Fetal-type variant of the posterior cerebral artery and concurrent bilateral cerebral infarctions in a Korean male cadaver / Variante de tipo fetal de la arteria cerebral posterior e infartos cerebrales bilaterales concurrentes en un cadáver masculino coreano

SUMMARY: Fetal-type variant of the posterior cerebral artery is a relatively common variant of the cerebral arterial circle (circle of Willis), but concurrent cerebral pathologies have not been well reported. We describe a case of fetal-type variant of the posterior cerebral artery and concurrent bilateral cerebral infarctions in the territories of the middle cerebral artery in a 78-year-old Korean male cadaver. Fetal-type variant of the posterior cerebral artery was found the right cerebral arterial circle, arose from the internal carotid artery with larger diameter than the pre-communicating segment from the basilar artery. Histopathological examination revealed that left supramarginal gyrus and right infraparietal lobule showed characteristic cerebral infarctions with chronological changes, respectively. Knowledge on the variation in the posterior cerebral artery combined with clinical features including cerebral infarction plays a pivotal role to anatomists and clinicians.

RESUMEN: La variante de tipo fetal de la arteria cerebral posterior es una variante relativamente común del círculo arterial cerebral (polígono de Willis) de arterial cerebral, pero las patologías cerebrales concurrentes no han sido bien informadas. Describimos un caso de variante de tipo fetal de la arteria cerebral posterior e infartos cerebrales bilaterales concurrentes en los territorios de la arteria cerebral media en un cadáver masculino coreano de 78 años. La variante de tipo fetal de la arteria cerebral posterior se encontró en la parte de derecha del círculo arterial cerebral, surgido de la arteria carótida interna con mayor diámetro que el segmento precomunicante de la arteria basilar. El examen histopatológico reveló que el giro supramarginal izquierdo y el lóbulo infraparietal derecho mostraban infartos cerebrales característicos con cambios cronológicos, respectivamente. El conocimiento sobre la variación en la arteria cerebral posterior combinado con las características clínicas, incluido el infarto cerebral es fundamental para los anatomistas y los médicos.

Evaluation of Engraftment of Superparamagnetic Iron Oxide-Labeled Mesenchymal Stem Cells Using Three-Dimensional Reconstruction of Magnetic Resonance Imaging in Photothrombotic Cerebral Infarction Models of Rats

OBJECTIVE: To evaluate engraftment by visualizing the location of human bone marrow-derived mesenchymal stem cells (hBM-MSCs) three-dimensionally in photothrombotic cerebral infarction (PTCI) models of rats. MATERIALS AND METHODS: Magnetic resonance imaging (MRI) of an agarose block containing superparamagnetic iron oxide (SPIO)-labeled hBM-MSCs was performed using a 3.0-T MRI, T2-(T2WI), T2*-(T2*WI), and susceptibility-weighted images (SWI). PTCI was induced in 6 rats, and 2.5 x 10(5) SPIO-labeled hBM-MSCs were infused through the ipsilateral internal carotid artery (ICA group) or tail vein (IV group). MRI was performed on days 1, 3, 7, and 14 after stem cell injection. Dark signal regions were confirmed using histology. Three-dimensional MRI reconstruction was performed using the clinical workflow solution to evaluate the engraftment of hBM-MSCs. Volumetric analysis of the engraftment was also performed. RESULTS: The volumes of SPIO-labeled hBM-MSCs in the phantom MRI were 129.3, 68.4, and 25.9 microL using SWI, T2*WI, and T2WI, respectively. SPIO-labeled hBM-MSCs appeared on day 1 after injection, encircling the cerebral infarction from the ventral side. Dark signal regions matched iron positive cells and human origin (positive) cells. The volume of the engraftment was larger in the ICA group on days 1, 3, and 7, after stem cell injection (p < 0.05 on SWI). SWI was the most sensitive MRI pulse sequence (p < 0.05). The volume of infarction decreased until day 14. CONCLUSION: The engraftment of SPIO-labeled hBM-MSCs can be visualized and evaluated three-dimensionally in PTCI models of rats. The engraftment volume was larger in the ICA group than IV group on early stage within one week.

A forced running wheel system with a microcontroller that provides high-intensity exercise training in an animal ischemic stroke model

We developed a forced non-electric-shock running wheel (FNESRW) system that provides rats with high-intensity exercise training using automatic exercise training patterns that are controlled by a microcontroller. The proposed system successfully makes a breakthrough in the traditional motorized running wheel to allow rats to perform high-intensity training and to enable comparisons with the treadmill at the same exercise intensity without any electric shock. A polyvinyl chloride runway with a rough rubber surface was coated on the periphery of the wheel so as to permit automatic acceleration training, and which allowed the rats to run consistently at high speeds (30 m/min for 1 h). An animal ischemic stroke model was used to validate the proposed system. FNESRW, treadmill, control, and sham groups were studied. The FNESRW and treadmill groups underwent 3 weeks of endurance running training. After 3 weeks, the experiments of middle cerebral artery occlusion, the modified neurological severity score (mNSS), an inclined plane test, and triphenyltetrazolium chloride were performed to evaluate the effectiveness of the proposed platform. The proposed platform showed that enhancement of motor function, mNSS, and infarct volumes was significantly stronger in the FNESRW group than the control group (P<0.05) and similar to the treadmill group. The experimental data demonstrated that the proposed platform can be applied to test the benefit of exercise-preconditioning-induced neuroprotection using the animal stroke model. Additional advantages of the FNESRW system include stand-alone capability, independence of subjective human adjustment, and ease of use.

Forensic clinical analysis on 25 cases of traumatic cerebral infarction / 法医学杂志

OBJECTIVE@#To investigate characteristics of forensic clinical identification on traumatic cerebral infarction(TCI).@*METHODS@#Twenty-five cases of TCI were analyzed retrospectively, including the general situation, location of infarction and clinical feature.@*RESULTS@#TCI occurred primarily in children and elderly. All the cases had definite cerebral trauma which was located mainly in the regions of basal ganglia-internal capsule, frontal, temporal and parietal cerebral cortex.@*CONCLUSION@#The consequence of TCI has direct correlation with location of cerebral infarction. More attention should be paid to this issue in forensic practice.

Contribution of Nitric Oxide Synthase [NOS] Activity in Blood-Brain Barrier Disruption and Edema after Acute Ischemia/ Reperfusion in Aortic Coarctation-Induced Hypertensive Rats

Nitric oxide synthase [NOS] activity is increased during hypertension and cerebral ischemia. NOS inactivation reduces stroke-induced cerebral injuries, but little is known about its role in blood-brain barrier [BBB] disruption and cerebral edema formation during stroke in acute hypertension. Here, we investigated the role of NOS inhibition in progression of edema formation and BBB disruptions provoked by ischemia/reperfusion injuries in acute hypertensive rats. Rats were made acutely hypertensive by aortic coarctation. After 7 days, the rats were randomly selected for the recording of carotid artery pressure, or regional cerebral blood flow [rCBF] using laser Doppler. Ishcemia induced by 60-min middle cerebral artery occlusion [MCAO], followed by 12-h reperfusion. A single i.p. dose of L-NAME [1 mg/kg] was injected before MCAO. After evaluation of neurological disabilities, rats were slaughtered under deep anesthesia to assess cerebral infarction volume, edema, or BBB disruption. A 75-85% reduction in rCBF was occurred during MCAO which returned to pre-occluded levels during reperfusion. Profound neurological disabilities were evidenced after MCAO alongside with severe cerebral infarctions [628 +/- 98 mm[3]], considerable edema [4.05 +/- 0.52%] and extensive BBB disruptions [Evans blue extravasation, 8.46 +/- 2.03 [microg/g]. L-NAME drastically improved neurological disabilities, diminished cerebral infarction [264 +/- 46 mm[3]], reduced edema [1.49 +/- 0.47%] and BBB disruption [2.93 +/- 0.66 microg/g]. The harmful actions of NOS activity on cerebral microvascular integrity are intensified by ischemia/reperfusion injuries during acute hypertension. NOS inactivation by L-NAME preserved this integrity and diminished cerebral edema

Nova abordagem das vertigens: correlação clínica / New boarding of the vertigo: clinical correlation

Este artigo consiste em uma revisão ampla sobre vertigem e seu diagnóstico diferencial.

This article consists on a comprehensive revision about vertigo and its differential diagnosis.

Granulocyte Stimulating Factor Attenuates Hypoxic-ischemic Brain Injury by Inhibiting Apoptosis in Neonatal Rats

PURPOSE: This study was undertaken to determine the neuroprotective effect of granulocyte stimulating factor (G-CSF) on neonatal hypoxic-ischemic brain injury. MATERIALS AND METHODS: Seven-day-old male newborn rat pups were subjected to 110 minutes of 8% oxygen following a unilateral carotid artery ligation. Apoptosis was identified by performing terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining and flow cytometry with a combination of fluorescinated annexin V and propidium iodide (PI) and JC-1 (5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolyl-carbocyanine iodide). The extent of cerebral infarction was evaluated at 2 weeks after recovery. RESULTS: With a single dose (50microgram/kg) of G-CSF treatment immediately after hypoxic-ischemic insult, hypoxia-ischemia induced increase in TUNEL-positive cells, annexinV+/PI- and JC-1 positive apoptotic cells in the ipsilateral cerebral cortex was significantly reduced at 24 hours, measured by flow cytometry, and the extent of cerebral infarction at 2 weeks after recovery was also significantly attenuated compared to the hypoxia-ischemia control group. CONCLUSION: Our data suggest that G-CSF is neuroprotective by inhibiting apoptosis, thereby reducing the ensuing cerebral infarction in a newborn rat pup model of cerebral hypoxia-ischemia (HI).

Functional recovery in ischemic stroke.

Functional outcome at three months was studied in 72 patients with ischemic stroke. The Canadian Neurological Scale was used to assess the severity of stroke at admission and functional outcome at 3 months was assessed using modified Rankin scale. The size and site of the infarct was noted from the initial CT. Risk factors like hypertension, diabetes, and serum cholesterol were analyzed. Initial neurological scoring at admission, and size and site of the infarct were significantly associated with functional recovery at 3 months.

Determinaçäo volumétrica do infarto cerebral na fase aguda usando tomografia computadorizada de crânio sem contraste: estudo comparando três métodos / Volumetric determination of cerebral infarction in the acute phase using skull computed tomography without contrast: comparative study of 3 methods

A determinaçäo volumétrica do infarto cerebral agudo (IC) tem importantes implicaçöes prognósticas e terapêuticas. Foram estudadas e comparadas três técnicas de determinaçäo do volume do IC agudo (técnica computadorizada, planimetria linear e fórmula A.B.C/2) em 27 doentes usando imagens de TC sem contraste realizadas à internaçäo (primeiras 48 horas de evoluçäo). As aferiçöes foram feitas por dois observadores independentes, sendo determinado o coeficiente de correlaçäo intraclasse (CCI). Os três métodos mostraram alta inter-relaçäo para determinaçäo do volume do IC. A planimetria linear e a fórmula A.B.C/2 exibiram alto grau de correlaçäo com o método computadorizado, com CCIs de 0,94 a 0,95 e 0,835 a 0,90, respectivamente. A planimetria linear e a fórmula referida também apresentaram alta inter-relaçäo, com CCI entre 0,97 e 0,99. O método computadorizado de aferiçäo deve ser recomendado onde disponível. A planimetria linear e a fórmula A.B.C/2 também exibem, entretanto, alta confiabilidade. A fórmula A.B.C/2 pode ser utilizada rotineiramente na determinaçäo volumétrica do IC por ser método de baixo custo, rápida realizaçäo, larga aplicabilidade e grande utilidade potencial

Effectiveness of propofol pretreatment on the extent of deranged cerebral mitochondrial oxidative enzyme system after incomplete forebrain ischemia/reperfusion in rats

It has been suggested that propofol has the protective effect on cerebral ischemia-reperfusion injury. The aim of this study is to evaluate the effect of propofol pretreatment on incomplete forebrain ischemia-reperfusion injury in rats. Thirty Sprague-Dawley rats were anesthetized with isoflurane in oxygen and randomly allocated into propofol group (n=13) and saline group (n=17). In propofol group, propofol was pretreated in a step-down scheme before inducing forebrain ischemia by occlusion of both common carotid arteries and arterial hypotension. After ischemia (20 min) and reperfusion (30 min), rats were decapitated. Brain was sliced to obtain coronal slices of 4-12 mm from frontal pole, which were reacted with 2% 2,3,5-triphenyl-2H-tetrazolium chloride (TTC) for 10 min to differentiate the damaged tissues from normal tissues. Median (interquartile range) values of the average percent infarct area were 0.0 (8.6)% and 20.1 (41.2)% in propofol and saline groups, respectively. There was significant difference between the groups. In conclusion, propofol may have a protective effect on incomplete forebrain ischemia-reperfusion injury.

The effects of peripheral leukocytes on the hippocampal neuronal changes in transient global ischemia and unilateral cerebral hemispheric infarction

The participation of activated leukocytes and subsequent production of chemical mediators has been well accepted in the pathophysiology of hypoxic-ischemic injury. This study was performed to see the effects of leukocytes on hippocampal neuronal damage in transient global ischemia induced by 10-min occlusion of bilateral common carotid arteries (CCAs) with reperfusion for various times, and in complete unilateral ischemia induced by 24-hr ligation of left CCA. Leukopenia was induced by intraperitoneal injection of cyclophosphamide for 4 days. The results showed that hippocampal neuronal damages were worse at 6-hr reperfusion in leukopenic experimental group than in the control group. In comparison, 24-hr and 3-day reperfusion leukopenic groups showed less numbers of damaged neurons and milder changes. The 5-day reperfusion group showed inconsistent changes. Unilateral CCA occlusion showed extensive infarction in 83.3% of gerbils in the control group, compared to 25% of gerbils in the experimental group (p<0.05). These results strongly suggest that the number of peripheral leukocytes were closely related to the development of delayed neuronal damage of hippocampus in transient global ischemia and the incidence of infarction induced by 24-hr unilateral CCA ligation.

Non-typhoid Salmonella meningitis complicated by a infarction of basal ganglia

A previously healthy 16-month-old Korean girl with symptoms of fever, vomiting, and generalized tonic seizure was diagnosed to have Group D non-typhoid Salmonella meningitis. The patient was treated with ceftriaxone (100 mg/kg/day) and amikin (22.5 mg/kg/day) initially and ciprofloxacin (30 mg/kg/day) was added later because of clinical deterioration and disseminated intravascular coagulation. Brain CT performed on the second day showed a well-demarcated low density lesion in the right lentiform nucleus and both caudate nuclei, without evidence of increased intracranial pressure. MRI performed on the 11th day confirmed CT scan findings as well as right subdural fluid collection, brain atrophy, and ventriculomegaly. She underwent subdural drainage and later ventriculo-peritoneal shunt operation. Despite receiving intensive treatment, she still has severe neurologic sequelae. Our case shows that infarctions of basal ganglia and thalami are not specific for tuberculous meningitis and that meningitis complicated by infarction is indicative of grave prognosis.

Síndrome de Sneddon: relato de três casos / Sneddon's syndrome: report of 3 cases

Descrita por Sneddon (1965) a síndrome consiste na ocorrência de acidente vascular encefálico (AVE) isquêmico em pacientes com livedo reticular. Trata-se de doença vascular sistêmica de causa desconhecida, em que há comprometimento de artérias de médio e pequeno calibres. Pode haver positividade dos anticorpos antifosfolípides. Säo apresentados três casos desta entidade, todos do sexo masculino com 7, 16 e 54 anos de idade. Em todos a instalaçäo do quadro deu-se por convulsöes focais seguidas de hemiparesia ou paralisia labio-glossofaríngea. Os pacientes näo tiveram outras manifestaçöes neurológicas em 2 anos de acompanhamento. A investigaçäo laboratorial demonstrou presença de anticorpos antifosfolípides e anticardiolipina em 1 caso. A investigaçäo neuro-radiológica forneceu os seguintes resultados: TCC e RM com infarto nos 3 casos, e angiografia com obstruçäo de vasos de médio e pequeno calibre. A síndrome de Sneddon näo parece ser täo rara e deve fazer parte de protocolos de investigaçäo de AVE, especialmente em grupos mais jovens

Fibrolamellar carcinoma of the liver--an unusual presentation.

Non-bacterial thrombotic endocarditis was found at autopsy in a 17 year old male patient of fibrolamellar type of hepatocellular carcinoma with pericardial metastases. This had resulted in multiple embolic cerebral infarcts with long standing hemiplegia and later death due to acute left ventricular failure.

Porencephalic cyst.

Porencephalic cyst with seizure is rare. It represents a part of diffuse cerebral maldevelopment. Porencephaly occurs as a result of imbalance between brain growth and its vascular supply and is picked up by CT scan.

Pathogenesis of small deep cerebral infarcts

Datos recientes sugieren que el impacto de la Hipertensión Arterial (HTA) ha sido probablemente exagerado y el rol de la enfermedad cardíaca y de la aterosclerosis de grandes vasos subestimado respecto de la patogenia de los pequeños (<1.5 cm) infartos de las arterias penetrantes profundas. En otras palabras, se puede decir que una arteriolopatía primaria local es menos importante de lo que se pensaba en el pasado, y que la embolia puede tener un rol más considerable que el que se le atribuía anteriormente.El tamaño máximo aceptado para un infarto pequeño (o sea "lacunar") ha sido fijado en 1.5 cm. Dentro de ese limite, parece apropiado considerar que las lagunas muy pequeñas (<0,5 cm) --habitualmente asintomáticas--, tienen una fuerte asociación con la arteriolopatia hipertensiva, pero las mas grandes y sintomáticas (0.5-1.5 cm) tienen un origen mucho más diverso. Como ni los sindromes clínicos ni los estudios de TC o RMI diferencian las causas de los diferentes infartos lacunares, parece aconsejable la búsqueda sistemática de enfermedad asociada de grandes vasos (estudios arteriales no invasivos), así como de posible embolia cardiogénica (ECG, ecocardiografía y Holter de ser necesario), tanto como en los infartos cerebrales