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A case of Rasmussen's encephalitis is reviewed. Focal seizures and hemiparesis in a 5-year-old child progressed over a period of 2 1/2 years. Neuroimaging findings showed progressive atrophy of the right temporal lobe. The diagnosis of this syndrome is possible using a combination of the clinical symptoms and neuroimaging findings.
UNLABELLED: FUNCTIONAL NEUROIMAGING: Although the primary imaging modality in the management of epilepsy is magnetic resonance imaging MRI, functional neuroimaging with positron-emission tomography (PET) and single photon emission computed tomography (SPECT) often provides complementary information and, in a number of situations, provides unique information that cannot be obtained with MRI. The most commonly used PET tracers used for epilepsy evaluation are 2-deoxy-2-[(18)F]fluoro-D: -glucose (FDG) and [(11)C]flumazenil (FMZ). Recently, interictal PET with alpha-[(11)C]methyl-L: -tryptophan was found to be highly specific for the epileptic focus and can differentiate between epileptogenic and nonepileptogenic lesions in the same patient (e.g., in patients with tuberous sclerosis). DISCUSSION: In this review, we discuss clinical applications of these three PET tracers in drug-resistant temporal and extratemporal lobe epilepsy, selected epilepsy syndromes of childhood, lesional and nonlesional epilepsy, and the challenges of imaging secondary epileptic foci. A brief discussion of SPECT applications in epilepsy is also included. With further development of new tracers highly sensitive and specific for epileptogenic brain regions, the presurgical evaluation of refractory epilepsy will be greatly facilitated. Approximately 0.5 to 1.0% of the population suffer from epilepsy, of which 15-20% are intractable. Infants and children, whose seizures have a focal onset are refractory to anticonvulsants and are prolonged, tend to have the worst cognitive outcome [Meador KJ, Neurology 58 (Suppl 5):S21-S26, 2002]. Seizures themselves affect the developing brain and contribute to an adverse neurologic outcome (Holmes, Pediatric Neurology 33:1-110, 2005). CONCLUSION: Therefore, in treating children with intractable epilepsy, it is important to consider seizure control and to give allowance for normal cognitive development.
In order to analyze the surgical outcome according to clinical characteristics and to evaluate the correlation between clinical improvement and neuroimaging changes, we retrospectively reviewed 32 children who had undergone endoscopic III ventriculostomy (ETV) from February 1994 to May 1998. There were 15 boys and 17 girls, with a mean age of 5.2 years (range: 1 month to 13 years). The etiology of the hydrocephalus was primary aqueductal stenosis in 18 patients, secondary aqueductal stenosis caused by tumors in 5, IV ventricle outlet obstruction in 5, and hydrocephalus associated with meningomyelocele in 4. The mean duration of follow-up was 19.4 months (range 1-50 months). Overall, surgical outcome was regarded as good in 21 of 29 patients. Surgical outcome was poor in patients younger than 1 year (P<0.05). Neuroimaging 1 month after ETV showed a decrease in ventricular size in 11 of the 16 patients with good surgical outcomes. Five showed minimal changes only. In patients with good outcomes, ventricular size tended to decrease as time passed. Resolution of periventricular edema, flow void in the III ventricle on T2-weighted axial images, and cine-MR imaging were sensitive indicators of good outcome. We suggest that ETV be considered as a primary treatment option in patients older than 1 year of age with noncommunicating hydrocephalus. In addition, time factors should be taken into consideration when surgical outcome is judged. Changes in ventricular size could not predict surgical outcome completely in themselves. Therefore, a comprehensive postoperative assessment should be made with the help of T2-weighted MRI and cine-MRI.
Functional neuroimaging and neuropsychological performance indicate a prefrontal dysfunction in schizophrenia patients. Frontal morphological brain abnormalities are also evident in these patients, but the relationship between neuropsychology and neuroimaging findings remains unclear. In this study, thirty patients with schizophrenia and 30 control participants were assessed using a neuropsychological test battery sensitive to fronto-striatal system dysfunction. Computed tomography (CT) scans were used to calculate the distance from the corpus callosum to the frontal pole corrected for brain size (anterioposterior length) in the group of patients and in a group of control participants with negative radiological findings. Schizophrenia patients performed significantly worse than controls in all frontal lobe tests. Corrected length from the corpus callosum to the frontal pole was reduced in patients with schizophrenia. This easy-to-perform measurement has not been used in previous studies, and indicates that schizophrenia patients have structural frontal abnormalities. However, correlations between structural and functional measures fail to show a clear relationship between the prefrontal performance and the main CT measures. As a rule, the trend observed in the correlation matrix pointed towards a relationship between CT parameters and a dysfunction on neuropsychological tests sensitive to frontal lobe damage.
Following the diagnostic indications of the Guidelines for the diagnosis and therapy of juvenile headache, we present the results of a prospective, multicentre study of headache patients aimed at evaluating the utility of neuroradiologic testing in the diagnosis of headache. A total of 6535 subjects up to age 18 were studied, and 1485 underwent neuroimaging testing based on the indications of the diagnostic Flow-Chart. Abnormal results were observed in 273 (18.5%) subjects. Incidental findings were observed in 138 (9.3%) subjects, not correlated with the headache pathology, whereas alterations that led to the diagnosis of secondary headache were observed in 135 (9.1%) subjects. In conclusion, our data support a greater incidence of positive neuroimaging examinations among patients who underwent testing based on suspicion of a secondary headache pathology when compared with the low percentages observed in study populations.
The first two decades of cognitive neuroimaging research have provided a constant increase of the knowledge about the neural organization of cognitive processes. Many cognitive functions (e.g.working memory) can now be associated with particular neural structures, and ongoing research promises to clarify this picture further, providing a new mapping between cognitive and neural function. The main goal of this paper is to outline conceptual issues that are particularly important in the context of imaging changes in neural function through recovery process. This review focuses primarily on studies made in stroke and traumatic brain injury patients, but most of the issues raised here are also relevant to studies using other acquired brain damages. Finally, we summarize a set of methodological issues related to functional neuroimaging that are relevant for the study of neural plasticity and recovery after rehabilitation.
Functional neuroimaging over the past decade has provided a new way to examine brain behavior relationships. Current noninvasive neuroimaging techniques, which can examine structure and function, have begun to clarify the networks involved in cognitive processes and how these are affected in aging and disease. Functional magnetic resonance imaging (fMRI) has demonstrated the interaction between medial temporal and prefrontal regions in episodic memory. The anatomical correlates of various components of spatial attention and working memory have emerged from elegant event-related fMRI designs. Distinct neural networks for different emotions are being mapped out, and the role of the anterior cingulate in depressed mood has been documented. This review highlights key recent studies that have illuminated the neural substrates of these important cognitive and affective processes.
The armamentarium available for treating acute stroke patients is growing as clinical trials show benefit of intravenous thrombolysis, intra-arterial clot lysis, and antiplatelet agents. Patients with dissection or severe atheromatous stenosis of major cerebrovascular vessels are commonly treated with anticoagulation to prevent recurrent artery-to-artery embolus or arterial thrombosis. These advances in acute stroke treatments demand an accurate means to quickly identify those patients most likely to benefit (or not benefit) from a specific therapy. Fortunately, advances in imaging cerebrovascular lesions, decreased brain perfusion, and even ischemic tissue injury now make it possible to consider tailoring therapy to the individual patient's cerebrovascular problem. Experience and controlled clinical data in this endeavor is meager. Here we describe the ability of various emergency neuroimaging tools to provide information on the state of brain blood flow, metabolism, and vascular anatomy. Most importantly, we present the rationale and limited available evidence relevant to how the neuroimaging information might be used to select optimal treatments for individual patients.
Contemporary neuroimaging studies using structural and functional techniques are critical in the evaluation of patients with localization-related epilepsy. Imaging procedures may be used to localize the epileptic brain tissue or determine the likely pathologic findings underlying the epileptogenic zone, or both. The diagnostic yield of magnetic resonance imaging (MRI) has been demonstrated in patients with partial epilepsy. The identification of an MRI epileptogenic lesion is almost invariably a reliable indicator of the site of seizure onset. Peri-ictal single photon emission computed tomography (SPECT) may be of particular benefit in patients with normal MRI studies. The use of neuroimaging in the care and management of patients with partial epilepsy is discussed here.
The basal ganglia and its associated circuitry can be assessed with a variety of neuroimaging methods that can provide information regarding specific neurotransmitter systems, the functional activity of brain regions, and the structural integrity of these regions. In Parkinson's disease (PD) and related atypical parkinsonian syndromes (APS), these imaging methods may be useful for many reasons, including aiding in differential diagnosis and measuring the efficacy of new therapies. This paper reviews recent developments in the application of neuroimaging to the assessment of PD and related APS.
Neuroimaging studies continue to provide important insights into the central nervous system disease pathology of multiple sclerosis (MS). Although conventional magnetic resonance imaging remains the mainstay of diagnosis and laboratory assessment of therapeutic response in MS, quantitative techniques continue to extend our understanding of both macroscopic and microscopic disease processes. Over the past year, many published studies have investigated measures of brain atrophy, gray matter involvement, vascular properties, and myelin and neuronal loss and have examined their relationship to clinical disease expression, genotype, and therapy. An important trend continuing over the past year is the development of targeted agents to improve the pathologic specificity of imaging measures. Specific disease measures such as endothelial activation, microglial activation, and cell trafficking are accessible to neuroimaging and offer significant promise for improved characterization of central nervous system involvement in MS.
Functional neuroimaging in child psychiatry presents unique scientific, ethical, and technical challenges. The study of childhood disorders presupposes knowledge of neurodevelopment and brain maturation. However, much of human brain science is based on inferences from animal work and indirect neurochemical measures from body fluids. Neuroimaging can examine brain development directly in humans. The benefits can be enormous for learning how and when to intervene to prevent or treat a disorder. These unprecedented potential gains are countered by complex and difficult ethical issues. Technical advances can reduce ethical concerns by minimizing risks. They also promise to enhance the sensitivity and specificity of the measures (eg, by improving spatial and temporal resolution). Judiciously designed investigations will permit the testing of a priori hypotheses built on rational models of neuropathology. Finally, it is the integration of scientific knowledge across the various fields of neuroscience and clinical research that will push the limits of our understanding of health and disease.
Neuroimaging methodologies have shown some of their greatest promise in studies of Alzheimer's disease (AD). Imaging outcome measures are now entering the arena of investigational trials for AD, to elucidate treatment mechanisms, optimize drug dosing, and perhaps serve as surrogate efficacy measures. Drugs that enhance central cholinergic neurotransmission have been extensively examined for their effects on regional cerebral blood flow, regional cerebral glucose metabolism, or levels of N-acetyl-aspartate in AD patients. Putative disease-modifying agents will be studied by structural magnetic resonance imaging for their ability to reduce rates of hippocampal or whole brain atrophy. When anti-amyloid therapies reach widespread clinical testing, their effects may be monitored by specific imaging probes for amyloid-beta peptide-containing senile plaques. Neuroimaging studies of AD patients and asymptomatic subjects who carry the apolipoprotein E e4 allele suggest that these individuals may be particularly suitable for testing candidate prevention therapies for AD.
Although Creutzfeldt-Jakob disease (CJD) is the prototypical rapidly progressive dementia, clinical heterogeneity in the disease can make diagnosis difficult. Creutzfeldt-Jakob disease affects multiple brain areas, which causes multifocal deficits that involve movement, cognition, and psychiatric status. Thorough neurologic, cognitive, and psychiatric examinations are necessary for observing its clinical features. Recent advances in neuroimaging techniques have allowed researchers and clinicians to discover imaging patterns that distinguish CJD from other neurologic diseases. This article discusses how these advances may make neuroimaging the most valuable noninvasive tool for diagnosing CJD, which helps to track the progression of the disease course and provides insight into clinical-anatomic correlations.
Neuroimaging techniques, including positron emission tomography (PET), are ideally suited for studies of addiction. These minimally invasive modalities yield information about acute and long-term drug-induced structural and functional changes in the brain over time. Changes can be observed in the brains of human and animal subjects during drug self-administration. Neuroimaging with PET allows precise quantification and visualization of the drug and its rates of movement in the body. In addition, imaging reveals recovery of function and reappearance of neuronal markers in abstinent drug users. Evidence that suggests that PET may have use in identifying individuals predisposed to become addicted is emerging. Finally, candidate pharmacotherapies for drug addiction can be critically evaluated. These unique assets clearly point to the use of these strategies for addiction studies.
Within the past several years, neuroimaging research on personality disorders has begun to develop. Personality disorders can be thought of as trait-like dysfunctional patterns in cognitive, affective, impulse control, and interpersonal domains. These domains of dysfunction have been linked to specific neural circuits. Developments in brain imaging techniques have allowed researchers to examine the neural integrity of these circuits in personality-disordered individuals. This article reviews the neuroimaging literature on borderline personality disorder, antisocial personality disorder (including psychopathy) and schizotypal personality disorder. Functional and structural studies provide support for dysfunction in fronto-limbic circuits in borderline and antisocial personality disorder, whereas temporal lobe and basal striatal-thalamic compromise is evident in schizotypal personality disorder.
The past decade has seen a rapid advance in understanding of the neural circuits of post-traumatic stress disorder (PTSD), which has largely been due to the application of neuroimaging to the study of this disorder. Based on studies in animals of the effects of stress on the brain, dysfunction of the medial prefrontal cortex, hippocampus, and amygdala have been hypothesized to underlie symptoms of PTSD. Neuroimaging studies in PTSD have been consistent with these hypotheses, with the most replicated findings showing decreased medial prefrontal cortical function in PTSD. Other replicated findings include decreased inferior frontal gyrus function, decreased hippocampal function, increased posterior cingulate function, and, in some behavioral paradigms, increased amygdala function. Several studies have now shown changes in structure (smaller volume) of the hippocampus in PTSD. These studies are beginning to map out a neural circuitry of PTSD that may have future implications for diagnosis and treatment.
This paper examines the use of neuroimaging to measure change in regional cerebral blood flow (rCBF) produced by pain in patients with fibromyalgia and in healthy individuals. Fibromyalgia patients differ from healthy persons in rCBF distribution in several brain structures involved in pain processing and pain modulation both at rest and during experimental pain induction. These abnormalities may contribute to abnormal pain sensitivity as well as the maladaptive pain behaviors that characterize many patients with fibromyalgia. We anticipate that future neuroimaging studies will enhance our understanding of abnormal pain sensitivity and of pain management interventions aimed at altering central nervous system function in patients with fibromyalgia.