A 10-year longitudinal study of deep white matter lesions on magnetic resonance imaging.

PURPOSE: Deep white matter lesions (DWMLs), T2 high-intensity areas in the subcortical white matter on magnetic resonance imaging (MRI), are a clinical phenotype of cerebral small vessel disease. Factors such as age and hypertension have been reported to significantly contribute to the presence and severity of DWMLs in cross-sectional studies. We herein report a 10-year longitudinal study on DWMLs in elderly Japanese subjects to reveal the clinical variables contributing to the progression of DWMLs. METHODS: A total of 469 Japanese subjects were invited to participate in the study. Of the participants at baseline, 259 subjects completed the revisit MRI study 10 years later. In those 259 subjects, we evaluated the correlation between the progression of DWMLs and clinical variables, such as the gender, age, and overt vascular risk factors. To clarify the role of hypertension, 200 subjects with grade 1 DWMLs at baseline were categorized into three groups according to their status of hypertension and its treatment. RESULTS: Of the 200 subjects with grade 1 DWMLs, 47 subjects (23.5%) showed progression of DWMLs (progression group). In the progression group, the percentage of subjects with hypertension and the systolic blood pressure values were higher than in the non-progression group. In addition, subjects ≥ 60 years old at baseline tended to show deterioration of DWMLs in the group with hypertension without antihypertensive treatment. CONCLUSION: The results of this 10-year longitudinal study imply a positive correlation between long-standing hypertension and the progression of DWMLs.

Serum albumin to globulin ratio is related to cognitive decline via reflection of homeostasis: a nested case-control study.

BACKGROUND: Recent research suggests that several pathogenetic factors, including aging, genetics, inflammation, dyslipidemia, diabetes, and infectious diseases, influence cognitive decline (CD) risk. However, no definitive candidate causes have been identified. The present study evaluated whether certain serum parameters predict CD. METHODS: A total of 151 participants were assessed for CD using the Mini-Mental State Examination (MMSE), and 34 participants were identified as showing CD. RESULTS: Among CD predictive risk factors, Helicobacter pylori seropositivity was significantly predictive of CD risk, more so than classical risk factors, including white matter lesions and arterial stiffness [adjusted odds ratio (OR) = 4.786, 95% confidence interval (CI) = 1.710-13.39]. A multivariate analysis indicated that the albumin to globulin (A/G) ratio was the only factor that significantly lowered CD risk (OR = 0.092, 95% CI = 0.010-0.887). A/G ratio also was positively correlated with MMSE scores and negatively correlated with disruption of homeostatic factors (i.e., non-high-density lipoprotein, hemoglobin A1c, and high-sensitive C-reactive protein). CONCLUSIONS: The current study results suggest that the A/G ratio is related to cognitive decline and may reflect homeostatic alterations.

The relationship between neurological worsening and lesion patterns in patients with acute middle cerebral artery stenosis.

BACKGROUND: Intracranial atherosclerotic disease is one of the most common causes of ischemic stroke especially in Asians, Hispanics and blacks. Although middle cerebral artery (MCA) stenosis is increasingly being recognized with the advent of magnetic resonance angiography (MRA) or transcranial Doppler ultrasonography, few studies have focused on acute neurological worsening (NW) in patients with MCA stenosis. We investigated the relationship between NW and lesion patterns detected by diffusion-weighted imaging (DWI). METHODS: We studied 44 consecutive patients out of a total of 2,863 consecutive patients who had symptomatic lesions in the territory of the MCA and in whom MRA and/or conventional angiography showed isolated MCA stenosis ≥50% in the MCA trunk. Acute DWI lesion patterns were classified as follows: (1) pial artery territory infarcts (PAI); (2) small cortical and/or subcortical infarcts (SCS); (3) deep penetrating artery territory infarcts (DPI); (4) cortical border zone infarcts (CBZ), and (5) internal border zone infarcts (IBZ). NW was defined as worsening by ≥2 points on the National Institutes of Health Stroke Scale (NIHSS) during the first 7 days. Functional outcome was assessed by the modified Rankin Scale (mRS) at 3 months after stroke onset. Poor outcome was defined as ≥3 on the mRS. The severity of MCA stenosis on MRA was further categorized as 50-75% (moderate) and >75% or focal signal loss with the presence of distal MCA signal (severe). RESULTS: There were 14 patients (31.8%) who showed NW and 16 patients (36.3%) who showed poor outcomes. Nine of the 14 patients with NW showed poor outcomes (64.2%). The most frequent lesions in the present study were SCS (n = 16, 36.3%), followed by IBZ (n = 12, 27.2%) and DPI (n = 11, 25.0%). Prevalence of IBZ was significantly higher in the group with NW compared to that without NW (p = 0.0081), while the prevalence of SCS, DPI, PAI and CBZ did not differ between the two groups. Logistic regression analysis showed significantly high age- and sex-adjusted odds ratios (ORs) for NW only for IBZ (OR 10.9, p = 0.0051). The degree of stenosis did not correlate with NW and lesion patterns. CONCLUSIONS: Only IBZ among various lesion patterns correlated strongly with NW. IBZ are considered to be more associated with hemodynamic compromise, while embolic pathogeneses contribute more to CBZ or SCS. Early interventional medical treatments such as thrombolytic or anti-platelet therapy or stenting should be considered in cases of IBZ in MCA stenosis.

A combined treatment for acute larger lacunar-type infarction.

Larger lacunar-type infarcts (LLIs), presumably caused by occlusion at the orifices or proximal portions of larger-caliber penetrating arteries by atheromatous plaque, are frequently associated with progressive motor deficits (PMD) and lead to poor functional outcome. This study was conducted to examine the efficacy of a combined treatment to prevent PMD or improve the functional outcome in patients with LLI. A total of 218 consecutive patients with LLI and motor lacunar syndrome were enrolled, including 138 patients with infarcts in the territory of the lenticulostriate artery and anterior choroidal artery (supratentrial group) and 80 patients with infarcts in the territory of the anterior pontine artery (pontine group). The prevalence of PMD and functional outcome represented by modified Rankin Scale (mRS) score at 1 month after ictus were compared between groups treated with a combined treatment approach consisting of cilostazol and edaravone (n = 100) and a conventional treatment approach (n = 118). The efficacy of the combined treatment provided in 2005-2009 was compared with conventional treatment provided in 2001-2005. There was no significant difference in the prevalence of PMD between the 2 treatment groups. The combined treatment group had significantly more favorable outcomes compared with the conventional treatment group in the total population (P = .0078, Wilcoxon Mann-Whitney test) and in the pontine group (P = .0042). Logistic regression analysis showed that an initial National Institutes of Health Stroke Scale score <4, the absence of PMD, and the novel combined treatment approach were independently associated with favorable functional outcome. The novel combined treatment approach was safe and effective in improving functional outcome in acute LLI, but not effective in preventing PMD.

Subdural haematoma, the great imitator, mimicking acute spinal cord lesion.

Acute non-traumatic paraparesis is usually caused by vascular, inflammatory or neoplastic myelopathies; however, it is sometimes caused by non-myelopathic pathologies, including polyradiculoneuropathies, myopathies, psychogenic aetiologies or parasagittal cortical pathologies. A 73-year-old woman reported weakness of the bilateral lower limbs and urinary incontinence. Together with the sensory level at the left T6 dermatome, we initially considered thoracic myelopathy as the most likely diagnosis. However, MRI of the cervicothoracic cord was negative and subsequent cranial CT revealed a bilateral subdural haematoma. A parasagittal cortical pathology should not be excluded from differential diagnoses as a rare cause of paraparesis until its possibility is carefully ruled out.

Temporal Changes in Brain Magnetic Resonance Imaging Findings over 16 Years in a Patient with Neuronal Intranuclear Inclusion Disease.

Leukoencephalopathy with high-intensity signals in the corticomedullary junction on diffusion-weighted imaging (DWI) is a diagnostic hallmark for neuronal intranuclear inclusion disease (NIID). We herein report a 65-year-old man who developed dementia and was diagnosed with NIID 2 years later. Of note, he had coincidentally undergone brain magnetic resonance imaging 14 and 10 years before the onset of dementia. No abnormalities were discerned on DWI on either of these occasions, but high-intensity signals in the corticomedullary junction on DWI were revealed two years before the clinical onset. The early recognition of this pathognomonic white matter change may facilitate the presymptomatic diagnosis of NIID.

Case Report: Dexmedetomidine for Intractable Clusters of Myoclonic Jerks and Paroxysmal Sympathetic Hyperactivity in Progressive Encephalomyelitis With Rigidity and Myoclonus.

Introduction: Progressive encephalomyelitis with rigidity and myoclonus (PERM) is a severe form of stiff-person spectrum disorder characterized by painful spasms, myoclonic jerks, hyperekplexia, brainstem dysfunction, and dysautonomia, which is sometimes resistant to γ-amino-butyric acid (GABA)-ergic agents. The response to immunotherapy varies depending on identified autoantibodies. We report a dramatic response to dexmedetomidine in a patient with glycine receptor (GlyR) antibody-positive PERM who developed intractable clusters of myoclonic jerks and paroxysmal sympathetic hyperactivity (PSH) that was highly refractory to conventional symptomatic treatment with GABAergic drugs and immunotherapy. Case Presentation: A 62-year-old Japanese man was transferred to our center for intermittent painful spasms that progressed in severity over the preceding 7 weeks. On admission, he had gaze-evoked nystagmus, and paroxysmal painful spasms/myoclonic jerks triggered by sound or touch. The myoclonic jerks rapidly worsened, along with the development of hyperekplexia, opisthotonus, and PSH, leading to prolonged apnea requiring mechanical ventilation. Brain and spinal cord magnetic resonance imaging was unremarkable. Cerebrospinal fluid (CSF) examination revealed mild pleocytosis and oligoclonal bands. Surface electromyography confirmed simultaneous agonist-antagonist continuous motor unit activity. Based on the clinico-electrophysiological features, PERM was suspected. He was initially treated with intravenous steroids, immunoglobulin, benzodiazepines, and propofol, but the symptoms persisted. On day 9, he received a continuous infusion of dexmedetomidine, which resulted in dramatic reduction in the frequency of clusters of myoclonic jerks and PSH. The effect of dexmedetomidine was confirmed by surface electromyography. The addition of plasma exchange resulted in further clinical improvement. GlyR antibodies were identified in the CSF but not the serum, leading to the diagnosis of GlyR antibody-positive PERM. Conclusions: PERM is an immune-mediated disorder, but dexmedetomidine, a highly selective α2-adrenergic agonist, may alleviate paroxysmal symptoms by decreasing noradrenergic neuronal activity, resulting in attenuation of antibody-mediated disinhibited increased motor and sympathetic activity. Dexmedetomidine may be useful as an adjunctive symptomatic therapy in PERM and related disorders.

Experimental infection of pigs with different doses of the African swine fever virus Armenia 07 strain by intramuscular injection and direct contact.

We experimentally infected pigs with the African swine fever virus (ASFV) Armenia 07 strain (genotype II) to analyze the effect of different dose injections on clinical manifestations, virus-shedding patterns, histopathology, and transmission dynamics by direct contact. Each three pigs and four pigs were injected intramuscularly with 0.1 fifty percent hemadsorbing doses (HAD50)/ml, 101 HAD50/ml and 106 HAD50/ml of ASFV Armenia 07 strain, respectively. Each two of three pigs injected with 0.1 HAD50/ml and 101 HAD50/ml died by 10 days post inoculation. All pigs had a gross lesion of splenomegaly. Perigastric and renal lymph nodes were enlarged and resembled blood clots in nine of ten pigs. It was revealed that 0.1 HAD50/ml of this ASFV was sufficient to infect healthy pigs by intramuscular injection and caused sub-acute lethal disease. For the transmission study, two 8-week-old pigs were injected intramuscularly with 103 HAD50/ml of the same virus. Each of the experimentally inoculated pigs was co-housed with two 8-week-old naive pigs. All contact pigs exhibited clinical manifestations at 6 or 7 days after the experimentally inoculated pigs developed pyrexia. These findings suggest that this strain may spread slowly within a herd. Histologically, lymph nodes resembled blood clots were formed by severe blood absorption and followed hemorrhage result of disruption of the lymphoid sinus filling with absorbed red blood cells. The severity of the gross and histological lesions depended on duration after infection, regardless of the difference of injection doses in this study.

Cerebral Infarction with Pulmonary Thromboembolism Due to Immobilization.

Arterial and venous thrombi can coexist without preexisting conditions, such as malignant disease, thrombotic predisposition, or arteriovenous shunt. We herein report a case of acute cerebral infarction and pulmonary thromboembolism in the absence of underlying disease. A 71-year-old woman presented with left hemiplegia. On an examination, her oxygen saturation was 91% on ambient air despite the absence of chest symptoms and clear lung fields on a chest radiograph. The patient was finally diagnosed with acute cerebral infarction caused by large artery atherosclerosis and acute pulmonary thromboembolism due to deep vein thrombosis, consequent to immobilization for three days after the onset of cerebral infarction.

Unusual Clinical Sequelae of Kawasaki Disease-Symptomatic Extracranial Internal Carotid Stenosis in Young Adult.

BACKGROUND: Kawasaki disease (KD) is an acute systemic vasculitis that primarily affects the coronary artery, but it does not commonly affect the carotid artery. Cerebral infarction (CI) with internal carotid artery stenosis (ICS) in patients with KD has not been reported until now. We report a patient with CI as a remote-phase complication of KD. CASE PRESENTATION: A 32-year-old man presented with impaired consciousness. Magnetic resonance imaging and digital subtraction angiography confirmed CI and ICS. He successfully underwent carotid endarterectomy. The resected plaque had pathologic findings of KD, which suggested that the internal carotid artery suffered from chronic inflammation. CONCLUSION: KD in childhood may cause symptomatic ICS as a sequela of a remote phase.

Association between α-Klotho and Deep White Matter Lesions in the Brain: A Pilot Case Control Study Using Brain MRI.

BACKGROUND: The anti-aging protein, α-Klotho, may be involved in cognitive decline and has potential as a surrogate marker that reflects dementia. However, the role of α-Klotho in the brain has not been sufficiently investigated. OBJECTIVE: Here, we investigated the association between α-Klotho and cognitive decline that is associated with cerebral deep white matter lesions (DWMLs). METHODS: Two hundred-eighty participants (187 males and 93 females, mean age: 70.8 years old) were evaluated for DWMLs, and the Fazekas scale (Grade) was assessed following brain magnetic resonance imaging. A questionnaire concerning lifestyle and neuropsychological tests was administered, and their associations with the blood α-Klotho level were retrospectively investigated. RESULTS: The α-Klotho level was 685.1 pg/mL in Grade 0 (68 subjects), 634.1 in G1 (134), 596.0 in G2 (62), and 571.6 in G3 (16), showing that the level significantly decreased with advanced grades. Significant correlations were noted between the α-Klotho level and higher brain function tests including the Mini-Mental State Examination and word fluency tests (p < 0.05). When a 90th percentile value of the level in the G0 group (400 pg/mL) or lower was defined as a low α-Klotho level, the odds ratio of the high-grade G3 group was 2.9 (95% confidence interval: 1.4-7.8) (after correction for age, sex, hypertension, and chronic kidney disease), which was significant. CONCLUSION: A reduced blood α-Klotho level was correlated with grading of cerebral DWMLs and was accompanied by cognitive decline as an independent risk factor. The α-Klotho level may serve as a useful clinical index of vascular cognitive impairment.

Association between Mid-Regional Proadrenomedullin Levels and Progression of Deep White Matter Lesions in the Brain Accompanying Cognitive Decline.

BACKGROUND: Adrenomedullin (ADM) is a vasoreactive physiological peptide with anti-inflammatory effects and vasodilative and immunomodulatory actions that is widely distributed throughout the vascular system of the brain. OBJECTIVE: To investigate mid-regional proADM (MR-proADM), a stable fragment of the ADM precursor, and cerebral deep white matter lesions (DWMLs) in association with cognitive decline. METHODS: The study participants were 288 patients (194 men, 94 women) who gave consent to participate in a 5-year longitudinal survey on arteriosclerosis from 2008 to 2013. The Fazekas classification system (Grade [G] 0 [normal] to G3 [severe]) was used for the evaluation of DWMLs on brain magnetic resonance imaging (MRI). In addition, all participants were asked to undergo cognitive function tests regarding word/letter fluency, the results of which were assessed for correlations with MR-proADM levels. RESULTS: MR-proADM levels significantly increased with DWML grade progression. The odds ratio for high MR-proADM levels was 3.08 (95% confidence interval: 1.49-5.17) in the groups graded G3 on brain MRI, suggesting that a high level of MR-proADM is an independent risk factor for DWMLs. A significant inverse correlation was observed between MR-proADM levels and cognitive test scores. MR-proADM levels were significantly increased in the G3 group in 2013 compared with 2008. CONCLUSION: MR-proADM levels were significantly different between the DWML groups and inversely correlated with cognitive function test scores, suggesting that high MR-proADM levels and DWMLs are associated with cognitive decline. Therefore, the MR-proADM level may be an effective candidate as a potential diagnostic surrogate marker of cognitive decline.

CD62-mediated activation of platelets in cerebral white matter lesions in patients with cognitive decline.

BACKGROUND: Vascular dementia is related to intracranial arteriosclerosis associated with deep white matter lesions (DWMLs). DWMLs have been linked to thrombogenesis due to sustained platelet activation; therefore, an accurate hematological marker is needed. This study was done to evaluate the usefulness of a new method to examine the function of activated platelets in order to assess DWMLs associated with cognitive decline. METHODS: A total of 143 individuals (70.4 ± 6.1 years old) who underwent hospital-based health screening using head MRI were evaluated. DWLs were evaluated on T2-weighted and FLAIR images by semi-quantitatively grading them from Grade 0 (none) to Grade 3 (severe) using the Fazekas classification. Cognitive function was evaluated using the MMSE and the word fluency test. Platelet activation was assessed using fluorescence-labeled anti-human platelet monoclonal antibodies and semi-quantitatively determining PAC-1- and CD62P-positive rates by flow cytometry. RESULTS: Significant increases in hypertension and CD62P levels were observed with increasing DWML grade (2.6% in Group 0, 3.1% in Group 1, 4.1% in Group 2, and 5.0% in Group 3). CD62P levels were defined as elevated when they were above the mean+2SD of the Grade 0 group, and the odds ratio of the Grade 2+3 group was 3.03. A significant negative correlation was observed between CD62P levels and word fluency tests or the MMSE score. CONCLUSION: Elevations in CD62P levels, which reflect platelet function activation, were associated with white matter lesions accompanied by a decline in cognitive function. CD62P levels may be useful as a sensitive clinical marker for the early detection of DWMLs with cognitive decline.

Oral Cnm-positive Streptococcus Mutans Expressing Collagen Binding Activity is a Risk Factor for Cerebral Microbleeds and Cognitive Impairment.

Cerebral microbleeds (CMBs) are an important risk factor for stroke and dementia. We have shown that the collagen binding surface Cnm protein expressed on cnm-positive Streptococcus mutans is involved in the development of CMBs. However, whether the collagen binding activity of cnm-positive S. mutans is related to the nature of the CMBs or to cognitive impairment is unclear. Two-hundred seventy nine community residents (70.0 years) were examined for the presence or absence of cnm-positive S. mutans in the saliva by PCR and collagen binding activity, CMBs, and cognitive function were evaluated. Cnm-positive S. mutans was detected more often among subjects with CMBs (p < 0.01) than those without. The risk of CMBs was significantly higher (odds ratio = 14.3) in the group with S. mutans expressing collagen binding activity, as compared to the group without that finding. Deep CMBs were more frequent (67%) and cognitive function was lower among subjects with cnm-positive S. mutans expressing collagen binding activity. This work supports the role of oral health in stroke and dementia and proposes a molecular mechanism for the interaction.

Ventricular Temperatures in Idiopathic Normal Pressure Hydrocephalus (iNPH) Measured with DWI-based MR Thermometry.

PURPOSE: The brain produces intense heat as a result of cerebral metabolism and cerebral blood flow, and the generated heat is removed mainly through circulation of the intracranial blood vessels and cerebrospinal fluid (CSF). Because magnetic resonance (MR) images are constructed from analysis of the spin of various molecules, the diffusion coefficient can be used as a parameter that reflects the temperature of water molecules. We used diffusion-weighted imaging (DWI)-based MR imaging to measure the temperature of the CSF around the lateral ventricles in patients with idiopathic normal pressure hydrocephalus (iNPH). METHODS: Our study included 33 cases of iNPH (Group N, mean age, 75.1 years) and 40 age-matched controls (Group C, mean age, 74.5 years). We calculated CSF temperature in the ventricular domain using the conversion formula to evaluate the feasibility of iNPH study. RESULTS: The mean temperatures were significantly higher in Group N (37.6°C ± 0.4°C) than Group C (36.7°C ± 0.5°C; P < 0.01). The cut-off value of 37.2°C (more than the mean + 2 standard deviations [SD] of the values in Group C) showed sensitivity of 72.4% and specificity of 77.5% for distinguishing the 2 groups. We confirmed improved CSF temperature in the lateral ventricles in all patients examined both before and after shunting. CONCLUSIONS: Elevated ventricular temperatures in patients with iNPH (Group N) may represent a disturbance in heat balance. Our results showed that thermometry using DWI-based MR imaging can help in the noninvasive and consistent evaluation of CSF temperature and may thus provide a useful supplementary brain biomarker for iNPH.

Characteristics of intracranial branch atheromatous disease and its association with progressive motor deficits.

BACKGROUND: Small deep brain infarcts are often caused by two different vascular pathologies: 1. atheromatous occlusion at the orifice of large caliber penetrating arteries termed branch atheromatous disease (BAD) and 2. lipohyalinotic degenerative changes termed lipohyalinotic degeneration (LD). We herein analyze and describe the characteristics of these 2 different pathologies. METHODS: We studied 394 patients with penetrating artery territory infarcts in the territories of the lenticulostriate arteries and anterior pontine arteries. Radiologically defined BAD of the lenticulostriate arteries was defined as infarcts with size more than 10mm in diameter on axial slice and visible for 3 or more axial slices, and that of the anterior pontine arteries was defined as unilateral infarcts extending to the basal surface of the pons. Within each of the 2 territory groups, differences between BAD and LD were compared. RESULTS: Ninety five patients in the lenticulostriate arteries group (36.1%) and 78 patients in anterior pontine arteries group (59.5%) were classified as BAD. Initial NIHSS, incidence of progressive motor deficits and poor functional outcome were significantly higher and incidence of concomitant silent lacunar infarcts tended to be lower in BAD than LD. In logistic regression analysis, BAD compared with LD was independently associated with PMD, in lenticulostriate arteries group (OR: 4.21, p=0.0001) and in anterior pontine arteries group (OR: 5.32, p=0.0018). CONCLUSIONS: Radiologically defined BAD and LD had different characteristics. BAD was significantly associated with progressive motor deficits and considered as a major vascular mechanism of progressive motor deficits in penetrating artery infarcts.

The infarct location predicts progressive motor deficits in patients with acute lacunar infarction in the lenticulostriate artery territory.

BACKGROUND AND PURPOSE: Patients with acute lacunar infarction in the lenticulostriate artery (LSA) territory often show progression of motor deficits (PMD) after admission. The purpose of our study is to identify predictors for PMD using the findings of diffusion-weighted imaging (DWI) on admission. METHODS: From January 2005 to December 2008, we studied 60 consecutive patients with acute lacunar infarction in the LSA territory within 24h after onset. To identify predictors for PMD, clinical characteristics including vascular risk factors and DWI findings were evaluated. DWI findings included the size and location of the infarcts and the slice numbers of infarcts visible on DWI. For the location, posterior type was defined as an infarct located in the posterior part of corona radiata on the second slice from the top among slices including corona radiata. RESULTS: Twenty-six patients (43%) showed PMD. In univariate analysis, age >or=75 (P=0.03), female sex (P=0.04), infarct slice number >or=3 (P=0.04), and posterior type infarct (P<0.001) were more frequent in the PMD group than in the no PMD group. In multivariate analysis, posterior type infarct was the only independent predictor among DWI findings for PMD (odds ratio, 14.83; 95% confidence interval, 3.54-87.21, P<0.001). CONCLUSIONS: Posterior type infarct was the independent predictor in DWI findings for PMD in patients with lacunar infarction in the LSA territory. We postulate that the posterior type infarct may affect the corticospinal tract to a greater degree and cause PMD.

Predictive factors for progressive motor deficits in penetrating artery infarctions in two different arterial territories.

BACKGROUND: Progressive motor deficits (PMD) are common in cerebral penetrating artery disease (PAD) during the acute stage and leads to severe disability. Reliable predictors and stroke mechanism for PMD in PAD have been yet to be elucidated. Moreover, difference of predictors between topographically classified PAD has not ever been systematically studied. METHODS: Three hundred ninety two consecutive patients with acute PAD (<20 mm) who showed lacunar motor syndrome and admitted within 24 h after onset were selected for this study. Patients were divided into 2 groups whose infarcts were topographically located within the territories of lenticulostriate arteries (LSA), and anterior pontine arteries (APA). Within each of the 2 groups, factors associated with PMD were analyzed. RESULTS: Progressive motor deficits were found in 55 patients (21.0%) in LSA group and 38 patients (29.0%) in APA group. In multivariate analysis, female sex and severity of motor deficit on admission (NIHSS 5 or more) were common independent predictors for PMD in both groups. The specific predictors were single infarcts without concomitant silent lacunar infarcts and preceding TIAs in LSA group and diabetes mellitus in APA group. CONCLUSIONS: Predictive factors for PMD were different in the 2 different territory groups. Diabetes mellitus was particularly associated with PMD in APA group.

Cognitive impairment and cerebral hypoperfusion in a CADASIL patient improved during administration of lomerizine.

A 64-year-old woman was admitted to our hospital for recurrent stroke and cognitive impairment and was diagnosed with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Iodine-123 iodoamphetamine single photon emission computed tomography showed hypoperfusion in the whole brain, but cerebral blood flow increased dramatically after the administration of acetazolamide in the cerebral cortex. Lomerizine, a diphenylmethylpiperazine Ca2+ channel blocker, can selectively increase cerebral blood flow. Cognitive decline and cerebral hypoperfusion improved during 2-year administration of lomerizine in this CADASIL patient, and thus, lomerizine is a potential candidate for treating cognitive impairment in CADASIL patients.