Attention biases,anxiety, and development: toward or away from threats or rewards?

Research on attention provides a promising framework for studying anxiety pathophysiology and treatment. The study of attention biases appears particularly pertinent to developmental research, as attention affects learning and has down-stream effects on behavior. This review summarizes recent findings about attention orienting in anxiety, drawing on findings in recent developmental psychopathology and affective neuroscience research. These findings generate specific insights about both development and therapeutics. The review goes beyond a traditional focus on biased processing of threats and considers biased processing of rewards. Building on this work, we then turn to the treatment of pediatric anxiety, where manipulation of attention to threat and/or reward may serve a therapeutic role as a component of Attention Bias Modification Therapy.     

Vascular dementia: dead or alive?

The term ‘Vascular Dementia’ remains popular as a diagnostic entity, since it encompasses a variety of vascular pathologies. This is in stark contrast to many clinical classificatory systems that weight their definitions strongly towards stroke alone. A diagnosis of vascular dementia is complicated by compounding factors that reduce both the validity and specificity of diagnostic systems. This review highlights some of the problems faced in epidemiological, clinical, neuropathological and radiological studies attempting to define a clear-cut syndrome of dementia associated with cerebrovascular disease. The role of non-stroke ischaemia is also discussed. It is concluded that the term ‘vascular dementia’ may have outlived its usefulness as a valid concept; alternative approaches are suggested. © 1998 John Wiley & Sons, Ltd.     

Treating anomia in semantic dementia: improvement, maintenance, or both?

A treatment programme for AK, an anomic patient with semantic dementia is described. The programme was based on home practice and resulted in re-learning the names of some objects AK could not name and/or comprehend prior to the treatment. The effects of treatment were still present one month post-treatment for items that AK could not name but could comprehend prior to treatment. In addition to items that AK could not name, items that she could both understand and name were also included in the programme. This allowed us to evaluate the influence of practice on the retention of words that appeared to be intact at the outset of the investigation. Results indicated that practice delayed the progression of loss. In addition, the programme was designed jointly with AK who made many important decisions related to treatment.     

Stalin's last years: delusions or dementia?

The sheer scale of Stalin's achievements and institutionalized terror has prompted some authors to label him as a paranoid megalomaniac. Whatever the merits of this diagnosis, his undeniable accomplishments and the rationality of many of his actions cannot be explained by the workings of a disturbed mind. In his last years, however, his life-long suspiciousness became florid paranoia. He eschewed medical advice, listening to a veterinarian and treating his hypertension with iodine drops. Stalin feared his own shadow and trusted no-one, even himself. He increasingly withdrew from official functions and he muttered menacingly to his close associates that it was time for another purge. Stalin suffered at least one stroke prior to his fatal intracerebral haemorrhage in 1953. Given his untreated hypertension and the autopsy report, it is probable that he had a number of lacunar strokes. These tend to predominate in the fronto-basal areas, and disconnect the circuits that underpin cognition and behaviour. The most plausible explanation of Stalin's late behaviour is the dimming of a superior intellect and the unleashing of a paranoid personality by a multi-infarct state.     

Alzheimer's dementia or cerebral toxoplasmosis? Case study of dementia following toxoplasmosis infection

Cerebral toxoplasmosis can lead to dementia in AIDS and in immunodeficient patients. We present a case study in which cerebral toxoplasmosis was associated with a dementia of Alzheimer type. Half a year to one year before the cognitive impairment began, the patient suffered a subacute infection of toxoplasmosis at the age of 56. Neuropsychological examination as well as MRI suggested a diagnosis of dementia with infectious genesis. However, serological tests showed only little evidence of infection. Since the results of the PET examination indicated changes in the glucose metabolism typical of Alzheimer's disease, we infer a comorbidity of cerebral toxoplasmosis and dementia of Alzheimer type.     

Frontotemporal dementia: one disease, or many?: probably one, possibly two

Accumulating evidence suggest that frontotemporal dementia is best viewed as a clinical syndrome even though there are distinct presentations of the behavioral variety, progressive aphasia, semantic dementia, corticobasal degeneration and progressive supranuclear palsy. Similarly the pathology should be regarded as a spectrum even though histological varieties are distinguished. More than half of FTD pathology is associated with ubiquitin positive and tau negative inclusions that are common in ALS. However the majority of FTD cases do not have ALS clinically and relatively few ALS cases develop FTD. The pathological and biochemical varieties can be dichotomized as tau positive and tau negative pathology and biochemistry. The genetics of the tau positive variety is associated with tau mutations and so far the tau negative variety is not, although some are linked to chromosome-17 also. There is a corresponding clinical dichotomy combining the behavioral variety of FTD presentation with semantic dementia and usually ubiquitin positive tau negative pathology on one hand and the association of primary progressive aphasia and cortical basal degeneration/PSP syndrome with tau positive pathology on the other. The overlap between them is too great to establish two separate diseases.     

Naming problems in dementia: Semantic or lexical?

Abstract

The naming behaviour was explored of patients moderately deteriorated with probable Alzheimer's disease (pAD) by analysing responses made on a picture naming and two word-picture matching tasks for the same items. Naming responses were classified into target and non-target and the relationship between non-target responses and their targets were explored. It was found that semantic relatedness influenced these non-target responses but frequency and imageability did not. The pAD participants performed significantly better on the two word-picture matching tasks than the naming task, while there was no difference on these within- and between-category tasks. These findings are explored with reference to a two-stage model of lexical access, which has separate storage of semantic, lexical and phonological information. The participants' difficulties appear to lie largely in retrieving the labels for items they comprehend.     

Alzheimer's disease versus vascular dementia -- dichotomy or interaction?

Alzheimer's dementia (AD) and vascular dementia (VD) are the two major forms of dementia in the elderly. They have been separated categorically on the basis of pathophysiological findings and clinical operationalized criteria. However, this strict separation has to be reevaluated in the light of recent data. The risk to develop a neurodegenerative dementia in old age is determined by various susceptibility genes and correlated with aging. In AD, the current understanding of pathophysiology focuses on the amyloid cascade hypothesis as the major endpoint of the complex cellular pathology. In VD, incomplete microangiopathic infarcts due to fibrohyalinosis are regarded as the major pathophysiological event. A controversial discussion exists about the coincidence or interaction of genetically determined risk factors of AD and/or VD. Further interactions between AD and VD exist with regard to perivascular mediators and those factors which impair cerebral blood flow. Based on these and other recent neuropathological and therapeutic findings the hypothesis is proposed that the two specific etiopathologies of AD and VD interact to precipitate clinical dementia in the individual and that the individual phenomenology of these dementias is modified by vascular risk factors. Neither, a categorical separation of AD and VD nor the recent idea to regard AD as a distinct form of vascular dementia, do appear convincing.     

Frontotemporal dementia and semantic dementia: anatomic variations on the same disease or distinctive entities?

Research into the non-Alzheimer dementias has exploded over the last 2 decades, and frontotemporal lobar degeneration has emerged as the most common cause of dementia in patients below the age of 65. In 1998, an international consortium of investigators focusing on this disease entity met and agreed upon the classification of 3 subtypes of frontotemporal lobar degeneration, using regional atrophy to distinguish them. These are: a frontally predominant form called frontotemporal dementia, a temporally predominant form called semantic dementia, and a left-frontally predominant syndrome, called progressive nonfluent aphasia. With the rise of genetic and neuropathologic findings, however, the usefulness of this subtype classification has been called into question. This paper discusses the major pertinent findings, and the implications of classifying the disease on the basis of atrophy versus genetic or molecular mechanisms.     

Is subjective memory loss correlated with MMSE scores or dementia?

OBJECTIVES: (1) To determine if subjective memory loss (SML) is associated with Mini-Mental State Examination (MMSE) scores, (2) to determine if this association persists after adjustment for other factors, and (3) to determine the sensitivity and specificity of SML for dementia. POPULATION: 1751 seniors sampled from a population registry. MEASURES: Age, sex, education, SML, the MMSE, and the Center for Epidemiologic Studies-Depression (CES-D) scale. Dementia was diagnosed by clinical examination. ANALYSIS: Linear regression models were constructed. The sensitivity and specificity of SML were determined with a diagnosis of dementia being the gold standard. RESULTS: SML was correlated with MMSE scores, even after adjusting for age, sex, education, and depressive symptoms. The sensitivity of SML was 0.58 (95% confidence interval [CI]: 0.45, 0.71), and the specificity was 0.76 (95% CI: 0.74, 0.78) for dementia. CONCLUSIONS: SML is correlated with MMSE score. However, SML is neither sensitive nor specific for dementia.     

Can episodic memory tasks differentiate semantic dementia from Alzheimer's disease?

The performance of two groups of patients with semantic dementia (SD), with predominant right (SDR) and left temporal lobe atrophy (SDL), was contrasted with that of cases with probable Alzheimer's disease (AD) on a range of standard episodic memory tasks. While the SDL group achieved a good score on a composite visual, but not a verbal, episodic memory measure, the AD and SDR groups were equivalently impaired at visual and verbal memory. The SD, but not the AD, groups were, by definition, impaired on simple tests of semantic memory. Standard verbal episodic memory tests, therefore, failed to discriminate patients with SD from those with probable AD and even visual memory tests may result in misclassification of SDR cases.