Bilateral oligodendroglial hamartomas: A rare cause of drug-resistant epilepsy in a pediatric patient.

Intractable or drug-resistant seizures in pediatric patients are often secondary to cortical malformations, hamartomas, or mass lesions. Various subtypes of intracerebral hamartomas, associated with seizure disorders, have been described. In this report, we describe a subtype of intracerebral hamartoma associated with intractable epilepsy in a 10-year-old patient. Initial MR imaging demonstrated a mildly expansile, T2/FLAIR hyperintense, T1 isointense, nonenhancing lesion with blurring of the gray-white junction in the left amygdala. Surgical resection was performed, and pathology confirmed oligodendroglial hamartoma. Patient's seizures recurred after a two-year interval with imaging demonstrating a similar lesion in the right amygdala which in retrospect was also seen on multiple imaging studies. This case report demonstrates the importance of recognizing oligodendroglial hamartomas as a cause of intractable seizures given the imaging findings, distinguishing it from ganglioglioma, dysembryoplastic neuroepithelial tumor, and oligodendroglioma, and the importance of closely looking/searching for contralateral lesions, which has important therapeutic and prognostic implications.

Neuroimaging of Pediatric Arteriopathies.

Pediatric arteriopathies are increasingly recognized in school-aged children with a variety of presenting symptoms ranging from headache, seizures, encephalopathy, and neuropsychiatric symptoms as well as focal neurologic deficits due to acute ischemic strokes. However, unlike the adult stroke population, there are differences in the clinical manifestations, the stroke mechanism, and risk factors in pediatric ischemic stroke. There has been increasing awareness and recognition of pediatric cerebral arteriopathies as a predominant stroke etiology. Prompt diagnosis of arteriopathies is essential to limit injury and prevent recurrent stroke. Based on predominant vessels involved and clinical symptoms, these arteriopathies can be broadly divided into two categories: large-medium size arteriopathies and small vessel arteriopathies. Each category can be further divided into inflammatory and noninflammatory according to their etiologies. The ability to distinguish between inflammatory and noninflammatory etiologies carries major prognostic implications for acute management and secondary stroke prevention as well as screening for systemic complications and counseling.

Pediatric Congenital Cerebrovascular Anomalies.

Congenital cerebrovascular anomalies in the pediatric age group are myriad with diverse etiologies. The purpose of this paper is to provide an imaging overview of congenital vascular malformations and vascular tumors, as these conditions are varied and the characteristic vascular abnormality may even suggest the underlying systemic condition in helping to guide further management. For example, the identification of an arterial anomaly such as agenesis/hypoplasia/duplication may warrant further evaluation for an associated syndrome. Recognition of other pertinent findings, such as persistent carotid-vertebrobasilar anastomoses for instance, would be particularly important for the planning of potential embolization/coiling of associated vascular malformation and/or aneurysm. Awareness of congenital dural sinus anomalies, including hypoplasia, aplasia, and or duplication, prevents the incorrect or overdiagnosis of sinus thrombosis. Moreover, multiple developmental venous anomalies in a patient may require further investigation for its familial association. In a similar context, there may be familial association with multiple cavernous malformations and children with central nervous system vascular malformations may have an association with other vascular conditions, eg, hereditary hemorrhagic telangiectasia, etc. An accurate description of vascular lesions is critical for understanding the natural history of the disease process and ultimately for guiding treatment. An important example of this includes Sturge-Weber syndrome, which is often incorrectly viewed as an arteriovenous malformation, but actually a type of venous malformation. Another example which is important to recognize includes the differentiation between an infantile hemangioma and a vascular malformation, particularly as the course of the pathology and the treatment is so different between the two.

The "pool sign" of metastatic adenocarcinoma.

The differential of a newly discovered solitary intracranial mass is a primary intracranial neoplasm and metastatic disease. Differentiating between the two entities on imaging is difficult, though there are clues on conventional imaging that suggest one over the other. The purpose of this article is to describe a new imaging finding on T2-weighted imaging, the "pool sign," that may be specific for metastatic adenocarcinomas and can help differentiate a solitary metastasis from a primary CNS neoplasm. We present a series of four patients with initial magnetic resonance imaging of a solitary intracranial mass demonstrating the "pool sign," and therefore predicted to be metastatic adenocarcinoma. All of these cases were confirmed to be metastatic adenocarcinoma on pathology.

Beyond stroke-uncommon causes of diffusion restriction in the basal ganglia.

In the emergency setting, a regional area of restricted diffusion involving the basal ganglia typically represents an acute infarct due to small vessel occlusion. However, it is important to consider additional differentials, specifically systemic causes. This article will review anatomy of the basal ganglia and pertinent associated vasculature, followed by other entities that can be a cause of restricted diffusion. These include hemolytic uremic syndrome, hypereosinophilic syndrome, fat embolism, meningitis, and hypoxic-ischemic injury. It is important to recognize presenting findings in these conditions, as the radiologist may be the first to give an accurate diagnosis or prompt additional testing.

Toxins in Brain! Magnetic Resonance (MR) Imaging of Toxic Leukoencephalopathy - A Pictorial Essay.

Toxic leukoencephalopathy results from damage to the white matter caused by various toxins. It manifests itself as white matter signal abnormalities with or without the presence of restricted diffusion. These changes are often reversible if the insulting agent is removed early, with the exception of posthypoxic leukoencephalopathy that can manifest itself 1-2 weeks after the initial insult. However, many other potential causes of white matter signal abnormalities can mimic the changes of toxic leukoencephalopathy. Thus, familiarity with the causes, clinical presentation and particularly imaging findings of toxic leukoencephalopathy is critical for early treatment and improved prognosis. The purpose of this pictorial essay is to familiarize the reader with the various causes of toxic leukoencephalopathy along with its differential diagnoses and mimics.

Magnetic resonance imaging of sellar and juxtasellar abnormalities in the paediatric population: an imaging review.

The sellar and juxtasellar regions in the paediatric population are complex both anatomically and pathologically, with magnetic resonance imaging (MRI) being the "gold standard" imaging modality due to the high contrast of detail. Assessment requires a detailed understanding of the anatomy, embryology, pathophysiology and normal signal characteristics of the pituitary gland and surrounding structures in order to appropriately characterise abnormalities. This article aims to provide an overview of the imaging characteristics of developmental/congenital and acquired disease processes which affect the sellar and juxtasellar region in the paediatric population. Main Messages • The sellar region is anatomically complex and covers a wide pathology spectrum. • MRI is the key imaging modality to assess sellar and juxtasellar pathology. • Numerous developmental anomalies may not be discovered until adulthood. • Knowledge of pathology alerts and guides the clinician towards appropriate management.

Idiopathic Intracranial Hypertension: Diagnostic Accuracy of the Transverse Dural Venous Sinus Attenuation on CT Scans.

Idiopathic intracranial hypertension (IIH) is a clinical disorder of unknown etiology. It may exhibit several non-specific imaging findings. We observed that patients with intracranial hypertension demonstrate intracranial venous sinus attenuation with changes in the contour and caliber of the distal transverse sinus. This can be seen on routine non-contrast sagittal reformatted CT images of the brain. We have termed this the venous attenuation sign (VAS). This study evaluated the VAS as a marker for IIH assessing the transverse sinuses on sagittal reformatted non-contrast CT for the presence of a VAS in 25 patients with IIH and 24 control patients. Scans were independently assessed in a blinded fashion by three readers. The readers identified the VAS in 96% of patients with IIH; 83.3% of the control patients were negative for VAS. Our study supports the VAS as an additional imaging marker which may be incorporated into the evaluation of patients suspected to have this condition.

CT perfusion in acute stroke: know the mimics, potential pitfalls, artifacts, and technical errors.

The CT perfusion (CTP) imaging of brain has been established as a clinically useful tool in multimodality imaging of acute stroke. All abnormalities seen on perfusion CT are not specifically related to acute infarct. There are many neurologic diseases causing symptoms simulating cerebrovascular disease produce an alteration of brain perfusion and thus can result in perfusion CT abnormalities. There are many pitfalls and artifacts in acquiring the data, calculation of maps and choosing arterial input function. We analyze and classify all these aspects, to allow the technician and the radiologist to know exactly what to avoid and what to choose, and we indicate the way to improve the quality of examination. The knowledge of mimics and pitfalls in acute stroke imaging can be helpful in accurate interpretation of these examinations.

Role of noncontrast head CT in the assessment of vascular abnormalities in the emergency room.

Noncontrast CT of the head is a widely used noninvasive investigation for a variety of acute and chronic neurological conditions. Since CT head without contrast is usually the first and often the only investigation in the emergency room for many neurological symptoms, it is imperative to detect subtle vascular changes, which in many patients can be life-saving. The vascular abnormalities may present with increased density and/or size of the vessels, filling defects, and be associated with parenchymal and bony changes. In this article, we present examples of several vascular pathologies which can be identified on the noncontrast CT of the head, and learn imaging and interpretation techniques to help recognize what often are nebulous changes. While some of the findings are diagnostic by themselves and others subtle, any suspicious abnormality should be followed with dedicated vascular imaging such as CT/MR angiogram, venogram, or catheter angiogram for confirmation and better characterization.

Lesions masquerading as acute stroke.

Rapid and accurate recognition of lesions masquerading as acute stroke is important. Any incorrect or delayed diagnosis of stroke mimics will not only increase the risk of being exposed to unnecessary and possibly dangerous interventional therapies, but will also delay proper treatment. In this article, written from a neuroradiologist's perspective, we classified these lesions masquerading as acute stroke into three groups: lesions that may have "normal imaging," lesions that are "symptom mimics" but on imaging clearly not a stroke, and lesions that are "symptom and imaging mimics" with imaging findings similar to stroke. We focused the review on neuroimaging findings of the latter two groups ending with a suggestion for a diagnostic approach in the form of an algorithm.

Your brain on drugs: imaging of drug-related changes in the central nervous system.

Drug abuse is a substantial problem in society today and is associated with significant morbidity and mortality. Various drugs are associated with serious complications affecting the brain, and it is critical to recognize the imaging findings of these complications to provide prompt medical management. The central nervous system (CNS) is a target organ for drugs of abuse as well as specific prescribed medications. Drugs of abuse affecting the CNS include cocaine, heroin, alcohol, amphetamines, toluene, and cannabis. Prescribed medications or medical therapies that can affect the CNS include immunosuppressants, antiepileptics, nitrous oxide, and total parenteral nutrition. The CNS complications of these drugs include neurovascular complications, encephalopathy, atrophy, infection, changes in the corpus callosum, and other miscellaneous changes. Imaging abnormalities indicative of these complications can be appreciated at both magnetic resonance (MR) imaging and computed tomography (CT). It is critical for radiologists to recognize complications related to drugs of abuse as well as iatrogenic effects of various medications. Therefore, diagnostic imaging modalities such as MR imaging and CT can play a pivotal role in the recognition and timely management of drug-related complications in the CNS.

Magnetic resonance imaging of neurosarcoidosis.

Neurosarcoidosis is an uncommon condition with protean manifestations. Magnetic resonance imaging (MRI) is often used in the diagnostic evaluation and follow-up of patients with neurosarcoidosis. Therefore, familiarity with the variety of MRI appearances is important. In this pictorial essay, the range of possible patterns of involvement in neurosarcoidosis are depicted and discussed. These include intracranial and spine leptomeningeal involvement, cortical and cerebral white matter lesions, corpus callosum involvement, sellar and suprasellar involvement, periventricular involvement, cranial nerve involvement, cavernous sinus involvement, hydrocephalus, dural involvement, ischemic lesions, perivascular involvement, orbit lesions, osseous involvement, nerve root involvement, and spinal cord intramedullary involvement. Differential diagnoses for each pattern of involvement of neurosarcoidosis are also provided.

Border zone infarcts: pathophysiologic and imaging characteristics.

Border zone or watershed infarcts are ischemic lesions that occur in characteristic locations at the junction between two main arterial territories. These lesions constitute approximately 10% of all brain infarcts and are well described in the literature. Their pathophysiology has not yet been fully elucidated, but a commonly accepted hypothesis holds that decreased perfusion in the distal regions of the vascular territories leaves them vulnerable to infarction. Two types of border zone infarcts are recognized: external (cortical) and internal (subcortical). To select the most appropriate methods for managing these infarcts, it is important to understand the underlying causal mechanisms. Internal border zone infarcts are caused mainly by hemodynamic compromise, whereas external border zone infarcts are believed to result from embolism but not always with associated hypoperfusion. Various imaging modalities have been used to determine the presence and extent of hemodynamic compromise or misery perfusion in association with border zone infarcts, and some findings (eg, multiple small internal infarcts) have proved to be independent predictors of subsequent ischemic stroke. A combination of several advanced techniques (eg, diffusion and perfusion magnetic resonance imaging and computed tomography, positron emission tomography, transcranial Doppler ultrasonography) can be useful for identifying the pathophysiologic process, making an early clinical diagnosis, guiding management, and predicting the outcome.