Vertebrobasilar insufficiency by persistent trigeminal artery stenosis

Persistent trigeminal artery is an embryonic remnant of the anastomotic channel linking the internal carotid artery and the basilar artery. Cases of vertebrobasilar insufficiency caused by the persistent trigeminal artery with internal carotid artery stenosis has been described previously, but vertebrobasilar insufficiency entirely due to in situ stenosis of the persistent trigeminal artery has not been reported. A 71-year-old man presented with frequent dizzy episodes. The brain MRI showed no parenchymal lesions. MR angiography showed poor visualization of vertebrobasilar system. He was diagnosed as having vertebrobasilar insufficiency. Cerebral angiography revealed that there was complete occlusion at the vertebrobasilar junction, and the basilar artery was supplied by the persistent trigeminal artery which had severe stenosis at its origin. There was no stenosis of the internal carotid artery of both sides. We believe that this is the first report of vertebrobasilar insufficiency due to stenosed persistent trigeminal artery, without internal carotid artery stenosis.

Increased Circulating Endothelial Microparticles and Carotid Atherosclerosis in Obstructive Sleep Apnea

BACKGROUND AND PURPOSE: Endothelial impairment is a linking mechanism between obstructive sleep apnea (OSA) and cardiovascular diseases. Profiles of endothelial microparticles (EMPs) and endothelial progenitor cells (EPCs) reflect the degree of endothelial impairment. The aims of this study were to measure the levels of EMPs and progenitor cells in OSA, determine the correlations between these factors and OSA severity and the degree of atherosclerosis, and document any changes in these factors after therapy. METHODS: Subjects with (n=82) and without (n=22) OSA were recruited prospectively. We measured the number of colony-forming units (CFU) in cell culture as the endothelial progenitor cell index, and the number of EMPs using flow cytometry with CD31 [platelet endothelial cell adhesion molecule (PECAM)], CD42 (platelet glycoprotein), annexin V, and CD62E (E-selectin) antibodies at baseline and after 4-6 weeks of continuous positive airway pressure (CPAP) therapy. Carotid intima-media thickness (IMT) was regarded as a marker of atherosclerosis. RESULTS: The levels of PECAM+CD42- (p<0.001), PECAM+annexin V+ (p<0.001), and E-selectin+ microparticles (p=0.001) were higher in OSA subjects than in non-OSA subjects. The number of CFU did not differ between the two groups. OSA severity independently predicted the levels of PECAM+CD42- (p=0.02) and PECAM+annexin V+ (p=0.004). Carotid IMT was correlated with OSA severity (p<0.001), PECAM+CD42- (p=0.03), and PECAM+annexin V+ (p=0.01). Neither OSA severity nor carotid IMT was correlated with either the number of CFU or E-selectin+. CPAP therapy decreased the occurrence of E-selectin+ (p<0.001) in 21 of the OSA subjects, but had no effect on the other microparticles of the number of CFU. CONCLUSIONS: OSA led to the overproduction of EMPs, which moderately correlated with OSA severity and the degree of atherosclerosis, and partly responded to therapy. The endothelial impairment might contribute to future cardiovascular events.

Neuropathologic and Clinical Features of Human Medial Temporal Lobe Epilepsy

BACKGROUND AND PURPOSE: There is recent evidence of various types of morphological changes in the hippocampus of a rodent model of medial temporal lobe epilepsy (mTLE). However, little is known about such changes in humans. We examined the histological changes [i.e., neuronal loss, cell genesis, and granule cell dispersion (GCD)] in surgical hippocampal specimens taken from patients with mTLE. METHODS: Nissl staining, and nestin and Prox1 immunohistochemistry were performed on human hippocampal specimens obtained from patients with medically intractable mTLE, thus allowing the analysis of neuronal loss, cell genesis, and GCD, respectively. We also assessed the correlations between clinical parameters and the histopathologic findings. RESULTS: The degree of cell genesis in the granule cell layer was significantly correlated with the severity of GCD, history of childhood febrile seizures, and frequent generalized seizures. Cell genesis was not correlated with cell death, age at seizure onset, duration of epilepsy, or the mean frequency of all seizures. CONCLUSIONS: Our results indicate that cell genesis in the dentate gyrus of patients with mTLE is associated with GCD and is influenced by the presence of febrile seizures during childhood and the frequency of episodes of generalized seizures.

Stroke Mimicking Encephalopathy as an Initial Manifestation of Diffuse Large B-Cell Lymphoma

BACKGROUND: Systemic lymphoma can be difficult to recognize due to its diverse manifestations. Paraneoplastic leukoencephalopathy has rarely been reported in the context of lymphoma. CASE REPORT: We report a 45-year-old man with systemic lymphoma whose initial manifestation was sudden-onset leukoencephalopathy, mimicking stroke. This patient, who was eventually diagnosed with diffuse large B-cell lymphoma, initially presented with sudden cognitive impairment and gait disturbance. Radiological studies suggested a paraneoplastic leukoencephalopathy. Chemotherapy for lymphoma resulted in clinical and radiological improvement. CONCLUSIONS: The presented case indicates that diffuse large B-cell lymphoma may initially appear as a treatable leukoencephalopathy.

Circulating Endothelial Progenitor Cells in Cerebrovascular Disease

Stroke is associated with high disability and mortality burdens worldwide, but there are few effective and widely available therapies. There is therefore a need to develop treatments that promote the repair and regeneration of ischemic brain tissue. In this regard, a population of adult stem cells-called endothelial progenitor cells (EPCs)-has been identified in peripheral blood that could provide novel approaches in regenerative medicine for curing patients with acute ischemic stroke. There is accumulating evidence that EPCs can repair damaged endothelia and attenuate the development and progression of atherosclerosis. Also, EPCs can be recruited in response to acute ischemic events and participate in reparative vasculogenesis. Most studies related to EPCs have involved patients with cardiovascular diseases, and there is emerging evidence that EPCs represent a risk marker and a potential therapeutic agent in cerebrovascular disease. Here we review the characteristics and biology of EPCs in cerebrovascular disease and discuss the challenges that must be addressed to clarify the role and therapeutic applicability of EPCs in cerebrovascular disease.

Analysis of 10,811 Cases with Acute Ischemic Stroke from Korean Stroke Registry: Hospital-Based Multicenter Prospective Registration Study

BACKGROUND: Although several hospital-based stroke studies were published, there has not been any reliable data representing the clinical characteristics of stroke in Korea. We analyzed the clinical characteristics of patients with ischemic stroke registered in the Korean Stroke Registry (KSR), which is the largest prospective hospital-based nation-wide stroke registry in Korea. METHODS: The KSR provided standardized protocols for collecting data, which includes the data of demographics, subtypes of stroke, risk factors, and neurological outcome at discharge. The brain imaging studies, including CT or MRI, were performed in all cases. RESULTS: KSR registered 10,811 patients of acute ischemic stroke between Nov. 2002 and Jun. 2004. The large-artery atherosclerosis was the most common subtype (37.3%), followed by small vessel occlusion (30.8%). Hypertension (65.4%) was the most common risk factor, followed by smoking (34.5%) and diabetes (28.3%). Although most of the hypertensive and diabetic patients had been diagnosed before the stroke, less than 45.4% and 32.5% of them were under regular control. The steno-occlusive lesion of extracranial carotid artery was only 29.3% and the ratio of intra- to extracranial artery disease was more than 2 in KSR. Only 20.5% of patients were admitted within 3 hours after stroke onset and 2.1% were treated with intravenous thrombolysis. In-hospital case-fatality was 5.2%, which is relatively comparable to those of previous studies. CONCLUSIONS: The KSR provided informative data in understanding the clinical characteristics of ischemic stroke in Korea. Further analysis of KSR will facilitate clinical trials and development of guidelines for the management of stroke patients.

Truncal Contrapulsion in Pretectal Syndrome

Truncal contrapulsion in association with pretectal syndrome has not been described previously. We report a patient with vertical-gaze palsy and severe truncal contrapulsion due to an infarction in the mesodiencephalic junction. Truncal contrapulsion in this patient may have resulted from the disruption of the ascending fibers in the crossed cerebellothalamic tract.

Endogenous Neural Stem Cell Proliferation after Intracerebral Hemorrhage in Rat Model

BACKGROUND: Focal and global ischemia was shown to be potent in inducing neurogenesis in the subventricular zone (SVZ). However, it is unknown whether these new neurons can replace those lost following damage, such as intracerebral hemorrhage (ICH). We tested the hypothesis that ICH leads to an increase of cell proliferation in the SVZ and that the new neurons migrate into the damaged area of the hemorrhagic striatum. METHODS: Experimental ICH was induced by an intrastriatal administration of collagenase in adult rats. Proliferating cells were labeled with intraperitoneal injections of 5-bromo-2'-deoxyuridine-5'-monophosphate (BrdU) over 3-day periods before sacrificing the animals, 0, 6, 9, 12 or 15 days after ICH. BrdU+ cells in the dorsolateral SVZ and the striatum were counted in three coronal sections per animal. RESULTS: BrdU+ cells were found in the bilateral SVZs, the third ventricle, and ipsilateral cortex near the needle insertion site. The number of BrdU+ cells in the damaged striatum and the ipsilateral SVZ reached maximum counts 9 days after ICH. The BrdU+ cells were double-labeled with a neuronal marker, neuronal nuclear antigen (NeuN), and a glial marker, the glial fibrillary acidic protein (GFAP), in the hemorrhagic hemisphere. The percentage of BrdU+ cells that expressed NeuN and GFAP was about 13% and about 72%, respectively. CONCLUSIONS: These results suggest new evidence that endogenous neural stem cells are activated in the dorsolateral SVZ after ICH, and that the newly formed cells play a role for ICH-induced neurogenesis in what may be an adaptive process that contributes to recovery after a hemorrhagic stroke.

Neural Stem Cells for Neurological Disorders

Recent progress shows that neurons suitable for transplantation can be generated from neural stem cells (NSCs) in culture, and that the adult brain produces new neurons from its own stem cells in response to injury. In this article, we discuss how the subventricular zone of the forebrain is the most active neurogenetic area and the richest source of NSCs. This review also focuses on the nature and functional properties of NSCs of the adult mammalian brain, and we propose our views on the strategy from bench to the clinic with particular concerns and considerations.

Forntal Lobe Epilepsy Presenting with Blinking and Leg Jerking

Eye blinking is a rare semiology in frontal lobe epilepsy. However, eye blinking with leg jerking as a manifestation of simple partial seizure has not been reported. We report a patient with frontal oligodendroglioma who showed simple partial seizure presenting with eye blinking and leg jerking.