Background and PurposeUnstable carotid atherosclerotic plaques are characterized by cap rupture, leading to thromboembolism and stroke. Matrix metalloproteinases (MMPs) have been implicated in the progression of atherosclerosis and plaque rupture. The aim of this study was to assess the relationship between the expressions of MMP-2 and MMP-9 and carotid plaque instability.MethodsEighty atherosclerotic plaques were collected from 74 patients undergoing carotid endarterectomy. Clinical information was obtained from each patient, and plaque morphology was examined at the macroscopic and microscopic levels. The immunohistochemical expressions of MMPs were graded using semiquantitative scales.ResultsMacroscopic ulceration (84.6% versus 63.4%, p=0.042) and microscopic cap rupture (79.5% versus 51.2%, p=0.010) were more common in symptomatic than in asymptomatic patients. Immunoreactivities of MMP-2 and MMP-9 were increased in 40 and 36 atheromatous plaques, respectively. Macroscopic ulceration was strongly correlated with the expressions of MMP-2 (p<0.001) and MMP-9 (p=0.001). There were significant correlations between increased MMP-2 expression and cap rupture (p=0.002), intraplaque hemorrhage (p=0.039), and a thin fibrous cap (p=0.002), and between increased MMP-9 expression and cap rupture (p=0.010) and a large lipid core (p=0.013).ConclusionsPlaque rupture was significantly associated with the development of vascular events in carotid atherosclerotic disease. MMP-2 and MMP-9 are strongly correlated with plaque instability.

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To evaluate prediction models of cognitive trajectories in patients with nonamnestic mild cognitive impairment (naMCI) using group-based trajectory analysis, we evaluated 121 patients with naMCI who underwent at least their first three yearly assessments. Group-based trajectory models were used to classify cognitive trajectories based on Clinical Dementia Rating Sum of Boxes scores over four years in patients with naMCI. A total of 22 patients (18.2%) were classified into the “fast-decliners” group, while 99 patients (81.8%) were classified into the “slow-decliners” group. The mean age was higher in the fast-decliners than in the slow-decliners (p = 0.037). Compared to the slow-decliners, the fast-decliners were more frequently impaired in the domains of language (p = 0.038) and frontal/executive functions (p = 0.042), and had more frequent multiple-domain cognitive impairment (p = 0.006) on baseline neuropsychological tests. The rate of conversion to dementia was significantly higher in the fast-decliners than in the slow-decliners (86.4% vs. 10.1%, p < 0.001). Our findings showed that there are indeed distinct patterns of cognitive trajectories in patients with naMCI. Close observation of naMCI patients’ baseline demographic and clinical profiles in clinical settings may help identify individuals at greatest risk for dementia.

We describe a 64-year-old man with scrub typhus who presented with both polyneuropathy and cerebral infarction. A neurological examination revealed a confused mental state, stiff neck, hearing impairment, symmetric weakness, sensory loss, and ataxia. Electrophysiologic studies showed demyelinating sensorimotor polyneuropathy and sensorineural hearing loss. Brain magnetic resonance imaging showed multiple infarctions. Brain involvement or polyneuropathy associated with scrub typhus has been rarely reported, and the pathogenic mechanism underlying the multiple neurological complications remains to be elucidated. Scrub typhus is a febrile illness caused by Orientia tsutsugamushi, and is characterized by fever, rash, eschar, myocarditis, and pneumonitis. Neurological involvement usually includes meningitis and hearing loss, possibly due to involvement of the eighth cranial nerve.1,2 However, involvement of the brain parenchyma and peripheral nerve is rarely reported. 3-5 Here we report a case of scrub typhus with cerebral infarction and polyneuropathy. CASE REPORTA 64-year-old man was admitted due to fever, myalgia, dysarthria, dizziness, and headache that had first appeared several days previously. He had worked at a sewage disposal plant in the northern rural area of Seoul. He had suffered from mild conductive hearing impairment of undetermined cause in the left ear for several years. On admission, his body temperature was 39℃ and his blood pressure was normal (110/70 mmHg). Eschar was not evident. A neurological examination revealed a confused mental state and neck stiffness. Limb weakness was absent, but he exhibited multidirectional sway on tandem gait.Laboratory tests showed leukocytosis (14.9×10 3 cells/μl) and thrombocytopenia (33×10 3 platelets/μl).Liver enzymes were elevated (aspartate aminotransferase = 214 IU/l, alanine aminotransferase = 151 IU/l) and renal function was impaired (blood urea nitrogen = 31creatinine = 1.6 mg/dl). Initial computed tomography (CT) of the brain was normal. (Fig. A), a chest radiograph indicated pulmonary edema, electrocardiography showed sinus tachycardia, and an echocardiogram was normal. Cerebrospinal fluid (CSF) was not examined due to the presence of thrombocytopenia. The patient was initially positive for serum indirect immunofluorescent antibody against O. tsutsugamushi (1:800),