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Neuroimaging is playing an increasing role in research of affective disorders, with investigators examining both volumetric changes of specific brain structures and vascular changes within white and gray matter. Recent studies have attempted to make clinical correlations between neuroimaging changes in unipolar and bipolar mood disorders. In this review, we focus particularly on those changes that are clinically meaningful. We conclude that there is enough evidence to begin to evaluate inclusion of neuroimaging findings in our mood disorder classification system. To this end, we propose two new mood disorder subtypes, vascular depression and vascular mania. Directions for future research in neuroimaging are then discussed.     

Neuroimaging and neurobiological models of depression

We review the data from structural neuroimaging studies (computed tomography and magnetic resonance imaging) related to depressive disorders. In addition, we review the relevant functional neuroimaging research, including studies of normal emotional processing, studies of the functional neuroanatomy of major depression, and neurochemical neuroimaging studies of depression. Finally, we discuss existing neurobiological models of depression and offer modifications based upon the body of neuroimaging research we have presented.     

Neuroimaging in psychiatry

The promise of neuroimaging as an aid to diagnosis is discussed, and findings from the most accessible imaging techniques are reviewed. In addition, some of the earliest findings from functional MR imaging and other technologies are presented with several illustrations. Strategies for interpretation, critique of imaging techniques, and review of major findings for brain injury, mood, anxiety, schizophrenia, and attention deficit disorders are offered. Examples of normal and pathologic images illustrate actual cases and examples of the newer imaging technologies.     

Neuroimaging in child and adolescent neuropsychiatric disorders

OBJECTIVE: To review the major findings and pathophysiological implications of imaging studies of neuropsychiatric disorders that onset in childhood or adolescence. METHOD: More than 200 neuroimaging studies were selected for review from Medline searches if the studies concerned developmental neuropsychiatric disorders such as autism, fragile X syndrome, Down syndrome, schizophrenia, obsessive-compulsive disorder, Tourette's syndrome, attention-deficit hyperactivity disorder, and dyslexia. RESULTS: Disordered central nervous system development may produce evidence of cortical neuronal migration abnormalities in autism, smaller cortical structures in Down syndrome, frontal lobe deficits and larger basal ganglia in schizophrenia, hypoplastic basal ganglia in Tourette's syndrome, aberrancies of the planum temporale in dyslexia, and hypoplastic cerebellar structures in numerous developmental disorders. Normal cerebral asymmetries appear to be disrupted in a number of disorders, including schizophrenia, Tourette's syndrome, attention deficit disorder, and dyslexia. CONCLUSIONS: Neuroimaging data regarding pathological central nervous system development in childhood are still sparse, and many of the findings in developmental disorders of childhood onset concern the study of adult subjects with those disorders. Nevertheless, imaging modalities previously used only in adults are with increasing frequency being applied to the study of children, which will likely continue to contribute to the understanding of pathological brain structure and function throughout childhood and to the improved treatment of these disorders.     

Dysmyelinating and demyelinating conditions in infancy

The myelin membrane is essential for rapid conduction of nerve impulses through the central nervous system. Failure of myelination--dysmyelination--may arise through several mechanisms. The synthesis of a particular myelin protein can be defective, as occurs for proteolipid protein in Pelizaeus-Merzbacher disease and for myelin basic protein in the 18q- syndrome. Delay in myelination with a more generalized diminution in white matter is characteristic of many inherited metabolic diseases, including galactosemia, pyridoxine-dependent seizure disorder, glutaric aciduria type 1, and infantile Refsum disease. Demyelination or breakdown in myelin is characteristic of metachromatic leukodystrophy, Krabbe disease, mitochondrial disorders, adrenoleukodystrophy, Canavan disease, Alexander disease, and orthochromatic leukodystrophy. A fourth category is reserved for malformation syndromes. These include Cockayne, Fukuyama, Walker-Warburg, and Angelman syndromes. Demyelination also occurs in HIV-infected individuals with central nervous system findings and in multiple sclerosis. Much of the evidence for leukodystrophy in these disorders comes from neuroimaging. Some of these disorders are treatable.     

Neuroimaging and the trimodal brain: applications for developmental communication neuroscience

New details generated by neuroimaging and other methods for studying the neural correlates of behavior have led to the formulation of a new model of brain organization, the Trimodal Brain. The model incorporates current biochemical; anatomical, and physiological concepts of prenatal brain growth and combines them with findings on right/left functional asymmetries. It provides a means of relating a wide range of human behaviors and clinical states according to a common base of neural organization, and stresses the utility of an organizational rather than a lesion model for understanding developmental communication disorders.     

Attention deficit hyperactivity disorder: advances in cognitive, neurobiological, and genetic research

Conceptual and technological advances in cognitive neuroscience and molecular genetics have the potential to identify the pathogenesis of psychiatric disorders. This article reviews the application of these technologies to the scientific study of attention deficit hyperactivity disorder. It begins with a summary of shifts in conceptualization and scientific study of this common condition. This is followed by a critical review of findings from recent cognitive, neuroimaging, and genetic studies. The available data do not yet permit an integration across these different levels of enquiry, but implicate problems in response inhibition, dysfunction of frontostriatal networks, and genetic factors in the pathogenesis of this complex behavioral phenotype. The review closes with suggestions for future interdisciplinary research.     

Glial reduction in the subgenual prefrontal cortex in mood disorders

Mood disorders are among the most common neuropsychiatric illnesses, yet little is known about their neurobiology. Recent neuroimaging studies have found that the volume of the subgenual part of Brodmann's area 24 (sg24) is reduced in familial forms of major depressive disorder (MDD) and bipolar disorder (BD). In this histological study, we used unbiased stereological techniques to examine the cellular composition of area sg24 in two different sets of brains. There was no change in the number or size of neurons in area sg24 in mood disorders. In contrast, the numbers of glia were reduced markedly in both MDD and BD. The reduction in glial number was most prominent in subgroups of subjects with familial MDD (24%, P = 0.01) or BD (41%, P = 0.01). The glial reduction in subjects without a clear family history was lower in magnitude and not statistically significant. Consistent with neuroimaging findings, cortical volume was reduced in area sg24 in subjects with familial mood disorders. Schizophrenic brains studied as psychiatric controls had normal neuronal and glial numbers and cortical volume. Glial and neuronal numbers also were counted in area 3b of the somatosensory cortex in the same group of brains and were normal in all psychiatric groups. Glia affect several processes, including regulation of extracellular potassium, glucose storage and metabolism, and glutamate uptake, all of which are crucial for normal neuronal activity. We thus have identified a biological marker associated with familial mood disorders that may provide important clues regarding the pathogenesis of these common psychiatric conditions.     

OTR-COTA collaboration in home health: roles and supervisory issues

Previous neuroimaging research has contributed insights regarding the neural substrates of specific psychiatric disorders. The purpose of this study was to determine the shared mediating neuroanatomy of anxiety symptoms across three different anxiety disorders. Data were pooled from 23 right-handed adult outpatients meeting criteria for obsessive-compulsive disorder, simple phobia, or posttraumatic stress disorder. Relative regional cerebral blood flow (rCBF) was measured using positron emission tomography in the context of symptom provocation paradigms. Symptom severity was measured via self-reports. The analysis of pooled imaging data indicated activation in right inferior frontal cortex, right posterior medial orbitofrontal cortex, bilateral insular cortex, bilateral lenticulate nuclei, and bilateral brain stem foci during the symptomatic versus control conditions. A positive correlation was found between rCBF at one brain stem locus and subjective anxiety scores (r = .744, p < .001). These findings suggest that elements of the paralimbic belt together with right inferior frontal cortex and subcortical nuclei mediate symptoms across different anxiety disorders. In addition, activation at one brain stem locus appears to be associated with the subjective severity of anxiety. Further studies are warranted to determine whether these same brain systems mediate normal anxiety states as well.     

Evaluation and management of pulmonary atresia with intact ventricular septum

The Consensus Conference of the American College of Medical Genetics has established guidelines regarding the evaluation of patients with mental retardation (MR) [Curry et al., Am. J. Med. Genet. 72:468-477, 1997]. They emphasized the high diagnostic utility of cytogenetic studies and of neuroimaging in certain clinical settings. However, data on the diagnostic yield of these studies in well-characterized populations of individuals with MR are scant. Majnemer and Shevell [J. Pediatr. 127:193-199, 1995] attained a diagnostic yield of 63%. However, this study included only 60 patients and the classification included pathogenetic and causal groups. The Stella Maris Institute has evaluated systematically patients with developmental delay (DD)/MR and performed various laboratory studies and neuroimaging in almost all patients. We report a retrospective analysis of the diagnostic yield of 120 consecutive patients observed at our Institute during the first 6 months of 1996. There were 77 males and 43 females; 47 were mildly delayed (IQ 70-50), 31 were moderately delayed (IQ 50-35), and 42 were severely delayed (IQ 35-20). Diagnostic studies (history, physical examination, standard cytogenetics, fragile X testing, molecular studies, electroencephalography, electromyography, nerve conduction studies, neuroimaging, and metabolic screening tests) yielded a causal diagnosis in 50 (41.6%) and a pathogenetic diagnosis in 47 (39.2%) of the 120 patients. Causal categories included chromosomal abnormalities (14), Fra(X) syndromes (4), known MCA/MR syndromes (19), fetal environmental syndromes (1), neurometabolic (3) disorders, neurocutaneous (3) disorders, hypoxic-ischemic encephalopathy (3), other encephalopathies (1), and congenital bilateral perisylvian syndrome (2). Pathogenetic categories included idiopathic MCA/MR syndromes (35), epileptic syndromes (10), and isolated lissencephaly sequence (2). Diagnostic yield did not differ across categories and degree of DD. Our results, while confirming the diagnostic utility of cytogenetic/molecular genetic, and neuroimaging studies, suggest the usefulness of accurate electroencephalogram recordings, and stress the importance of a thorough physical examination. Referral to a university child neurology and psychiatry service, where a comprehensive assessment with a selected battery of investigations is possible, yields etiologic findings in a high percentage of DD/MR patients, with important implications for management, prognosis and recurrence risk estimate.     

Developmental dyslexia and animal studies: at the interface between cognition and neurology

Recent findings in autopsy studies, neuroimaging, and neurophysiology indicate that dyslexia is accompanied by fundamental changes in brain anatomy and physiology, involving several anatomical and physiological stages in the processing stream, which can be attributed to anomalous prenatal and immediately postnatal brain development. Epidemiological evidence in dyslexic families led to the discovery of animal models with immune disease, comparable anatomical changes and learning disorders, which have added needed detail about mechanisms of injury and plasticity to indicate that substantial changes in neural networks concerned with perception and cognition are present. It is suggested that the disorder of language, which is the cardinal finding in dyslexic subjects, results from early perceptual anomalies that interfere with the establishment of normal cognitive-linguistic structures, coupled with primarily disordered cognitive processing associated with developmental anomalies of cortical structure and brain asymmetry. This notion is supported by electrophysiological data and by findings of anatomical involvement in subcortical structures close to the input as well as cortical structures involved in language and other cognitive functions. It is not possible at present to determine where the initial insult lies, whether near the input or in high-order cortex, or at both sites simultaneously.     

Senile dementia of the Binswanger's type

Senile dementia of the Binswanger's type is a term used to describe a dementia syndrome characterized by onset in the sixth or seventh decade of life, subcortical neurologic deficits, psychiatric disorders and evidence of hypertension or systemic vascular disease. The status of senile dementia of the Binswanger's type as a distinct entity is a matter of some controversy. The array of neuroimaging abnormalities and clinical findings attributed to this condition overlap with a number of other neuropathologies. Leukoaraiosis, or attenuation of subcortical white matter, seen on computed tomographic scans or magnetic resonance imaging of the brain, is a hallmark of senile dementia of the Binswanger's type. The clinical findings associated with Binswanger's disease are varied but typically include a progressive dementia, depression and "subcortical" dysfunction such as gait abnormalities, rigidity and neurogenic bladder. Treatment is largely supportive and includes a discussion about advanced directives, social support and antidepressant therapy. Control of hypertension and aspirin prophylaxis may help prevent further progression of white matter disease.     

Prediction of children's reading skills using behavioral, functional, and structural neuroimaging measures.

The ability to decode letters into language sounds is essential for reading success, and accurate identification of children at high risk for decoding impairment is critical for reducing the frequency and severity of reading impairment. We examined the utility of behavioral (standardized tests), and functional and structural neuroimaging measures taken with children at the beginning of a school year for predicting their decoding ability at the end of that school year. Specific patterns of brain activation during phonological processing and morphology, as revealed by voxel-based morphometry (VBM) of gray and white matter densities, predicted later decoding ability. Further, a model combining behavioral and neuroimaging measures predicted decoding outcome significantly better than either behavioral or neuroimaging models alone. Results were validated using cross-validation methods. These findings suggest that neuroimaging methods may be useful in enhancing the early identification of children at risk for poor decoding and reading skills. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Post-infectious demyelinating diseases

Post-infectious demyelinating disorders are uncommon. In the Hospital Pediatrico de la Misericordia de Santafé de Bogotá there were 14 cases in three years. The commonest age group was the new born, as is found in the literature. The infections involved in these neurological changes are probably viral, since at the time the patient is seen most symptoms have cleared up spontaneously. According to several authors, the viruses are most often found to be those of measles or mumps. Between the infection and the development of neurological symptoms there is an interval of approximately two weeks. The main clinical findings are motor changes such as hemiparesis, involvement of cranial nerves and alterations of consciousness. The aetiology is not completely clear. Firm diagnosis is made on histopathological studies which are seldom available. Usually neuroimaging techniques and cerebrospinal fluid analysis are the basis of the diagnosis. Computerized axial tomography and magnetic resonance are the most useful noninvasive techniques for assessing the involvement of the white matter, the extent and sites of the lesions. It is useful to know the classification of the demyelinating disorders so as to prescribe, the most suitable treatment and give the prognosis in each case. There is still no specific treatment for these disorders. Supportive measures, the control of epileptic crises and the prevention of complications are the main aims. This paper reviews the definition, classification, diagnosis and management of these disorders.     

Phylogenetic relationships of artiodactyls and cetaceans as deduced from the comparison of cytochrome b and 12S rRNA mitochondrial sequences

Functional neuroimaging studies in schizophrenia have often been confounded by various factors including medication status. To explore the effects of antipsychotic medications on relative regional cerebral perfusion, we scanned a group of 33 persons with schizophrenia twice, while receiving a stable dose of antipsychotic and after being off antipsychotics for 3 weeks, using technetium-99m hexamethyl-propyleneamine oxime single photon emission computed tomography (Tc-99m HMPAO-SPECT. We found that antipsychotic significantly increased the mean relative cerebral perfusion in the left basal ganglia. Additionally, patients receiving thiothixene (n = 9) had a significantly greater increase in relative cerebral perfusion in the basal ganglia than patients receiving haloperidol (n = 12). These findings indicate that antipsychotics lead to regional increases in cerebral perfusion and that antipsychotic status must be controlled for in functional neuroimaging studies. Functional neuroimaging techniques such as SPECT may be useful in furthering our understanding of the mechanism of antipsychotics.     

Traumatic brain injury in children and adolescents: psychiatric disorders at two years

OBJECTIVE: To extend findings regarding predictive factors of psychiatric outcome from the first to the second year after traumatic brain injury (TBI) in children and adolescents. METHOD: Subjects were children aged 6 to 14 years at the time they were hospitalized after TBI. The study used a prospective follow-up design. Assessments of preinjury psychiatric, behavioral, adaptive functioning, family functioning and family psychiatric history status were conducted. Severity of injury was assessed by standard clinical scales and neuroimaging was analyzed. The outcome measure was the presence of a psychiatric disorder, not present before the injury ("novel"), during the second year after TBI. RESULTS: Fifty subjects enrolled, and the analyses focused on 42 subjects followed at 24 months. Severity of injury, preinjury family function, and preinjury lifetime psychiatric history predicted the development of a "novel" psychiatric disorder present in the second year. CONCLUSION: These data suggest that there are children, identifiable through clinical assessment, at increased risk for "novel" psychiatric disorders in the second year after TBI.     

Merosin-negative congenital muscular dystrophy, occipital epilepsy with periodic spasms and focal cortical dysplasia. Report of three Italian cases in two families

We report clinical, EEG and neuroimaging findings of three patients in two Italian families with merosin-negative congenital muscular dystrophy (CMD), drug-resistant occipital epilepsy, diffuse persistent cerebral white matter changes and focal cortical dysplasia. Clinical and epilepsy histories, EEG and neuroimaging findings were very similar in all patients. Seizures started in childhood and mainly consisted of periodic spasms, a particular type of partial seizure characterized by clusters of epileptic spasms. The motor expression of the spasms was very mild so that they had been frequently missed or misinterpreted as non-convulsive generalized absence seizures. Interictal EEG showed occipital spike-waves and bilateral synchronous slow spike-wave discharges. Ictal EEG showed prolonged periodic sequences of slow waves with associated fast rhythm complexes, characteristic of periodic spasms. Two patients had normal intelligence, one patient presented moderate mental retardation. Focal cortical dysplasia in the posterior areas of the brain, in addition to marked diffuse white matter alterations, was detected in the magnetic resonance images of all patients. Findings in these patients indicate that in merosin-negative CMD brain involvement can include cortical dysplasia, in addition to white matter changes. In such cases the brain damage can lead to a childhood-onset localization-related symptomatic occipital epilepsy. Epileptic seizures and cortical dysplasia can be, however, difficult to detect in CMD. The clinical semiology of epileptic seizures may in fact be modified because of muscular weakness. This implies that epilepsy may be misdiagnosed or even missed and EEG-polymyographic recordings may be necessary to identify it. Similarly, cortical dysplasia may be very localized and visible by neuroimaging only if it is carefully investigated on the basis of epileptological and EEG-polymyographic findings.     

Cystic meningiomas: unusual forms of intracranial neoplasms

OBJECTIVE: We report eight patients with cystic intracranial meningiomas to outline the neuroimaging spectrum of this unusual form of intracranial tumors. METHODS: Both CT and MRI were equally effective for the detection of peritumoral or intratumoral cystic lesions. However, neuroimaging findings were nonspecific and did not allow a correct preoperative diagnosis in most cases. CONCLUSIONS: Only a high index of suspicion permits the neurosurgeon a proper recognition of cystic meningiomas and its differentiation from the more common and malignant gliomas.     

T lymphocytes and macrophages, but not motile spermatozoa, are a significant source of human immunodeficiency virus in semen

Sixty-three children with new-onset temporal lobe epilepsy (TLE) underwent extensive clinical, EEG, and neuroimaging investigation as part of a prospective, community-based cohort study of the natural history of TLE in childhood. Complex partial seizures occurred in 94% of the children, and tonic-clonic seizures occurred in 14%. Developmental, behavioral, or learning problems were present in 38%. Eighteen children (29%) had a significant illness/event prior to the onset of TLE, including febrile status epilepticus in seven, meningitis in four, respiratory arrest in two, and head injury in one. Magnetic resonance imaging or computed tomography revealed structural abnormalities of the temporal lobe in 24 children (38%), including hippocampal sclerosis (HS) in 13 and tumor in eight. There was a strong association between HS and a history of significant illness/event prior to the onset of TLE (p < 0.001). Analysis of past history and neuroimaging findings led us to propose three etiologically defined subgroups of TLE; developmental TLE (10 children with long-standing, nonprogressive temporal lobe tumors and malformations), TLE with HS/significant antecedents (18 children with HS or a history of a significant illness/event), and cryptogenic TLE (34 children with normal neuroimaging findings and no significant past history). Etiologic differences between children with new-onset TLE may confer prognostic information that will be useful for counselling families and planning treatment.     

Primary antibody deficiency in Arabs: first report from eastern Saudi Arabia

The purpose of this study was to determine whether a staged, algorithmic evaluation of infantile spasms could be developed to minimize patient discomfort, treatment delay, and overall costs. A retrospective chart review of patients diagnosed with infantile spasms at the authors' institution during a 10-year period was performed, with 29 patients identified; 28 charts were reviewed. By history and physical examination, 21 were classified as symptomatic and seven as cryptogenic. Of the 21 symptomatic patients, 13 had a known etiology at presentation; with further testing the specific etiology was determined in two more. Two in the cryptogenic group were reclassified on the basis of neuroimaging findings. Evaluations included neuroimaging (27, 15 abnormal), cerebrospinal fluid studies (nine, all normal), comprehensive metabolic studies (17, all normal), chromosomal analysis (11, two abnormal), and ophthalmologic evaluation (27, six abnormal). The average cost of the studies per patient was $5,076 at the authors' institution. Etiologic yield was increased by 20% with neuroimaging. The other investigations either confirmed a known etiology or were noncontributory. On the basis of these findings, the authors propose an algorithm for a more focused evaluation of infantile spasms. Using the algorithm, the authors suggest directly proceeding to therapy in patients with specific etiologies determined by history and examination. Further evaluation should start with neuroimaging. Subsequent evaluations should be on the basis of those results. The authors estimate a potential 60-90% reduction in total costs if this algorithm is applied.