Acute symptomatic hypoglycaemia mimicking ischaemic stroke on imaging:a systemic review

<p>Abstract</p> <p>Background</p> <p>Acute symptomatic hypoglycaemia is a differential diagnosis in patients presenting with stroke-like neurological impairment, but few textbooks describe the full brain imaging appearances. We systematically reviewed the literature to identify how often hypoglycaemia may mimic ischaemic stroke on imaging, common patterns and relationships with hypoglycaemia severity, duration, clinical outcome and add two new cases.</p> <p>Methods</p> <p>We searched EMBASE and Medline databases for papers reporting imaging in adults with symptomatic hypoglycaemia. We analysed the clinical presentation, outcome, brain imaging findings, duration and severity of hypoglycaemia, time course of lesion appearance, including two new cases.</p> <p>Results</p> <p>We found 42 papers describing computed tomography or magnetic resonance imaging in 65 patients, plus our two cases with symptomatic hypoglycaemia. Imaging abnormalities on computed tomography and magnetic resonance were uni or bilateral, cortical or sub-cortical. Thirteen (20%) mimicked cortical or lacunar stroke. Acute lesions had restricted diffusion on magnetic resonance or low attenuation on computed tomography, plus swelling; older lesions showed focal atrophy or disappeared, as with ischaemic stroke. The association between the depth or duration of hypoglycaemia, the severity or extent of neurological deficit, and the imaging abnormalities, was weak.</p> <p>Conclusion</p> <p>Imaging abnormalities in patients with hypoglycaemia are uncommon but very variable, weakly associated with neurological deficit, and about a fifth mimic acute ischaemic stroke. Blood glucose testing should be routine in all patients with acute neurological impairment and hypoglycaemia should be included in the differential diagnosis of imaging appearances in patients presenting with acute stroke.</p

Cis P-tau is induced in clinical and preclinical brain injury and contributes to post-injury sequelae

Traumatic brain injury (TBI) is characterized by acute neurological dysfunction and asso- ciated with the development of chronic traumatic encephalopathy (CTE) and Alzheimer’s disease. We previously showed that cis phosphorylated tau (cis P-tau), but not the trans form, contributes to tau pathology and functional impairment in an animal model of severe TBI. Here we found that in human samples obtained post TBI due to a variety of causes, cis P-tau is induced in cortical axons and cerebrospinal fluid and positively correlates with axonal injury and clinical outcome. Using mouse models of severe or repetitive TBI, we showed that cis P-tau elimination with a specific neutralizing antibody administered immediately or at delayed time points after injury, attenuates the development of neuropathology and brain dysfunction during acute and chronic phases including CTE-like pathology and dysfunction after repetitive TBI. Thus, cis P-tau contributes to short-term and long-term sequelae after TBI, but is effectively neutralized by cis antibody treatment

<i>Cis</i> P-tau is induced in clinical and preclinical brain injury and contributes to post-injury sequelae

Induction of the cis form of phosphorylated tau (cis P-tau) has previously been shown to occur in animal models of traumatic brain injury (TBI), and blocking this form of tau using antibody was beneficial in a rodent model of severe TBI. Here the authors show that cis P-tau induction is a feature of several different forms of TBI in humans, and that administration of cis P-tau targeting antibody to rodents reduces or delays pathological features of TBI

Bare stent-graft technique: A new method of endoluminal vascular reconstruction for the treatment of giant and fusiform aneurysms

We present our initial experience with a newly developed endovascular stent graft technique in the treatment of two patients with giant aneurysms. In both of these patients, surgery and conventional endovascular techniques were likely to fail. The technique resulted in the successful management of the aneurysms in both cases. Our technique is described, and related experiences in the literature are discussed

Spinal dural involvement in Erdheim-Chester disease: MRI findings

There are very few reported cases of Erdheim-Chester disease that document involvement of dura at the level of the spinal cord. Among these reports, we know of no publication that includes detailed MRI findings. To the best of our knowledge, the case presented here is the first published report of this specific manifestation of Erdheim-Chester disease that includes detailed MRI findings in addition to the related history. Spinal manifestations of Erdheim-Chester disease in our patient were at the dorsal and lumbar levels (T1-T6 and T12-T11 respectively). Both epidural and subdural linear large masses were present, causing spinal cord compression at the dorsal level and epidural thickening at the lumbar level

The role of dynamic contrast-enhanced magnetic resonance imaging parameters in head-neck tumors

We evaluated dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) in various head-neck masses, some of which are very rare tumors whose DCE-MRI have not been published to date. The purpose of this study was to investigate DCE-MRI in the differentiation of benign versus malignant lesions and to evaluate the DCE-MRI parameters most predictive for malignancy. Forty-one head-neck tumors including parotid gland tumors in 41 patients were examined at gadolinium-enhanced dynamic MR imaging. There were 26 malignant and 15 benign tumors. DCE-MR images were obtained between four and six minutes. Time-signal intensity curves (TICs) of the tumors on dynamic MR images were plotted, and then time of peak enhancement (Tpeak), and enhancement ratios (ER) with different times (such as ER30 ER60 ER90, ER120, ERmax) were also calculated. Data of the benign and malignant group with head-neck masses were compared by Mann-Whitney U-test. The mean values of time to peak (Tpeak) were found to be significantly shorter for the malignant group than the benign tumors (P&lt;0.05). The mean enhancement rates of malignant lesions were ER30: 60.62±52.62, ER60: 105.65±56.26, ER90: 113.17±45.83, ER120: 116.59±46.75 and ERmax: 128.56±56.51 whereas the mean enhancement rate of benign lesions were ER30: 67.35±60.78, ER60: 79.79±63.33, ER90: 84.53±64.92, ER120: 88.41±67.07 and ERmax: 112.06±66.48. The mean signal intensity values of the 60th second (ER60) and 90th second (ER90) were significantly different from other values for predicting malignancy (P&lt;.05). The parameters obtained from the time-signal intensity curve are important in differentiating benign and malignant enhancing lesions in dynamic head-neck MR imaging. DCE-MRI cannot replace standard MR imaging sequences for evaluating head-neck masses, but in addition to routine MR imaging it will improve differentiation between benign and malignant lesions

MR imaging findings of spinal dural involvement with Wegener granulomatosis

Summary: Involvement of the brain and meninges is rare in cases of Wegener granulomatosis, occurring in 2% to 8% of cases. Meningeal involvement in association with Wegener granulomatosis has scarcely been reported as being confined to the dura mater of brain on images and is thought to represent granulomatous infiltration. There are a few reported cases of Wegener granulomatosis that document involvement of dura at the level of the spinal cord. We present the case of a 52-year-old man with Wegener granulomatosis involving the cervical spinal dura and include detailed MR imaging findings

MRI findings of hypoxic cortical laminar necrosis in a child with hemolytic anemia crisis

We present magnetic resonance imaging findings of a 5-year-old girl who had a rapidly installing hemolytic anemia crisis induced by trimethoprim-sulfomethoxazole, resulting in cerebral anoxia leading to permanent damage. Magnetic Resonance imaging revealed cortical laminar necrosis in arterial border zones in both cerebral hemispheres, ischemic changes in subcortical white matter of left cerebral hemisphere, and in the left putamen. Although cortical laminar necrosis is a classic entity in adulthood related to conditions of energy depletions, there are few reports available in children. A wide review of the literature is also presented