Relationship between the Angle of the Posterior Inferior Cerebellar Artery and Cardioembolic Stroke.

BACKGROUND: In patients with unilateral posterior inferior cerebellar artery (PICA) territory infarction, the absence of relevant vessel stenosis may make it difficult to determine the etiology of the infarction. The incidence of cardioembolic (CE) infarction and the factors associated with infarction in such patients remains largely unknown. We hypothesized that the PICA angle would affect the flow direction of embolic sources. Thus, we analyzed the association between high-risk CE sources and the PICA angle. METHODS: Patients with an isolated unilateral PICA territory infarction without relevant vessel stenosis who were admitted between 2014 and 2017 were included from the Korea University Stroke Registry, which includes data from 3 university hospitals. We classified patients according to the presence of CE sources. For each case, we measured the angle between the vertebral artery (VA) and the proximal PICA. RESULTS: In all, 71 patients met the final study entry criteria. Multivariable analysis showed that the PICA angle was independently associated with the risk of a CE source. The optimal cut-off value using Youden's index was 89°. We classified the PICA shape based on the optimal cut-off value. A CE source was identified in 83.3% of cases in which the PICA angle exceeded 89°. CONCLUSIONS: The angle between the PICA and VA was an independent predictor of unilateral PICA stroke with high-risk CE sources without relevant artery stenosis, suggesting that an angle greater than 89° could be a new image marker for determining the stroke subtype.

C-reactive protein is a predictor of early neurologic deterioration in acute ischemic stroke.

Although the association between elevated C-reactive protein (CRP) level and long-term outcome after ischemic stroke is well known, the association between CRP and early neurologic deterioration (END) has not yet been thoroughly studied. We investigated the impact of CRP on END in patients with acute ischemic stroke. From a prospectively collected, multicenter stroke registry, 428 patients with acute ischemic stroke diagnosed within 24 hours of onset were enrolled in the study. Patients with hemorrhagic stroke, transient ischemic attack, and thrombolysis were excluded. END was defined as a >2-point increase in the National Institutes of Health Stroke Scale score within a 72-hour period. Data considered potentially associated with CRP level and the END were collected. END was observed in 47 patients. CRP level, time before arrival at the hospital, age, female sex, hematocrit, high-density lipoprotein (HDL) cholesterol level, hemoglobin A(1c) level, and internal carotid artery occlusion were significantly associated with END. On logistic regression analysis, CRP level, internal carotid artery occlusion, and HDL cholesterol proved to be independent variables. Our data suggest that CRP level at admission is significantly associated with END in acute ischemic stroke. HDL cholesterol and internal carotid artery occlusion are also associated with END.

Prevalence of sleep-disordered breathing in acute ischemic stroke as determined using a portable sleep apnea monitoring device in Korean subjects.

OBJECTIVES: It has been suggested that there is a strong association between sleep-disordered breathing (SDB) and stroke. However, this connection has not been studied in Korean subjects. METHODS: Sixty-one patients with acute cerebral infarction (ACI) and 13 patients with transient ischemic attack (TIA) were consecutively enrolled. SDB was evaluated within 48 h of stroke or TIA onset using a portable screening device, which allowed incidents of apnea, hypopnea, and snoring to be automatically analyzed. Clinical and sleep-related variables, including body mass indices (BMI), cardiovascular risk factors, stroke severity and disability, and Epworth sleepiness scale, Stanford sleepiness scale, and Berlin questionnaire scores were assessed. Sixty-four age-matched patient's spouses or family members with no history of physician-diagnosed stroke were enrolled as controls. RESULTS: Mean apnea-hypopnea index (AHI) was significantly higher in TIA (14.6 ± 10.4) and ACI (15.6 ± 14.7) patients than in the controls (7.8 ± 7.0; p = 0.001). The prevalences of SDB were 69.2% in TIA and 50.8% in ACI patients and 32.8% in controls. BMI and systolic blood pressure (SBP) were significantly higher in patients with SDB than in patients without SDB. Sleep-related stroke onset occurred in 17 patients (22.9%), and these patients had significantly higher AHIs. Multiple logistic regression analysis showed that BMI (odds ratio, 1.293; p = 0.027) and SBP (odds ratio, 1.030; p = 0.004) were found to independently predict SDB in patients with TIA or ACI. CONCLUSIONS: SDB is prevalent during the 48 h following ACI or TIA in Korean subjects. The authors recommend that SDB be evaluated after an ACI or TIA, especially in those with a high BMI and an elevated SBP.

Complete Freund's adjuvant-induced intervertebral discitis as an animal model for discogenic low back pain.

BACKGROUND: Although numerous animal models for low back pain associated with intervertebral disk (IVD) degeneration have been proposed, insufficient data have been provided to make any conclusions regarding pain. Our aim in this study was to determine the reliability of complete Freund's adjuvant (CFA) injection into the rat spine as an animal model representing human discogenic pain. METHODS: We studied IVD degenerative changes with pain development after a 10-microL CFA injection into the L5-6 IVD of adult rats using behavioral, histologic, and biochemical studies. Serial histologic changes were analyzed to detect degenerative changes. Expression of calcitonin gene-related peptide (CGRP), prostaglandin E (PGE), and inducible nitric oxide synthase (iNOS) were determined using immunohistochemistry or real-time polymerase chain reaction as support data for pain development. In addition, CGRP immunoreactivity (ir) at the IVD was considered indirect evidence of neural ingrowth into the IVD. RESULTS: There was a significant increase of the hindpaw withdrawal response in the CFA group until 7 wk postoperatively (P < 0.05). Histologic analyses revealed progressive degenerative changes of the disks without any damage in adjacent structures, including nerve roots. In the CGRP-ir staining study, the bilateral dorsal horns and IVD had positive ir after intradiscal CFA injection. CGRP mRNA expression was increased in the dorsal root ganglion (DRG) at 2 and 4 wk, whereas PGE and iNOS mRNAs were markedly increased at 2 wk. The increment of CGRP expression was higher in allodynic rats compared with nonallodynic rats. CONCLUSION: Intradiscal CFA injection led to chronic disk degeneration with allodynia, which was suggested by pain behavior and expression of pain-related mediators. The increment of CGRP, PGE, and iNOS also suggest pain-related signal processing between the IVD and the neural pathway in this animal model. This animal model may be useful for future research related to the pathophysiology and development of novel treatment for spine-related pain.

Brachial plexopathy following herpes zoster infection: two cases with MRI findings.

There are few reports of brachial plexopathy following the onset of a herpes zoster skin rash. Moreover, the MRI findings of zoster-induced brachial plexopathy have rarely been described. In the present study, we describe two cases of zoster brachial plexopathy and their MRI findings. MRI of the brachial plexus demonstrated T2 hyperintensity and contrast enhancement in the part of the brachial plexus that was compatible with both the clinical symptoms and the electrophysiological findings. Especially, MR imaging reflected the functional impairments more accurately than electrophysiological studies in the acute phase, during which MRI showed more extensive inflammatory involvement of the brachial plexus. MRI findings in the present cases suggest that, in addition to electrophysiological studies, MRI of the brachial plexus could provide valuable information for evaluating the location and extent of lesions and for understanding the pathophysiological mechanisms of zoster brachial plexopathy.

Symptomatic SUNCT syndrome associated with ipsilateral paranasal sinusitis.

Sinusitis has rarely been associated with short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) syndrome. We describe a case of symptomatic SUNCT syndrome caused by sinusitis, which showed typical features of SUNCT syndrome. The patient's symptoms completely resolved without recurrence after endoscopic sinus surgery followed by antibiotic treatment. We suggest that ipsilateral paranasal sinusitis accompanied by the spreading of inflammation through a dehiscence in the lamina papyracea could lead to the development of SUNCT syndrome.

Carotid atherosclerosis and heart rate variability in ischemic stroke.

The significant association between heart rate variability (HRV) and the outcomes of stroke has led to a particular interest in alterations of HRV in stroke patients. To date, several clinical variables have been associated with alterations of HRV in stroke patients. The present study adds the new information that carotid atherosclerosis may affect HRV alterations in stroke patients.

Correlation of coronary artery atherosclerosis with atherosclerosis of the intracranial cerebral artery and the extracranial carotid artery.

BACKGROUND: Investigating atherosclerosis of the coronary artery in ischemic stroke patients is clinically important because comorbidity is relatively common in such patients. We studied the relationship of atherosclerosis of the coronary artery to atherosclerosis of the intracranial cerebral artery and extracranial carotid artery. Further investigation was performed for determining the factors independently associated with coronary artery atherosclerosis in ischemic stroke patients. METHODS: We consecutively recruited ischemic stroke patients who had no history of coronary artery disease, and they underwent vascular examination. Patient-based vascular assessment was performed with magnetic resonance angiography of the cerebral arteries and computed tomography coronary angiography. The factors independently associated with coronary artery stenosis (> or =50%) were obtained from the conventional vascular risk factors and cerebral arterial stenosis using the logistic regression model. RESULTS: Coronary artery stenosis was observed in 25.4% of the patients and this was associated with age (OR: 1.16, 95% CI: 1.03-1.30) and the presence of stenosis of the extracranial carotid artery (OR: 11.37, 95% CI: 1.88-68.75) after logistic regression analysis. Intracranial arterial stenosis was not independently related to coronary stenosis. CONCLUSION: Careful concern about coronary artery disease is needed when treating ischemic stroke patients who have atherosclerosis of the extracranial carotid artery.

The impact of hyperthermia and infection on acute ischemic stroke patients in the intensive care unit.

INTRODUCTION: Despite the recognized deleterious effects of hyperthermia on critically ill neurological patients, few investigations have studied hyperthermia after an ischemic stroke in the intensive care unit (ICU) setting. METHODS: Acute ischemic stroke patients admitted to the ICU were assigned to one of three groups: normothermia, mild hyperthermia (MH), or severe hyperthermia (SH). The etiology of hyperthermia was further divided into infectious and non-infectious groups. RESULTS: Among the 150 patients included in the study, MH and SH were observed in 15 and 40 patients, respectively. Hyperthermia and the Glasgow coma scale (GCS) score were independently related to in-hospital mortality and increased length of stay in the ICU (ILOS, > or =4 days). DISCUSSION: Infection (39 patients) was more prevalent in the SH group than in the MH group and was associated with greater ILOS. CONCLUSIONS: Monitoring and managing infection and reducing body temperature may be important factors for determining the outcomes of patients with acute ischemic stroke admitted to the ICU.

Effect of endovascular hypothermia on acute ischemic edema: morphometric analysis of the ICTuS trial.

INTRODUCTION: Pilot studies of hypothermia for stroke suggest a potential benefit in humans. We sought to test whether hypothermia decreases post-ischemic edema using CT scans from a pilot trial of endovascular hypothermia for stroke. METHODS: Eighteen patients with acute ischemic stroke underwent therapeutic hypothermia (target = 33 degrees C) for 12 or 24 h followed by a 12-h controlled re-warm using an endovascular system. CT scans obtained at baseline, 36-48 h (right after cooling and re-warming) and 30 days were digitized, intracranial compartment volumes measured using a validated stereological technique, and the calculated change in CSF volume between the three time-points were used as an estimate of edema formation in each patient. Patients were grouped retrospectively for analysis based on whether they cooled effectively (i.e., to a temperature nadir of less than 34.5 degrees C within 8 h) or not. RESULTS: Eleven patients were cooled partially or not at all, and seven were effectively cooled. Baseline demographics and compartment volumes and densities were similar in both groups. At 36-48 h, the total CSF volume had significantly decreased in the not-cooled group compared to the cooled group (P < 0.05), with no significant difference in mean volume of ischemia between them (73 +/- 73 ml vs. 54 +/- 59 ml, respectively), suggesting an ameliorative effect of hypothermia on acute edema formation. At 30 days, the difference in CSF volumes had resolved, and infarct volumes (73 +/- 71 ml vs. 84 +/- 102 ml, respectively) and functional outcomes were comparable. CONCLUSIONS: Endovascular hypothermia decreases acute post-ischemic cerebral edema. A larger trial is warranted to determine if it affects final infarct volume and outcome in stroke.

Clinical and laboratory characteristics of cerebral infarction in tuberculous meningitis: a comparative study.

Cerebral infarction as a complication of tubercular (TB) meningitis is not uncommon, but an adequate comparison of patients with and without stroke has not been carried out. This study was performed to evaluate the clinical characteristics of cerebral infarction secondary to TB meningitis, and to investigate predictive factors for cerebral infarction in patients with TB meningitis. Patients with TB meningitis were recruited over a period of 56 months. They were divided into two groups, those with and those without stroke. Demographic features and clinical, laboratory, and neuroradiological findings were compared between the two groups. We classified strokes into subtypes using neuroimaging findings. Of the 38 patients who were diagnosed with TB meningitis, eight also experienced cerebral infarction. The percentage of cerebrospinal fluid leukocytes that were neutrophils was significantly higher in patients with stroke (68%) than in patients without stroke (31%; p=0.0001). Upon initial CT imaging, meningeal enhancement was found in 11 patients, and of these patients, six experienced stroke. There were no significant differences between the groups with respect to other clinical and laboratory features, including demographic features, time between meningitis onset and treatment initiation, peripheral white blood cell count, and cerebrospinal fluid findings. Five of the eight patients who developed stroke had lacunar infarcts. One of the three patients with territorial nonlacunar infarction died due to herniation. When treating patients with TB meningitis, the possibility of cerebral infarction should be considered when patients develop focal neurological signs, meningeal enhancement on a CT scan, and sustained polymorphic cerebrospinal fluid pleocytosis.

Prevalence of Parkinson's disease in Korea.

The prevalence of neurodegenerative disorders is not well documented in Korea. We assessed the prevalence of Parkinson's disease in an elderly population in a newly industrialized city in a rural region. Subjects for this study were randomly selected from a community-based cohort study. The sample in the cohort represented approximately 1.3% (4700) of 362 625 adults (age>18 years) listed in the city register in 1998. Among this group, 4218 subjects (1086 subjects aged>60 years) agreed to be interviewed and underwent a physical examination and neuropsychological tests administered by a neurologist and neuropsychologist. All participants were examined. Participants who had bradykinesia and at least one other possible cardinal sign of parkinsonism at the neurologic screening, and those who reported that they had Parkinson's disease, or were taking antiparkinsonian drugs were identified. In our study, 16 subjects showed evidence of Parkinson's disease. The prevalence in this population was 0.37%. Prevalence increased with age, and prevalence was 1.47% for those aged older than 60 years. Postural instability and gait disturbance were more common in the older age group. The results of neuropsychological tests were as follows: (1) only two subjects had low scores (<20) in the Korea-version mini-mental status examination; (2) seven subjects scored 0.5, one subject scored 2 and the other eight subjects scored 0 in the clinical dementia rating. The results of our prevalence study are similar to those of studies carried out in Western countries. Age is a risk factor for Parkinson's disease in Korea.

Stroke-evoked angiogenesis results in a transient population of microvessels.

The role of angiogenesis after stroke is unclear; if angiogenesis supports long-term recovery of blood flow, then microvessel hyperdensity consequent to angiogenesis should persist in infarcted cortex. Here, we assess the long-term stability of ischemia-induced microvessels after 2-h transient rat middle cerebral artery occlusion (tMCAo) followed by 30, 90, or 165 days of reperfusion. Stereological measures of microvessel density were taken adjacent to and within cortical cysts. Vascular permeability was documented by extravasation of immunoglobulin (IgG) and of fluorescein-dextran. After 30 days reperfusion, a significantly increased microvessel volume density (V(V)) was restricted to the inner margin of cystic infarcts as compared with the region external to the infarct or contralateral control cortex (F=42.675, P<0.001). The hyperdense ischemic vasculature was abnormally leaky to IgG and fluorescein-dextran. Between 30 and 90 days of reperfusion, this vessel hyperdensity regressed significantly and then regressed further but less drastically between 90 and 165 days. Phagocytic macrophages were restricted to the infarct and dynamic changes in their number correlated with microvessel regression. Additional ED-1 labeled inflammatory cells were widely distributed inside and external to the infarct, even after 165 days of reperfusion. These data show that ischemia evoked angiogenesis results, at least in part, in transient populations of leaky microvessels and phagocytic macrophages. This suggests that a major role of this angiogenesis is for the removal of necrotic brain tissue.