Caplan Syndrome

Koch DG, Caplan M, Reuben A. · Division of Gastroenterology and Hepatology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA. · Liver Transpl. · Pubmed #19326402 No free full text.

Abstract: Hepatopulmonary syndrome and portopulmonary hypertension are the most common pulmonary vascular complications in patients with cirrhosis. Usually but not universally mutually exclusive, they each may present prior to liver transplantation and, if severe enough, may be a contraindication to transplant. However, there have been a number of case reports describing patients developing pulmonary hypertension de novo after liver transplantation. This report describes one such patient from our institution and reviews the medical literature describing this unusual clinical entity.

Otsuki T, Maeda M, Murakami S, Hayashi H, Miura Y, Kusaka M, Nakano T, Fukuoka K, Kishimoto T, Hyodoh F, Ueki A, Nishimura Y. · Department of Hygiene, Kawasaki Medical School, Matsushima 577, Kurashiki 7010192, Japan. · Cell Mol Immunol. · Pubmed #17764616 links to  free full text

Abstract: Silicosis patients (SILs) and patients who have been exposed to asbestos develop not only respiratory diseases but also certain immunological disorders. In particular, SIL sometimes complicates autoimmune diseases such as systemic scleroderma, rheumatoid arthritis (known as Caplan syndrome), and systemic lupus erythematoses. In addition, malignant complications such as lung cancer and malignant mesothelioma often occur in patients exposed to asbestos, and may be involved in the reduction of tumor immunity. Although silica-induced disorders of autoimmunity have been explained as adjuvant-type effects of silica, more precise analyses are needed and should reflect the recent progress in immunomolecular findings. A brief summary of our investigations related to the immunological effects of silica/asbestos is presented. Recent advances in immunomolecular studies led to detailed analyses of the immunological effects of asbestos and silica. Both affect immuno-competent cells and these effects may be associated with the pathophysiological development of complications in silicosis and asbestos-exposed patients such as the occurrence of autoimmune disorders and malignant tumors, respectively. In addition, immunological analyses may lead to the development of new clinical tools for the modification of the pathophysiological aspects of diseases such as the regulation of autoimmunity or tumor immunity using cell-mediated therapies, various cytokines, and molecule-targeting therapies. In particular, as the incidence of asbestos-related malignancies is increasing and such malignancies have been a medical and social problem since the summer of 2005 in Japan, efforts should be focused on developing a cure for these diseases to eliminate nationwide anxiety.

Caplan JD, Waxman S, Nesto RW, Muller JE. · InfraReDx Inc., Burlington, Massachusetts 01803, USA. · J Am Coll Cardiol. · Pubmed #16631516 No free full text.

Abstract: This review describes efforts to use near-infrared (NIR) spectroscopy to identify chemical components of coronary artery plaques as a means to assess vulnerability. Near-infrared spectroscopy has been well-validated by the physical sciences as a method to characterize chemical composition of various bio-materials and could be ideal to detect vulnerable coronary plaques in patients. Recent studies in aortic and coronary artery autopsy specimens have confirmed the ability of the technique to identify lipid-rich thin-cap fibroatheromas through blood. A catheter-based system has been developed to address the challenges-of access to the coronary artery, blood, motion, and the need to scan-that must be overcome for use in patients. Initial clinical experience in six patients with stable angina demonstrates that high-quality NIR spectra can be safely obtained. Additional studies are planned to validate the ability of the technique to identify lipid-rich coronary artery plaques and ultimately link chemical characterization with subsequent occurrence of an acute coronary syndrome.

Caplan LR. · Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. · Neurology. · Pubmed #16401854 No free full text.

Abstract: Many patients with congestive heart failure develop neurologic dysfunction. This may take the form of a cardiac encephalopathy that shares clinical features with other metabolic encephalopathies. The causes are multiple. There is a particular, previously unreported, syndrome that occasionally develops in some patients with congestive heart failure that resembles the findings in patients with normal pressure hydrocephalus. This syndrome is characterized by apathy and abulia with preserved alertness; it is caused by fluid retention within the cranial cavity. The syndrome may also develop in patients with other conditions that cause anasarca, e.g., severe liver or kidney disease or hypoalbuminemia. Because patients with these conditions are often quite ill, it has been difficult to verify the pathophysiologic aspects of the syndrome so that its mechanism must remain a hypothesis that awaits more definitive study in a series of patients. I have not seen this syndrome discussed in any cardiology or neurology texts or reports, and it seems to be completely unknown to cardiologists and neurologists. I have recognized about one patient per year with this syndrome.

Moulin P, Lehucher-Michel MP. · Faculté de médecine de Marseille, Université de la Méditerranée, Assistance Publique-Hôpitaux de Marseille, Hôpital de la Timone. · Presse Med. · Pubmed #15615243 No free full text.

Abstract: CRYSTALLINE SILICA: Crystalline silica is an abundant mineral found in multiple occupational exposures. It is a recognised occupational risk factor for some systemic auto-immune diseases such as progressive systemic scleroderma and Caplan-Colinet's syndrome, or just suspected in Goujerot-Sjögren's syndrome, periarteritis nodosa and systemic lupus erythematosus. WEGENER'S GRANULOMATOSIS: A rare disease of unknown of unknown aetiology, the disease is characterised by granulomatous vasculitis affecting the upper respiratory tracks, lungs and kidneys, associated with glomerulonephropathy. THE ROLE OF SILICA PARTICLES: Studies have shown that crystalline silica may be implied in Wegener's disease. Associated with other factors, notably with a genetic predisposal, silica particles might, through the release of reactive oxygen radicals and inflammatory cytokines, trigger-off immunopathological mechanisms. The latter would be manifested by exocytosis of the proteinase 3 and myeloperoxidase antigens on the surface of the polynuclear neutrophils.

Baur X. · Ordinariat und Zentralinstitut für Arbeitsmedizin, Hamburg. · Pneumologie. · Pubmed #14961440 No free full text.

Abstract: The long-term exposure to dust in the hard coal mining industry can lead to various pathological lung changes, especially to chronic bronchitis without and with obstructive ventilation disorder, lung emphysema, pneumoconiosis (coal miner's pneumoconiosis, in Germany categorized as silicosis) and silicotuberculosis. These health disorders show a close pathogenetic and pathophysiological association and should not necessarily be regarded as individual entities. Most exposed subjects demonstrate more or less all of these pathological disorders. On account of individual (genetic?) susceptibility, their degree differs greatly. Some individuals are largely resistent, other subjects show severe effects like emphysema, progressive massive pneumoconiosis, or the Caplan syndrome. Several studies showed that the pathologically verified degree of lung fibrosis is associated with lung crystalline SiO(2) content whereas the emphysema score is inversely correlated with the coal content. With regard to diagnostics and medical expert opinion, it is important that conventional radiology has a low sensitivity. Further, health impairments of miners engaged for longtime which are insurance relevant (MdE) exist in cases without (BK 4111 if beginning after 12/31/1992) or with coalworkers' pneumoconiosis even for categories < 2/3.

Arakawa H, Honma K, Shida H, Saito Y, Morikubo H. · Department of Radiology, Dokkyo University School of Medicine, Mibu, Tochigi, Japan. · J Comput Assist Tomogr. · Pubmed #14501367 No free full text.

Abstract: We report a case of Caplan syndrome complicated with tuberculosis, which was clinically followed up for 18 years and underwent autopsy. Initial chest radiograph showed 2 large nodules against the background of smaller pneumoconiotic nodules. One of the large nodules showed cavitation during follow-up. Computed tomography (CT) was helpful in identifying calcification in another large nodule. Autopsy confirmed the 2 large nodules as burned-out rheumatoid nodules and revealed additional rheumatoid nodules that were indistinguishable from silicotic nodules by CT.

Chrisler JC, Caplan P. · Department of Psychology, Connecticut College, New London 06320, USA. · Annu Rev Sex Res. · Pubmed #12836734 No free full text.

Abstract: In this article we trace the historical, cultural, political, and economic forces that led to the social construction of premenstrual syndrome (PMS) and premenstrual dysphoric disorder (PMDD). The popularity of these diagnostic labels among medical professionals, the general public, and women themselves is considered and explored, as is the damage that the labels can do to women in general, as well as those who receive a diagnosis. Suggestions are provided for psychotherapists who might work with women who present with premenstrual symptoms.

Scarisbrick D. · No affiliation provided · Practitioner. · Pubmed #11852619 No free full text.

This publication has no abstract.

Loeb C. · Department of Neurosciences and Vision, University of Genoa, Via de Toni 5, I-16132 Genoa, Italy. · Neurol Sci. · Pubmed #11441570 No free full text.

Abstract: The clinicopathological findings reported by Binswanger are insufficient to qualify as distinct entity the condition named "Binswanger's disease", and subsequently by Olszewski (1962) "subcortical arteriosclerotic encephalopathy (SAE) (Binswanger's type)". A short summary of the characteristic pathological, clinical and neuroimaging features of SAE is reported. The white matter changes detected by neuroimaging must be considered aspecific, since identical changes may be found in normal elderly as well as in patients with different diseases: different biochemical mechanisms can undoubtedly underlie identical neuroimaging patterns. Two other relevant points are noteworthy: the occurrence of pathological features of SAE in other diseases (CADASIL, pseudoxanthoma elasticum, antiphospholipid antibody syndrome) and the observation of some patients with pathological changes of SAE but an incomplete clinical picture. The clinicopathological features described as Binswanger's disease do not qualify as a separate entity since they are common to a variety of illnesses. The pathological picture identified by Olszewski can rightly be named, according to Caplan, "chronic microvascular leukoencephalopathy" (CML). The clinicopathological features of the so-called Binswanger's disease constitute a syndrome, the CML syndrome (CMLS), which can be found in some hereditary diseases and in acquired conditions. This syndrome shows peculiar cerebrovascular changes and, when clinically associated with dementia, identifies one of the subtypes of vascular dementia.

Dell'Angelica EC, Mullins C, Caplan S, Bonifacino JS. · Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-5430, USA. · FASEB J. · Pubmed #10877819 links to  free full text

Abstract: Lysosomes are membrane-bound cytoplasmic organelles involved in intracellular protein degradation. They contain an assortment of soluble acid-dependent hydrolases and a set of highly glycosylated integral membrane proteins. Most of the properties of lysosomes are shared with a group of cell type-specific compartments referred to as 'lysosome-related organelles', which include melanosomes, lytic granules, MHC class II compartments, platelet-dense granules, basophil granules, azurophil granules, and Drosophila pigment granules. In addition to lysosomal proteins, these organelles contain cell type-specific components that are responsible for their specialized functions. Abnormalities in both lysosomes and lysosome-related organelles have been observed in human genetic diseases such as the Chediak-Higashi and Hermansky-Pudlak syndromes, further demonstrating the close relationship between these organelles. Identification of genes mutated in these human diseases, as well as in mouse and Drosophila: pigmentation mutants, is beginning to shed light on the molecular machinery involved in the biogenesis of lysosomes and lysosome-related organelles.

Brandt T, Steinke W, Thie A, Pessin MS, Caplan LR. · Department of Neurology, University Hospital of Heidelberg, Germany. · Cerebrovasc Dis. · Pubmed #10773642 No free full text.

Abstract: Only a few large series of posterior cerebral artery (PCA) stroke exist, and clinical features and causes have not been studied as extensively as in other vascular territories. The PCA syndrome includes more clinical signs than the well-known visual field deficits. Concomitant findings are frequently sensory, slight motor and neuropsychological deficits. Unilateral headaches are the common presenting symptom making complicated migraine an important differential diagnosis. Combined deep and superficial PCA territory infarcts involving the lateral thalamus are more frequent than commonly assumed and are mostly associated with sensory and reversible slight motor deficits. Occlusion of the precommunal PCA segment with associated paramedian midbrain infarction causes severe motor deficits, oculomotor signs, and decreased consciousness and has a poorer outcome than other PCA territory infarcts. Embolism from a cardiac or undetermined source is the leading mechanism accounting for up to half of the cases, whereas arterial embolism from significant proximal vertebrobasilar disease is less frequent. Local atherothrombotic stenosis or occlusion of the PCA is uncommon. In spite of thorough diagnostic evaluation, the etiology of PCA territory infarction cannot be determined in at least one quarter of patients. Among the rare causes of PCA territory infarction carotid artery disease is important while the significance of migraine remains controversial.

Fleischmann KE, Orav EJ, Lamas GA, Mangione CM, Schron EB, Lee KL, Goldman L, Anonymous00096. · Department of Medicine, The University of California-San Francisco, 505 Parnassus Ave., San Francisco, CA 94143, USA. · Am Heart J. · Pubmed #19540395 No free full text.

Abstract: BACKGROUND: In the Mode Selection Trial (MOST) of 2,010 patients with sinus node dysfunction, dual-chamber-paced patients had less atrial fibrillation (AF) and heart failure and had slightly improved health-related quality of life (QOL) compared with rate modulated right ventricular-paced patients. Our objective was to assess the impact of AF on QOL within MOST. METHODS: We analyzed serial QOL measures (Short Form-36, Specific Activity Scale, time trade-off) in 3 groups: (1) those without AF; (2) those with paroxysmal AF (PAF), but not chronic AF (CAF); and (3) those with CAF. We carried forward the last known QOL before crossover for all subsequent time points in patients randomized to rate modulated right ventricular pacing who crossed over to dual-chamber pacing for severe pacemaker syndrome. RESULTS: Three hundred seventeen patients (15.8%) had AF in the year after implantation, 206 patients within 3 months (191 PAF, 15 CAF), and another 159 (124 PAF, 35 CAF) between 3 and 12 months. There were no significant differences among groups in individual Short Form-36 subscales or time trade-off scores at 12 months as compared with baseline or 3 months. Cardiovascular health status was better at 12 months as compared with baseline or 3 months in those without AF. CONCLUSIONS: Atrial fibrillation after pacemaker implantation in elderly patients with sick sinus syndrome was not a major determinant of QOL. However, there was a trend toward better cardiovascular functional status in patients without AF.

Foster AR, Caplan JP. · Dept. of Psychiatry, University of Arizona College of Medicine, Tucson, AZ, USA. · Psychosomatics. · Pubmed #19377018 No free full text.

Abstract: BACKGROUND: Paraneoplastic limbic encephalitis (PLE) is a syndrome characterized by the development of neuropsychiatric symptoms due to a misdirected tumor-activated antibody response that damages host neural tissue. Definitive treatment relies on the identification and ablation of the underlying tumor. Few publications describe the management of psychiatric symptoms associated with PLE. OBJECTIVE: Given the plethora of neuropsychiatric symptoms that may mimic primary psychiatric illness, and the possibility that PLE may herald a life-threatening malignancy, it is important that psychiatrists become familiar with this condition. METHOD: The authors review and discuss the consensus literature on the various aspects of PLE. DISCUSSION: In this review, authors summarize proposed mechanisms and treatments of PLE.

Goette A, Huth C, Behrens-Baumann W, Evert M. · University Hospital Magdeburg, Division of Cardiology, Leipziger Str.44, 39120 Magdeburg, Germany. · Eur J Intern Med. · Pubmed #19237064 No free full text.

This publication has no abstract.

Malinin NL, Zhang L, Choi J, Ciocea A, Razorenova O, Ma YQ, Podrez EA, Tosi M, Lennon DP, Caplan AI, Shurin SB, Plow EF, Byzova TV. · Department of Molecular Cardiology, Joseph J. Jacobs Center for Thrombosis and Vascular Biology, NB50, The Cleveland Clinic, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA. · Nat Med. · Pubmed #19234460 No free full text.

Abstract: Monogenic deficiency diseases provide unique opportunities to define the contributions of individual molecules to human physiology and to identify pathologies arising from their dysfunction. Here we describe a deficiency disease in two human siblings that presented with severe bleeding, frequent infections and osteopetrosis at an early age. These symptoms are consistent with but more severe than those reported for people with leukocyte adhesion deficiency III (LAD-III). Mechanistically, these symptoms arose from an inability to activate the integrins expressed on hematopoietic cells, including platelets and leukocytes. Immortalized lymphocyte cell lines isolated from the two individuals showed integrin activation defects. Several proteins previously implicated in integrin activation, including Ras-associated protein-1 (RAP1) and calcium and diacylglycerol-regulated guanine nucleotide exchange factor-1 (CALDAG-GEF1), were present and functional in these cell lines. The genetic basis for this disease was traced to a point mutation in the coding region of the KINDLIN3 (official gene symbol FERMT3) gene. When wild-type KINDLIN-3 was expressed in the immortalized lymphocytes, their integrins became responsive to activation signals. These results identify a genetic disease that severely compromises the health of the affected individuals and establish an essential role of KINDLIN-3 in integrin activation in humans. Furthermore, allogeneic bone marrow transplantation was shown to alleviate the symptoms of the disease.

Barnes GN, Paolicchi JM. · Vanderbilt University, Medical Center, Nashville, TN 37232, USA. · Nat Clin Pract Neurol. · Pubmed #19015658 No free full text.

Abstract: This Practice Point commentary discusses a cross-sectional study by Caplan et al. that identified frequent comorbidities associated with childhood absence epilepsy (CAE). The authors found that children with CAE exhibited subtle cognitive deficits (25%), linguistic difficulties (43%), and psychiatric diagnoses (61%) -- in particular, attention deficit hyperactivity disorder and anxiety. The severity of the comorbidities was related to epilepsy duration, seizure frequency, and antiepileptic drug treatment. Only 23% of the children in the study were receiving interventions to treat the comorbidities. Although epilepsy associated with CAE seems to have a 'benign' outcome in most cases, a subpopulation of patients with CAE will continue to experience seizures and associated comorbidities, perhaps accounting for the poor outcomes of such patients in adulthood. The diagnosis and treatment of the CAE syndrome might be enhanced by use of a multidisciplinary approach involving an epileptologist, cognitive-developmental physicians, and child psychiatrists.

Caplan JM, Khalpey Z, Gates J. · Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. · Emerg Med J. · Pubmed #18955626 No free full text.

Abstract: Dural sinus thrombosis (DST) has an annual incidence of 3-4 per million and can result from many aetiologies. Presentation of the disease can vary considerably, as can the aetiology and delay of symptoms to clinical detection. Symptoms on presentation include headache, seizures, focal neural deficits and altered mental status. There are many aetiological risk factors associated with DST, which include hypercoagulable states, oral contraceptive use, infection and mechanical causes such as cranial trauma. DST as a result of trauma is rare and aetiologies range from mechanical falls with or without skull fracture, firework explosions, gunshots to the head, blunt trauma to the head and closed head injury. Internal jugular vein thrombosis is also a rare disease and as with DST, traumatic aetiologies are uncommon. More common aetiologies include iatrogenic causes related to catheterisation as well as infectious causes (eg, Lemierre's syndrome). A case of thrombosis of the transverse sinus, sigmoid sinus and internal jugular vein associated with a closed head injury as the result of a motorcycle accident is presented.

Saposnik G, Noel de Tilly L, Caplan LR. · Stroke Research Unit, Division of Neurology, Department of Medicine, St Michael's Hospital, University of Toronto, 55 Queen St E, Ste 931, Toronto ONM5C1R6, Canada. · Arch Neurol. · Pubmed #18852355 No free full text.

Abstract: BACKGROUND: Little is known about stroke mechanisms in patients with fluctuating symptoms and the role of branch atherosclerotic disease. OBJECTIVE: To report a novel stroke presentation associated with a paramedian pontine infarct due to branch disease with a fluctuating course. DESIGN: Case report. SETTING: Academic research. Patient A 63-year-old man with hypertension, diabetes mellitus, and dyslipidemia was seen with fluctuating right-sided weakness and dysarthria. He had had 2 episodes of complete bilateral horizontal conjugate gaze palsy with unimpaired consciousness lasting for 5 minutes each. His pupils were 4 mm and were equal and reactive to light. Vertical gaze and convergence were preserved. His neurologic status fluctuated between 3 and 15 on the National Institutes of Health Stroke Scale. MAIN OUTCOME MEASURES: Results of computed tomographic angiography, perfusion, and magnetic resonance imaging. RESULTS: Intravenous tissue plasminogen activator was administered within a 3-hour window. Fluctuations in motor weakness persisted for 12 hours after receiving thrombolytic therapy. Neuroimaging showed an acute left paramedian pontine infarct with a patent basilar artery. CONCLUSIONS: Branch disease is a common mechanism in pontine infarctions. We coined the term "pontine warning syndrome" to characterize recurrent stereotyped episodes of motor or sensory dysfunction, dysarthria, or ophthalmoplegia associated with a high risk of imminent basilar artery branch infarction and a permanent deficit resembling those of capsular warning syndrome.

Caplan JP. · Massachusetts General Hospital, Boston, MA 02114, USA. · Psychosomatics. · Pubmed #18448781 links to  free full text

Abstract: BACKGROUND: Delirium is a significant and costly complication of medical hospitalization, and it has been shown to be a significant predictor of morbidity and mortality. It is often noted as a symptom in reported cases of refeeding syndrome, which is a potentially fatal complication in the treatment of patients suffering from malnutrition. OBJECTIVE: A case of delirium due to refeeding syndrome in a 61-year-old man is presented to help clinicians recognize this entity. The pathophysiology of refeeding syndrome and its possible role as an as-yet poorly-identified iatrogenic cause of delirium are discussed. METHOD: A diagnosis of delirium due to refeeding syndrome was made, and a nutrition consult was requested. Per nutrition recommendations, the patient was placed on a restricted calorie regimen, with aggressive supplementation of magnesium and phosphate. RESULTS: With his new dietary regimen, his mental status gradually improved, with complete resolution of his delirium by the 8th hospital day. He suffered no further episodes of confusion or disorientation. CONCLUSION: The relationship between refeeding syndrome and delirium may be of particular significance in the elderly, since malnutrition, medical hospitalization, and delirium are prevalent phenomena in this population.

Solomon M, Ozonoff S, Carter C, Caplan R. · Department of Psychiatry & Behavioral Sciences, University of California, Davis, 2230 Stockton Blvd., Sacramento, CA, 95817, USA. · J Autism Dev Disord. · Pubmed #18297385 No free full text.

Abstract: This study investigated whether children with autism spectrum disorders (ASDs) exhibit formal thought disorder (FTD), and whether this is related to ASD symptoms, executive control, and anxiety. Participants aged 8-17 with ASDs exhibited significantly more illogical thinking and loose associations than matched typically developing control subjects. In participants with ASDs, illogical thinking was related to aspects of cognitive functioning and to executive control. Loose associations were related to autism communication symptoms and to parent reports of stress and anxiety. When FTD is present in ASDs, it generally is not a co-morbid schizophrenia symptom, but is related to pragmatic language abnormalities found in ASDs. The clinical and neurobiological significance of this work is discussed.

Cheruvu PK, Finn AV, Gardner C, Caplan J, Goldstein J, Stone GW, Virmani R, Muller JE. · Harvard Medical School, Boston, Massachusetts, USA. · J Am Coll Cardiol. · Pubmed #17765120 No free full text.

Abstract: OBJECTIVES: Our purpose was to quantify the frequency and distribution of suspected vulnerable lesions, defined as thin-capped fibroatheroma (TCFA) and ruptured plaque, in human coronary artery autopsy specimens. BACKGROUND: Most acute coronary events and sudden death are believed to arise from rupture of a TCFA followed by thrombosis. Although there is general agreement that clinical events are usually caused by focal lesions, there is considerable debate over the relative importance of focal versus systemic factors in the pathogenesis of atherosclerosis. METHODS: We longitudinally sectioned coronary arteries from 50 whole hearts taken from patients (mean age 73 years, 64% men) dying of cardiovascular (n = 33), noncardiovascular (n = 13), and unknown (n = 4) causes. A total of 3,639 longitudinal segments of length 3 mm were sectioned from 148 arteries, accounting for 10.9 m of total tissue length. Specimens were classified on the basis of histology and computer-aided morphometry. RESULTS: Twenty-three TCFA and 19 ruptured plaques were found (mean +/- SD: 0.46 +/- 0.95 and 0.38 +/- 0.70 per heart, respectively), and these lesions accounted for only 1.6% and 1.2%, respectively, of the total length of the coronary tree examined in patients dying of cardiovascular causes. The majority of TCFA and ruptured plaque localized in the proximal third of the major coronary arteries, and in 92% of cases these lesions clustered within 2 or fewer nonoverlapping 20-mm segments. CONCLUSIONS: The suspected precursors of rupture-mediated thrombosis occur in a limited, focal distribution in the coronary arteries.

Jones JE, Watson R, Sheth R, Caplan R, Koehn M, Seidenberg M, Hermann B. · Department of Neurology, University of Wisconsin School of Medicine and Public Health, 600 N. Highland, Madison, WI 53742, USA. · Dev Med Child Neurol. · Pubmed #17593119 No free full text.

Abstract: The aim of this study was to characterize the distribution, timing, and risk factors for psychiatric comorbidity in children with recent onset epilepsy. Children aged 8 to 18 years with recent onset epilepsy (<1 year in duration) of idiopathic etiology (n=53) and a healthy comparison group (n=50) underwent a structured psychiatric diagnostic interview to characterize the spectrum of lifetime-to-date history of comorbid psychiatric disorder. There was no significant difference between the children with recent onset epilepsy and healthy comparison children in sex (31 males, 22 females vs 23 males, 27 females) or mean age 12.7y [SD 3.3] vs 12.7y [SD 3.2]). Children with recent onset epilepsy exhibited an elevated rate of lifetime-to-date Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) Axis I disorders compared with the comparison group. They showed significantly higher rates of depressive disorders (22.6 vs. 4%, p=0.01), anxiety disorders (35.8 vs 22%, p<0.05), and attention-deficit-hyperactivity disorder (26.4 vs 10%, p=0.01) with elevated but less prevalent rates of oppositional defiant and tic disorders. A subset of children with epilepsy (45%) exhibited DSM-IV Axis I disorders before the first recognized seizure, suggesting the potential influence of antecedent neurobiological factors that remain to be identified. The increased prevalence of psychiatric comorbidity antedating epilepsy onset may be consistent with the presence of underlying neurobiological influences independent of seizures, epilepsy syndrome, and medication treatment.

Carlson T, Reynolds CA, Caplan R. · UCLA Semmel Institute of Neuroscience and Human Behavior, UCLA Medical Center, Los Angeles, CA 90024, USA. · J Am Acad Child Adolesc Psychiatry. · Pubmed #17314721 No free full text.

Abstract: This case report describes two children who developed hyperammonemia together with frank manic behavior during treatment with a combination of valproic acid and risperidone. One child had been maintained on valproic acid for years and risperidone was added. In the second case, valproic acid was introduced to a child who had been treated with risperidone for years. In both cases, discontinuing the valproic acid resulted in normalization of ammonia levels and cessation of the manic behavior. This case report alerts physicians to the importance of obtaining serum ammonia levels in children treated with valproic acid and risperidone who present with manic behavior.

Zimmermann-Górska I, Kołczewska A. · Katedra i Klinika Reumatologiczno-Rehabilitacyjna i Chor6b Wewnetrznych Akademii Medycznej im. Karola Marcinkowskiego w Poznaniu. · Pol Arch Med Wewn. · Pubmed #17278785 No free full text.

Abstract: We describe a 56-year old man with rheumatoid arthritis and pulmonary nodules detected by HRCT. Needle biopsy confirmed the diagnosis of Caplan syndrome.