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Gabriel Gold

Publications and source records attributed to Gabriel Gold.

24 records · Page 2Linked to original sources

Metabolic correlates of behavioral and affective disturbances in frontal lobe pathologies.

OBJECTIVE: Although previous studies have shown that the human frontal cortex is involved in the experience of emotions as well as in social behavior, data regarding the exact anatomical substrates of behavioral and affective deficits in frontal lobe pathologies are still scarce. The aim of this study was to investigate the metabolic correlates of these deficits in a group of non-selected consecutive patients with frontal lobe lesions. PATIENTS AND METHODS: Clinicometabolic correlations between several emotional and social parameters and metabolic patterns in the frontal cortex and amygdala were investigated in 32 patients with frontal lobe pathologies. The behavioral disturbances were evaluated using the Lhermitte's informant questionnaire. Regional cerebral glucose metabolism was measured with [(18)F] fluorodeoxyglucose and high-resolution positron emission tomography. Statistical analysis was performed using both single variable correlation and multiple regression analyses. RESULTS: Both single variable and multivariate analyses demonstrate that decreased regional glucose metabolism in the right medial area 10 was associated with apathy. There were also significant negative relationships between metabolism in the right orbitofrontal cortex and stereotypy and indifference to rules. Impulsiveness, personality disturbances and loss of emotional control were associated with decreased metabolism in the left amygdala. CONCLUSIONS: In terms of clinicometabolic correlations, the present data support the implication of different functional anatomic systems in frontal lobe-related behavioral and affective disturbances. In particular, they imply that the classically described symptoms of impaired behavioral control may be related to right orbitofrontal cortex hypometabolism whereas impaired regulation of emotions may result from a functional damage of the left amygdala.

Adult↗

Vascular dementia: a diagnostic challenge.

Although vascular dementia was described over a century ago, it remains a difficult and challenging diagnosis. Several sets of clinical criteria have been published in an effort to establish the presence or absence of vascular dementia in a standardized fashion. Clinical studies have demonstrated that they identify different groups of patients and are thus not interchangeable. Retrospective clinicopathological correlations have shown that most are insufficiently sensitive, although they are generally relatively specific. They accurately exclude pure Alzheimer's disease but may include 9% to 39% of mixed dementia cases (Alzheimer's disease and vascular dementia combined). Further studies are needed to develop better performing criteria that could lead to a broad consensus on the clinical diagnosis of vascular and mixed dementia.

Aged↗

Stereologic evidence for persistence of viable neurons in layer II of the entorhinal cortex and the CA1 field in Alzheimer disease.

The entorhinal cortex and hippocampus are the first cortical regions to be affected by the degenerative cellular process that leads to Alzheimer disease (AD) and display a limited degree of neuronal alterations in normal aging. Several quantitative studies have reported a substantial loss of neurons in these regions and a parallel increase in the number of neurofibrillary tangles (NFTs). However, accurate quantitative data on the dynamics of NFT formation are lacking. Here, we performed a stereologic assessment of the proportions of intracellular and extracellular (ghost) NFTs (iNFTs and eNFTs, respectively) and unaffected neurons in layer II of the entorhinal cortex and in the pyramidal cell layer of the CA1 field of the hippocampus in elderly control cases compared to cases with varying degrees of cognitive dysfunction. The data revealed differential rates of formation of iNFTs and eNFTs between the 2 regions and confirmed the presence of a severe disease-associated, but not age-related, neuronal loss. They also revealed that large numbers of neurons may persist either unaffected or in a transitional stage of NFT formation until the late stages of AD progression. These neurons with viability potential constitute 73% of the total numbers of profiles in layer II of the entorhinal cortex and 77% in the CA1 field in cases with a Clinical Dementia Rating score of 3. Whereas it is not possible in the present study to assess how functional such neurons with altered physiology might be, it is nonetheless likely that these transitional neurons open new options for potential therapeutic interventions aimed at protecting neurons vulnerable to neurofibrillary degeneration.

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Mixed dementia: epidemiology, diagnosis, and treatment.

Alzheimer's disease (AD) and vascular dementia (VaD) are the most frequent causes of dementia in older people. Although AD can be diagnosed with a considerable degree of accuracy, the distinction between isolated AD, VaD, and mixed dementia (MD), where both pathologies coexist in the same patient, remains a controversial issue and one of the most difficult diagnostic challenges. Although MD represents a very frequent pathology, especially in older people, as reported in neuropathological studies, the respective importance of degenerative and vascular lesions, their interaction in the genesis of dementia, and the mere existence of MD are still debated. Accurate diagnosis of MD is of crucial significance for epidemiological purposes and for preventive and therapeutic strategies. Until recently, pharmacological studies have generally focused on pure disease, AD or VaD, and have provided little information on the best therapeutic approach to MD. This article provides an overview of MD in older people. A retrospective review of the recent literature on prevalence, incidence, course, risk factors, diagnosis, and treatment of MD was performed. The article also emphasizes the need for further studies, including neuropsychological and functional evaluations, and neuroimaging and clinicopathological correlations to develop a better understanding of MD, which appears to be one of the most common forms of dementia.

Aged↗

End-of-life care of persons with dementia.

Many clinicians with different training and practice are involved in the care of persons with dementia. Whereas neurologists and psychiatrists focus their attention on the early phase of dementia, geriatricians and palliative care specialists are particularly involved at the end of demented patients' lives. To summarize the progress of knowledge in this field, it seems possible to answer four fundamental questions. When? Several longitudinal studies of cohorts of demented and nondemented patients showed clearly that dementia is a risk factor for early death. There are no survival differences between Alzheimer's and Lewy body disease patients. Patients with vascular dementia have the worst prognosis. These results need to be analyzed with consideration of associated comorbidity, types and intensity of care, and dementia treatment. Why? Studies conducted on the basis of death certificates appear to be biased. A large autopsy study performed in the geriatric department of Geneva University Hospital showed no difference existed in immediate causes of death between demented and nondemented hospitalized old patients. On the other hand, cardiac causes are significantly more frequent in vascular dementia than in Alzheimer's disease or mixed dementia patients. How? Deaths of demented patients raise a lot of ethical considerations. It is always difficult to know demented patients' awareness of the end of life. It is really difficult to accompany these patients, with whom communication is essentially nonverbal. During this delicate phase of the end of life, how can formal health professionals help the family members who are afraid of both death and dementia? And after? Suffering of family members and caregivers has to be strongly considered. This goal includes the improvement of our communication skills with the patient, and the facilitation of interdisciplinary exchanges with the caregiver's team and with the family members to allow acceptance of the death.

Aged↗

Clinicopathological validation study of four sets of clinical criteria for vascular dementia.

OBJECTIVE: The authors' goal was to validate the clinical criteria for vascular dementia of the State of California Alzheimer's Disease Diagnostic and Treatment Centers (ADDTC), the National Institute for Neurological Disorders and Stroke-Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN), DSM-IV, and ICD-10. METHOD: Sensitivity and specificity were assessed by comparing the clinical with the neuropathological diagnosis of 89 autopsied patients with dementia from a geriatric and psychiatric hospital. All cases were reviewed by a clinician and a neuropathologist who were blind to each other's findings. RESULTS: Neuropathologically there were 20 cases of vascular dementia, 23 cases of mixed dementia, and 46 cases of Alzheimer's disease among the autopsied patients. The sensitivity was 0.50 for DSM-IV criteria for vascular dementia, 0.70 for ADDTC criteria for possible vascular dementia, 0.55 for NINDS-AIREN criteria for possible vascular dementia, 0.20 for ICD-10 criteria for vascular dementia, 0.25 for ADDTC criteria for probable vascular dementia, and 0.20 for NINDS-AIREN criteria for probable vascular dementia. Specificity was 0.84, 0.78, 0.84, 0.94, 0.91, and 0.93, respectively. The proportion of cases clinically classified as vascular dementia ranged from 0% to 13% for neuropathologically confirmed cases of Alzheimer's disease and 9% to 39% for neuropathologically confirmed cases of mixed dementia. There was no statistically significant relationship between the neuropathological diagnosis and three of the clinical criteria sets studied (ICD-10 criteria for vascular dementia and ADDTC and NINDS-AIREN criteria for probable vascular dementia). CONCLUSIONS: Clinical criteria for vascular dementia are not interchangeable. The ADDTC criteria for possible vascular dementia are the most sensitive for the detection of vascular dementia; however, the DSM-IV criteria for vascular dementia and the NINDS-AIREN criteria for possible vascular dementia may be more effective in excluding mixed dementia. Given their inability to detect the vast majority of cases of vascular dementia, the ICD-10 criteria for vascular dementia and the ADDTC and NINDS-AIREN criteria for probable vascular dementia should be revised.

Aged↗