{"title":"Pharmacotherapy of late life mood disorders.","authors":"N Herrmann, K E Bremner, C A Naranjo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The pharmacotherapy of elderly patients with affective illnesses presents clinicians with a number of challenges. Changes associated with normal aging, as well as concomitant medical illnesses and their treatment, can affect the pharmacokinetics and pharmacodynamics of psychotropic drugs. Furthermore, the relative paucity of controlled trials with elderly patients necessitates a reliance on studies done on younger populations, which may be inappropriate. This review attempts to highlight how knowledge of the effects of aging on pharmacokinetics and pharmacodynamics can help clinicians optimize therapy for their older patients with affective disorders.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 1","pages":"41-7"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20011242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Molecular and biochemical events within the brain subjected to cerebral ischemia (targets for therapeutical intervention).","authors":"T Kogure, K Kogure","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We review the molecular and biochemical events that occur within the brain during cerebral ischemia, based on recent investigations of focal cerebral ischemia models. Occlusion of the middle cerebral artery in rats produces focal ischemia. In contrast to the core where ischemia is severe and infarction develops rapidly, areas surrounding the core (called the penumbra) show a more moderate decrease of blood flow and can tolerate longer durations of ischemic stress. Reperfusion and pharmacological interventions can help to salvage the penumbra. Ischemic insult alters the genomic properties of the brain cells and selective production of heat shock proteins can be seen. Heat shock proteins are necessary in the repair of cell integrity, and is thought to be induced as a rescue program. Pre-ischemic induction of these proteins is known to cause ischemic tolerance, and methods to manipulate genes into inducing HSPs may be effective in protecting neurons from ischemia. Genes that promote apoptosis are also expressed after ischemia, and may cause secondary expansion of the infarction. Strategies to denote expression of these genes may be effective in reducing ischemic neuronal death. Activation of the inflammatory cells such as neutrophils and macrophages, in the ischemic region, may cause further post-ischemic damage. Investigations on the role and mechanics of inflammatory systems in ischemic neuronal injury may present a new target for therapeutic intervention against stroke.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 4","pages":"179-83"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20132597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of Ca+2 and other second messengers in excitatory amino acid receptor mediated neurodegeneration: clinical perspectives.","authors":"A Schousboe, B Belhage, A Frandsen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Neurodegeneration associated with neurological disorders such as epilepsy, Huntington's Chorea, Alzheimer's disease, and olivoponto cerebellar atrophy or with energy failure such as ischemia, hypoxia, and hypoglycemia proceeds subsequent to overexposure of neurons to excitatory amino acids of which glutamate and aspartate may be quantitatively the most important. The toxic action of glutamate and aspartate is mediated through activation of glutamate receptors of the N-methyl-D-aspartate (NMDA) and non-NMDA subtypes. Antagonists for these receptors can act as neuroprotectants both in in vitro model systems (e.g., cultured neurons) and in vivo. Activation of receptors leads to an increase in the intracellular Ca++ concentration and also to an increase in other second messengers such as cGMP. Thus, Ca++ channel antagonists may have neuroprotective action under certain conditions.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 4","pages":"194-8"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20132599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Magnetic resonance imaging in optic neuropathy.","authors":"I Moseley, A Gass","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Magnetic resonance imaging has revolutionised the ability to investigate intrinsic disease of the anterior optic pathways. We review the data accumulated from this technique not only in the conditions, such as neoplasia, which have traditionally been the domain of neuroimaging, but also in inflammatory, metabolic and degenerative diseases.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 5","pages":"302-19"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20233239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Anterior ischemic optic neuropathy.","authors":"S S Hayreh","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Anterior ischemic optic neuropathy (AION), one of the most prevalent and visually crippling diseases in the middle-aged and elderly, potentially bilateral, is due to acute ischemia of the optic nerve head. For a logical understanding of its pathogenesis, underlying causes, clinical features, and management, it is essential to comprehend the basic scientific issues involved; these are discussed briefly in this paper. Clinically, AION is of two types: (1) arteritic AION (due to giant cell arteritis) and (2) nonarteritic AION (due to other causes). Arteritic AION is an ophthalmic emergency because of its potential of causing rapid, bilateral complete blindness which is almost always preventable if treated immediately with large doses of systemic corticosteroids. Clinical parameters which help to differentiate the two type of AION, and their management are discussed.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 5","pages":"251-63"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20233343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neuroimaging in late-life mood disorders.","authors":"A Kumar, D Miller","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Neuroanatomical and physiological imaging provide unprecedented opportunities to examine the biological substrates of major mental disorders such as late life major depression (MDD). Studies using positron emission tomography (PET) and single photon emission computed tomography (SPECT) demonstrate focal and global abnormalities in patients with MDD when compared with controls. Magnetic resonance imaging (MRI) allows us to examine specific neuroanatomical perturbations in depression and to study the impact of comorbid medical disorders on brain structure and function. These technologies have the potential to provide biological information critical to a better understanding and conceptualization of the neuroscientific basis and treatment of the major mental disorders in late life.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 1","pages":"8-15"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20011237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lexical-semantic organization: evidence from aphasia.","authors":"R S Berndt, C C Mitchum","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The emerging field of clinical neuroscience requires the combination of diverse theoretical and methodological approaches to the study of brain function. The study of neurogenic language disorders has played a central role in the development of models of language/brain relationships. These contributions are reviewed with regard to the study of word processing impairments in aphasia, where data from brain-damaged patients has been used to guide the development of models of lexical/semantic organization. It is argued that the study of aphasic patients will continue to occupy a central role in both neuroscience and clinical research as new technologies are developed for functional brain imaging and as theoretically driven treatments for aphasia are designed and tested.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 2","pages":"57-63"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20014859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Childhood aphasias.","authors":"I P Martins","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The study of acquired childhood aphasia has shown that the aphasic syndromes found in adults are reproducible in children with identical lesion sites and that some brain areas are essential for aphasia recovery. Besides, language deficits and learning difficulties are very common in the long-term follow-up of those children. This suggests that the adult pattern of cerebral organization for speech is established early in life and alternative organizations have a lasting price. Yet in contradiction with this, children with focal lesions sustained pre- or perinatally do not show developmentally the aphasic syndromes observed in older children and adults. One possible explanation is that the areas responsible for learning a function are different from those subserving that function as a more mature stage of development. Concerning specific language impairment in children, there is a growing evidence that such syndromes are genetically determined, but there is still a missing link between this predisposition and the structural/functional defects underlying them. The finding that these children are often impaired in other areas of mental development indicates that there may be a more basic cognitive defect underlying their language disorders.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 2","pages":"73-7"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20014861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of nitric oxide in retinal cell death.","authors":"S Roth","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide from L-arginine, exists in three major isoforms, neuronal, endothelial, and immunologic. Neuronal and immunologic NOS has been detected in the retina. Neuronal NOS may be responsible for producing nitric oxide in photoreceptors and bipolar cells. Nitric oxide stimulates guanylate cyclase of photoreceptor rod cells and increases calcium-channel currents, which may be significant in the photoresponse. Inducible nitric oxide synthase, found in Müller cells and in retinal pigment epithelium, may be involved in normal phagocytosis of the retinal outer segment, in infectious and ischemic processes, and in the pathogenesis of diabetic retinopathy. Nitric oxide contributes to basal tone in the retinal circulation. To date, findings are conflicting with respect to its role in retinal autoregulation. During glucose and oxygen deprivation, nitric oxide may increase blood flow and prevent platelet aggregation, but it may also mediate the toxic effects of excitatory amino acid release. Nonspecific inhibition of NOS appears to protect the retina from ischemic damage, suggesting an important role of nitric oxide in the pathogenesis of retinal ischemic injury, and possible therapeutic approaches in patients with retinal vascular occlusion.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 5","pages":"216-23"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20233338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Autonomic neuropathy: clinical and instrumental findings.","authors":"V Spallone, G Menzinger","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The development of sensitive techniques evaluating functions under autonomic control has allowed the early detection of widespread abnormalities in diabetes mellitus. However, despite a high frequency of functional abnormalities, an overt clinical syndrome develops slowly and is quite rare. Characteristic clinical features, more recent methods for evaluating autonomic function, diagnostic procedures, and main instrumental findings in a diabetic population are reported. Emphasis is given to more promising techniques evaluating autonomic control of the cardiovascular system, such as myocardial scintigraphy and assessment of 24-h blood pressure and heart rate variability. The clinical meaning of the number of functional abnormalities observed in diabetic patients is considered. While the role of autonomic neuropathy in the pathogenesis of gastrointestinal motor disorders, hypoglycaemia unawareness or diabetic impotence needs to be revised, the importance of autonomic-related sweating and blood flow abnormalities in the pathogenesis of diabetic foot lesions is now better documented. Moreover, growing evidence of the importance of autonomic control of cardiovascular system, together with cardiovascular dysfunction linked to diabetic autonomic neuropathy, supports the hypothesis of a possible role of autonomic neuropathy in the increased cardiovascular morbidity and mortality observed in diabetic patients.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 6","pages":"346-58"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20289778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}