RESUMEN
BACKGROUND CONTEXT: Gorham disease of massive osteolysis is a spontaneous, idiopathic, and progressive form of primary osteolysis. It has no age, sex, or race predilection, and patients are mostly asymptomatic until severe deformity or pathological fracture becomes evident. PURPOSE: A patient with craniocervical involvement is presented, describing imaging findings with a review of the literature to provide an insight into the disorder. STUDY DESIGN/SETTING: Case report and review of the literature. METHODS: X-ray, computed tomography, and magnetic resonance imaging findings of a patient with findings related to the site of involvement. RESULTS: All images demonstrate osteolysis typically described for the disease. Differential diagnosis and key features are indicated. Operative findings and pathological analysis were also consistent with the findings. Patient's follow-up is also reported. CONCLUSIONS: This benign appearing yet disabling disease may become fatal in relation to the site involved. Acknowledging imaging findings may provide early diagnosis for timely intervention or supportive management.
Asunto(s)
Articulación Atlantoaxoidea/patología , Vértebras Cervicales/patología , Osteólisis Esencial/patología , Adulto , Articulación Atlantoaxoidea/diagnóstico por imagen , Vértebras Cervicales/diagnóstico por imagen , Humanos , Imagen por Resonancia Magnética , Masculino , Osteólisis Esencial/diagnóstico por imagen , Tomografía Computarizada por Rayos XRESUMEN
The neuroprotective effect of alpha lipoic acid (ALA; 100 mg/kg, po), a dithiol antioxidant, on experimentally induced subarachnoid hemorrhage (SAH) was assessed in Wistar albino rats. Neurological examination scores recorded at the 48th h of SAH induction were increased in SAH groups, which were accompanied with significant increases in the formation of reactive oxygen species, DNA fragmentation ratios, malondialdehyde levels and myeloperoxidase activity, while significant decreases in the brain glutathione content and Na(+), K(+)-ATPase activity were observed. On the other hand, ALA treatment reversed all these biochemical indices as well as SAH-induced histopathological alterations. Increased brain edema, impaired blood-brain-barrier permeability and neurological scores were also improved by ALA treatment. The results demonstrate that ALA exerts neuroprotective effects via the enhancement of endogenous antioxidant enzyme activity, the inhibition of neutrophil accumulation and free radical generation, suggesting a therapeutic potential in reducing secondary injury after SAH in patients.
Asunto(s)
Antioxidantes/farmacología , Barrera Hematoencefálica/efectos de los fármacos , Barrera Hematoencefálica/patología , Estrés Oxidativo/efectos de los fármacos , Hemorragia Subaracnoidea/metabolismo , Hemorragia Subaracnoidea/patología , Ácido Tióctico/farmacología , Animales , Arteria Basilar/fisiología , Conducta Animal/efectos de los fármacos , Edema Encefálico/patología , Edema Encefálico/prevención & control , Fragmentación del ADN , Azul de Evans , Glutatión/metabolismo , Luminiscencia , Masculino , Malondialdehído/metabolismo , Fármacos Neuroprotectores/farmacología , Permeabilidad/efectos de los fármacos , Peroxidasa/metabolismo , Ratas , Ratas Wistar , Vasoespasmo Intracraneal/metabolismo , Vasoespasmo Intracraneal/patologíaRESUMEN
Cerebral vasospasm influences morbidity and mortality following subarachnoid haemorrhage (SAH). Inflammation is believed to play a role in post-haemorrhagic vasospasm. Meloxicam is a non-steroidal anti-inflammatory drug. We investigated the effect of meloxicam on a rat femoral artery vasospasm model using the radial wall thickness and cross-sectional lumen area as parameters under light, scanning and transmission electron microscopy examination. Rats were randomly separated into SAH, SAH+ meloxicam and control groups. Rats in the SAH+ meloxicam group were given meloxicam at 2 mg/kg daily for 7 days. Femoral arteries were examined by light microscopy and scanning and transmission electron microscopy, and for morphometric analysis. A statistically significant difference (p<0.001) was detected between the SAH and SAH+ meloxicam groups. Meloxicam treatment reduced ultrastructural and morphometric vasospastic changes. These findings support the hypothesis that inflammation may play a role in the pathophysiologyical pathways of post-haemorrhagic cerebral vasospasm.
Asunto(s)
Antiinflamatorios no Esteroideos/uso terapéutico , Arteria Femoral/efectos de los fármacos , Tiazinas/uso terapéutico , Tiazoles/uso terapéutico , Vasoespasmo Intracraneal/tratamiento farmacológico , Vasoespasmo Intracraneal/patología , Animales , Modelos Animales de Enfermedad , Meloxicam , Distribución Aleatoria , Ratas , Ratas Sprague-Dawley , Hemorragia Subaracnoidea/inducido químicamente , Vasoespasmo Intracraneal/etiologíaRESUMEN
BACKGROUND: Nosocomial meningitis is a rare complication following neurosurgical procedures and is associated with high morbidity and mortality. AIM: The aim of this study was to describe the clinical characteristics and the risk factors associated with mortality in patients who developed nosocomial meningitis following neurosurgical operations. SETTING AND DESIGN: Tertiary care hospital and an observational study. MATERIALS AND METHODS: The study subjects included 2265 patients who underwent various neurosurgical operations during 2003-05. The diagnosis of nosocomial meningitis was based on the Center for Disease Control criteria. STATISTICAL ANALYSIS: It was performed by using Statistical Package for Social Sciences for Windows 10.0 program. RESULTS: The incidence of postoperative nosocomial meningitis was 2.7% (62 episodes in 49 patients among 2265 patients operated). Staphylococcus aureus and Acinetobacter spp. were the most frequently isolated pathogens. Of the 49 with meningitis 20 (40.8%) patients died. In the logistic regression analysis model, Glascow coma scale score less than 10 (Odds Ratio (OR): 19.419, 95% Confidence Interval (CI); 1.637-230.41, P = 0.001), and low cerebrospinal fluid glucose level (< or = 30 mg/ dL) (OR: 10.272, 95% CI; 1.273-82.854, P = 0.002), and presence of concurrent nosocomial infection (OR: 28.744, 95% CI;1.647-501.73, P =0.001) were the independent risk factors associated with mortality. CONCLUSION: The mortality in patients who developed meningitis was high. The high percentage of concurrent nosocomial infections was associated with a high mortality rate which was a serious problem.
Asunto(s)
Meningitis Bacterianas/terapia , Complicaciones Posoperatorias/terapia , Infecciones por Acinetobacter/microbiología , Infecciones por Acinetobacter/mortalidad , Infecciones por Acinetobacter/terapia , Anciano , Femenino , Humanos , Masculino , Meningitis Bacterianas/microbiología , Meningitis Bacterianas/mortalidad , Persona de Mediana Edad , Complicaciones Posoperatorias/microbiología , Complicaciones Posoperatorias/mortalidad , Estudios Prospectivos , Factores de Riesgo , Infecciones Estafilocócicas/microbiología , Infecciones Estafilocócicas/mortalidad , Infecciones Estafilocócicas/terapiaRESUMEN
BACKGROUND: Allopurinol is a xanthine oxidase inhibitor that prevents the generation of free radicals and may play a role in the protection of the cells during cerebral ischemia. METHODS: We evaluated the protective and therapeutic effect of allopurinol on reversible focal cerebral ischemia-reperfusion model in rats. Cerebral blood flow to the left hemisphere of adult Sprague-Dawley rats (n = 40) was temporarily interrupted by middle cerebral artery (MCA) and bilateral common carotid artery (CCA) occlusion for 3 hours in 5 groups of 8 rats each. Allopurinol (50 mg/kg) was given intraperitoneally 2 hours and immediately before ischemia and immediately and 2 hours after reperfusion in 4 different groups of rats, respectively. Animals were kept alive 24 hours after reperfusion. After sacrifice, infarction volumes and ratios of the brain slices were calculated, and the results were compared with those of the control group. RESULTS: The difference between the allopurinol-administered group and the control group 2 hours before for both infarction volumes and infarction ratios achieved statistical significance. Regarding the allopurinol-administered group immediately before ischemia, infarction volumes and infarction ratios were diminished, but there was no statistically significant difference. The difference between allopurinol-administered and control group immediately after and 2 hours after reperfusion for both infarction volumes and infarction ratios achieved no statistical significance. CONCLUSION: This study showed that allopurinol has a protective effect, but not a therapeutic effect, on cerebral ischemia.
Asunto(s)
Alopurinol/uso terapéutico , Isquemia Encefálica/prevención & control , Inhibidores Enzimáticos/uso terapéutico , Daño por Reperfusión/prevención & control , Xantina Oxidasa/fisiología , Alopurinol/administración & dosificación , Animales , Isquemia Encefálica/patología , Isquemia Encefálica/fisiopatología , Modelos Animales de Enfermedad , Esquema de Medicación , Inhibidores Enzimáticos/administración & dosificación , Masculino , Ratas , Ratas Sprague-Dawley , Daño por Reperfusión/patología , Daño por Reperfusión/fisiopatología , Xantina Oxidasa/antagonistas & inhibidoresRESUMEN
BACKGROUND: Antifibrinolytic therapy is effective in preventing rebleeding in cases of aneurysmal subarachnoid hemorrhage (SAH). The major disadvantage of this therapy is the increase in ischemic complications, which is supposed to be due to cerebral vasospasm. In this study the effect of short-term antifibrinolytic therapy on arterial vessel narrowing after SAH was investigated utilizing the rat femoral artery vasospasm model. METHODS: Twenty-four rats were divided into four groups of six animals each. Autologous blood (0.1 mL) was applied to the 1-cm segment of right femoral artery wrapped with a silicone cuff. In Group 1 the animals did not receive any treatment. In Groups 2, 3, and 4 150 mg/kg tranexamic acid (AMCA) was given orally for 3, 5, or 7 days respectively, starting from postoperative day 1. A 1 cm segment of each femoral artery was harvested on the 8(th) postoperative day. Morphologic analyses were performed using the parameters, radial wall thickness and cross luminal area under the light microscope. In addition, two samples from each group were examined by transmission electron microscope (TEM) to confirm the morphologic changes. RESULTS: There was a gradual decrease in cross luminal area and gradual increase in vessel wall thickness directly proportional with time. However, the vasospastic changes that occurred in Group 2 (received AMCA for 3 days) were not significantly different from those of Group 1 (nontreated). CONCLUSION: It was concluded that antifibrinolytic treatment for the first 3 days may prove useful in cases of clinical aneurysmal SAH. However, if this treatment is used for more than 3 days, arterial vessel narrowing is significantly increased.