1,721,132 research outputs found
Dissecting vertebrobasilar aneurysm in a child
No full textIntroduction: Paediatric intracranial aneurysms are rare. The pattern of disease is different to that in adults and there is far less literature available. I provide a case as an example of the presentation and progress of a child with a dissecting vertebrobasilar artery aneurysm. Presentation: 11-year-old boy presented to his local hospital with sudden-onset headache, photophobia and vomiting. Bloods and observations were normal - discharged. Symptoms recurred more severely the following day. Managed as meningitis. 4 lumbar punctures were 'bloody' and considered failed. MRI brain 2 days post-admission demonstrated a vertebrobasilar aneurysm. Transferred to the regional Neurosurgical centre. Transfer to Neurosurgical/Neurovascular centre: Cerebral angiography revealed dissecting vertebrobasilar aneurysm (1298910mm). Fusiform component extending beyond AICI/ PICA origins. Wide-necked saccular component. Procedure and progress: Loaded with Aspirin and Clopidogrel. Underwent endovascular procedure the following day - coil embolization, flow-diverting stent to the aneurysm. Ongoing low dose dual anti-platelet therapy. Made an excellent recovery with no neurological deficits. Further imaging - X-ray cervical spine for possible arcuate foramen or atlantoaxial instability, normal. Ultrasound liver/spleen, normal. Discharged home 10 days post-transfer. Patient background: Past medical history - under the GP for 18 months of headaches. Trauma - significant fall from bicycle 2 years before with forced lateral flexion of the neck. Posited that this may have been a contributing factor in aneurysm development. No significant family history. Lifestyle - an active boy, enjoys weightlifting and motocross. Weightlifting also posited as a contributing factor. Conclusions: I provide a case which I hope will raise awareness of paediatric intracranial aneurysms and stimulate discussion concerning their management and aetiology
Papel de la resistencia a la proteina C activada (R-PCA) en el ictus pediatrico
No full textIntroduction. Activated protein C resistance is a recently identified thrombophylic state which results from a mutation in the factor V gene and has been shown to be an important risk factor for peripheral venous thrombosis. We report a case of paediatric stroke in whom we have identified APC resistance. Clinical case. A boy presented acutely at the age of 6 year with a severe right sided headache, vomiting, unsteadiness and drowsiness which worsened over a period of 40 hours. Prior to this episode, he was neurologically and developmentally normal except for occasional headaches. CT showed low attenuation in the left cerebellar hemisphere, and occipital lobe associated with acute hydrocephalus. Excision biopsy of the left cerebellar cortex revealed inflammation and possible infarction. Although he remained in a 'locked-in' state with a flaccid quadriparesis for six months, he improved and was left with a left side hemiplegia, multiple cranial nerve palsies and a visual field defect. He represented at the age of thirteen years with transient ischaemic attacks and was found be heterozygous for the factor V Leiden mutation. Since he has been warfarinised, his symptoms have improved. Conclusions. Although cerebellar stroke in childhood is rare, it has been underdiagnosed in the past. As recurrence is common, patients should be fully investigated and followed up long term. Screening for new factor such as APC- resistance is recommended.</p
Peripheral neuropathy and neuromuscular blockade presenting as prolonged respiratory paralysis following critical illness
No full textWe report two patients who following critical illness presented with generalised paralysis associated with persistent failure to breathe. Both patients eventually recovered and were weaned from the ventilator. The cause of the paralysis was an unusual peripheral neuropathy in the first patient and persistent neuromuscular blockade secondary to vecuronium in the second. It is important to consider a reversible, possibly even iatrogenic, cause of this type of complication.</p
Central nervous system complications and management in sickle cell disease (vol 127, pg 829, 2016)
No full textErratum for DeBaun et al. 127(7):82
Cardiopulmonary bypass temperature and brain function
No full textA debate has emerged in recently published studies about the optimum cardiopulmonary bypass temperature for good neurological outcome - warm vs. cold, i.e. normothermic vs. hypothermic. Although many comparative studies have been performed, the results of these studies are inconclusive and are difficult to interpret. Brain function has been studied in terms of neurological and neuropsychological outcome, protein S100β levels as a marker of brain damage, and cerebral oxygenation using jugular bulb oximetry and near-infrared spectroscopy. The studies produce no conclusive proof of the superiority of warm or cold cardiopulmonary bypass. However, it appears that any degree of bypass hypothermia (< 35 °C) may protect the brain. On the other hand, even a slight increase in bypass temperature to > 37 °C may cause marked brain injury.</p
Brain T2-weighted signal intensity ratio in children with sickle cell disease with and without stroke
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