figure 2). Asymmetric skin temperature can occur among patients with Wallenberg syndrome associated with Horner syndrome due to a disturbance of the descending sympathetic tract that causes ipsilateral hypohidrosis and increased cutaneous blood flow.
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AUTHOR CONTRIBUTIONSDr. Takahashi: study concept, interpretation of data, and drafting the manuscript. Dr. Shinya: revision of the manuscript for intellectual content. Dr. Sekiguchi: study supervision. Dr. Kitazono: study supervision. Dr. Inaba: study supervision. Dr. Orimo: revision of the manuscript for intellectual content and study supervision.
STUDY FUNDINGNo targeted funding reported.
DISCLOSUREThe authors report no disclosures relevant to the manuscript. Go to Neurology.org for full disclosures.
To examine the impact of the plasma homocysteine level on the anti-atherosclerotic effects of pitavastatin treatment, we retrospectively examined 59 patients who had a history of stroke and had been prescribed pitavastatin for the treatment of dyslipidemia at the Neurology department of Toho University Ohashi Medical Center Hospital. The patients were classified into two groups according to their homocysteine levels. Carotid artery plaque progression was determined before and after pitavastatin treatment. Plasma levels of high-sensitivity C-reactive protein, platelet molecular markers, and von Willebrand factor were measured. Pitavastatin treatment had beneficial effects on the lipid profiles of these patients and slowed atherosclerosis progression. These effects were observed in both the high and low homocysteine groups. Proactive lipid intervention using pitavastatin may inhibit the progression of atherosclerosis and contribute to secondary prevention of stroke in high-risk patients. We conclude that this statin could inhibit progression at any stage of disease and should therefore be proactively administered to these patient groups, regardless of disease severity.
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