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Abstract:We investigated an association between olfaction and cardiac 123 I-metaiodobenzylguanidine (MIBG) uptake in patients with Parkinson's disease (PD) and multiple system atrophy (MSA). There was a significant positive correlation between cardiac MIBG uptake and the CrossCultural Smell Identification (CCSI) score in patients with PD (r ‫؍‬ 0.56; P ‫؍‬ 0.003) independent of the disease duration or clinical rating of motor status. However, patients with MSA did not show a significant correlation between cardiac MIBG uptake and the CCSI score. Our findings suggest that the functional losses of the olfactory and cardiac sympathetic systems are closely coupled in PD.

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We investigated olfactory function and its relation to cardiac 123I-metaiodobenzylguanidine (MIBG) uptake in 15 patients with drug induced parkinsonism (DIP). The mean Cross Cultural Smell Identification (CCSI) score was significantly greater in patients with DIP than in those with Parkinson's disease (PD: 6.9 (1.6) vs 4.4 (2.2); p<0.001); however, the mean CCSI score in patients with DIP was not significantly different from controls. One patient with DIP, whose CCSI score was significantly reduced, also exhibited decreased cardiac MIBG uptake. DIP patients with CCSI scores within the normal range had normal cardiac MIBG uptake. Our study suggests that an olfactory function test may be a useful tool for detecting DIP unrelated to PD and for identifying patients with DIP who have subclinical PD.

<i>Background:</i> Lacunar stroke has been defined as an infarct <15 mm in diameter in the presence of symptoms of lacunar syndromes. We investigated a new approach in predicting whether a deep infarct is caused by small arterial occlusion. <i>Methods:</i> A total of 319 consecutive patients with acute symptomatic infarcts within the striatocapsular territory underwent diffusion-weighted imaging (DWI) and diagnostic workups, including vascular and cardiological studies. Predictors for nonlacunar mechanisms were evaluated by logistic regression analysis, with the size of infarct (1-mm increase) and stroke syndrome (traditional vs. atypical lacunar syndrome vs. cortical syndrome) graded rather than dichotomized. <i>Results:</i> Amongst the 171 patients who did not meet the established criteria for lacunar stroke, that is, deep infarct of ≧15 mm or presenting symptoms of nontraditional lacunar syndrome, a documented etiology could not be determined in 97 (56.7%) patients. In contrast, amongst the 148 patients who met the criteria, 27 (18.2%) had nonlacunar mechanisms. Logistic regression analysis identified the variables that predicted nonlacunar stroke mechanisms with statistical significance as nontraditional lacunar syndromes (OR 2.19 for atypical lacunar syndrome, and OR 6.72 for cortical syndrome), infarct size on DWI (OR 1.05 per 1-mm increase), and unilateral multiple deep infarcts on DWI (OR 2.22, p < 0.05 in all cases). Receiver operating characteristic curves showed that discrimination power of the model derived from logistic regression analysis (grading system) was better than that of the previously established dichotomizing criterion in predicting nonlacunar mechanisms (p = 0.004). <i>Conclusions: </i>A clinically significant proportion of clinical MRI lacunae are associated with underlying nonlacunar mechanisms. Decisions regarding the extent of diagnostic procedures in patients with subcortical infarcts can be guided by the point value in terms of the stroke syndrome and infarct patterns, as well as the size of infarct.

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Background and PurposeThe National Institutes of Health Stroke Scale (NIHSS) score is known to be effective in predicting the likelihood of recovery after stroke. However, the baseline NIHSS score predicts long-term outcomes rather crudely because early changes in stroke scores may influence the stroke outcomes. Therefore, a precise prognostic algorithm or a cutoff point for predicting long-term outcomes based on data from serial NIHSS scores is needed.MethodsWe serially assessed 437 patients with acute symptomatic ischemic stroke within the middle cerebral artery territory who presented with nonlacunar stroke and were followed-up for at least 6 months after symptom onset. The NIHSS score was serially checked at 0, 1, 3, 7, and 14 days after admission. In all patients, the Barthel index (BI) and the modified Rankin Scale (mRS) score were checked, with a poor outcome defined as any of the following endpoints: death, modified mRS score of >3, or BI of <60.ResultsA marked neurological improvement or worsening (i.e., a change in the NIHSS score of at least 4) was seen in 13.5% or 5.5% of the patients, respectively, during the first 7 days after admission. About 25% of the 437 patients had poor long-term outcomes. Analysis of receiver operating characteristic curves showed that the NIHSS score at day 7 after admission was better for predicting poor long-term outcomes than was the baseline score (P=0.003). In addition, we analyzed the cutoff point of the 7th-day NIHSS score for predicting a poor outcome at 6 months after symptom onset. An NIHSS score of at least 6 at day 7 after admission predicted poor long-term outcomes with a sensitivity of 84% [95% confidence interval (CI), 76-90%], a specificity of 92% (95% CI, 88-94%), and positive and negative predictive values of 77% and 95%, respectively. A logistic regression analysis revealed that age, diffusion-weighted imaging lesion volume, stroke history, and 7th-day NIHSS score were independently associated with poor outcome. However, no score used in addition to the 7th-day NIHSS score improved the prediction of a poor outcome.ConclusionsAn NIHSS score of at least 6 on day 7 after admission accurately forecasts a poor long-term outcome after stroke. Our data may be helpful in predicting the long-term prognosis as well as in making decisions regarding novel therapeutic applications in subacute-stroke trials.

BackgroundThe role of several cardiogenic risk factors, including patent foramen ovale, in patients with cryptogenic stroke has been extensively studied. However, little attention has been paid to the role of non-cardioembolic causes of cryptogenic stroke. We therefore sought to identify the characteristics of cryptogenic stroke.MethodsWe studied 832 patients with acute infarction in the middle cerebral arterial territory. We divided the patients into four subtypes: 402 with large artery atherosclerosis (LAA), 133 with cardioembolism, 182 with small arterial occlusion (SAO), and 115 with cryptogenic stroke. We compared risk factors and lesion patterns observed by diffusion-weighted imaging (DWI) between patients with cryptogenic stroke and those with stroke of other subtypes.ResultsBoth risk factors and DWI lesion patterns differed between the cryptogenic and cardioembolic groups (P<0.05). Risk factors for cryptogenic stroke were similar to those for the LAA and SAO groups. Similarly, DWI lesion patterns for cryptogenic stroke were similar to LAA patients. Large cortical infarcts on DWI were more common in the cardioembolic group than in the LAA or cryptogenic groups (P<0.001). In contrast, deep, non-lacunar (OR 5.02; 95% CI 2.68~9.40; P<0.001) and superficial perforator infarcts (OR 2.23; 95% CI 1.08~4.59; P=0.029) were independently associated with the cryptogenic group.ConclusionsOur results indicate that non-cardioembolic causes, such as macro- and microangiopathy, are important mechanisms in the pathogenesis of cryptogenic stroke.