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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnostic evaluation of dementia is directed toward the identification of treatable causes. It can be facilitated by classification of the dementia into one of four categories: attentional, amnestic, cognitive, and intentional. Intentional dementia reflects dysfunction of frontal lobe systems, components of which include the frontal cortex, basal ganglia, thalamus, limbic structures, and subcortical white matter. Disorders that affect one or more of these components and produce intentional dementia include Binswanger's disease, Parkinson's disease, Huntington's disease, HIV infection, closed head injury, normal pressure hydrocephalus, neoplasms, syphilis, vitamin B12 deficiency, multiple sclerosis, and a number of uncommon degenerative and acquired syndromes. Depression may resemble intentional dementia. Guidelines for diagnosis and management are discussed.
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PMID:Multi-infarct dementia, subcortical dementia, and hydrocephalus. 203 8

This psychopathological study about the experience of anxiety in 160 melancholic and 93 neurotic depressive patients (diagnostic criteria acc. to ICD-9) aims at reconsidering earlier findings about the anthropological essence of melancholia. Anxiety seems to be especially appropriate to examine changes in time experience emphasized by phenomenological authors. Only 5% of the melancholic patients spontaneously report on alterations of the experience of time. Self reports point to a "basic disturbance of temporal development" (von Gebsattel) in melancholia. The temporal structure of the experience of anxiety however, more depends on the respective content of anxiety than on the patient group examined. On the contrary the natural matter of course in dealing with hitherto familiar affairs gets lost more often in melancholia than in non-melancholic states: Anxiety about all and everything and anxiety related to depersonalization prove to be characteristic of melancholia, even with regard to the severity of depression. The data confirm that beyond changes of time experience a "separateness from the essential conditions of natural experience" (Binswanger) comes to light in melancholia.
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PMID:[Phenomenologic findings in melancholia in relation to empirical studies]. 239 61

Two cases of subcortical arteriosclerotic encephalopathy (Binswanger's disease) are reported. The two patients lacked a clinical history of hypertension, relevant pathogenetic factor in the development of the small and medium size cerebral arteries atherosclerosis, which is the main pathologic finding of the disease. The two subjects clinically showed a marked intellectual deterioration, together with mood depression and focal neurological signs, that were an expression of the multifocal neurologic involvement. In both cases CT scans evidentiated a mainly periventricular leucoencephalopathy associated, in the first patient, with small multiple ischemic lesions and, in the second, with a unique hypodense area in the centrum semiovale. A review of the literature on the subjects is proposed, together with an attempt of pathogenetic interpretation of our two cases.
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PMID:[2 cases of Binswanger's disease not associated with arterial hypertension: clinical-instrumental and neuropsychological evaluation]. 305 88

The authors describe four elderly patients with Binswanger's disease in whom depression was prominent. Therapy with antidepressant drugs in three patients produced major improvement in psychological and physical functions. The one patient who could not be given an adequate course of antidepressant therapy because of intercurrent illness improved spontaneously after many months. The authors conclude that depression associated with Binswanger's disease is reversible despite persistence of neurological abnormalities. They speculate that this depressive syndrome is an example of organic affective disorder due to diffuse subcortical white matter ischemic lesions of the cerebral hemispheres and discuss the possible neuroanatomical basis of the depression.
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PMID:Reversible depression in Binswanger's disease. 333 86

A series of 79 patients with multi-infarct dementia (MID) were divided into 2 groups designated cortical MID and subcortical MID, according to whether the computed tomography (CT) scan showed the presence or absence of cortical infarcts, and an absent to mild or moderate to severe degree of white matter low attenuation (WMLA). Cortical MID was characterized by repeated atherothrombotic and cardiogenic strokes, moto-sensory hemiparesis, a severer degree of aphasia, and abrupt onset of cognitive failure. Subcortical MID typically showed the following features: lacunar strokes, bulbar signs including dysarthria, pure motor hemiparesis, depression and emotional lability. WMLA was found in all patients with subcortical MID but also in over 60% of those with cortical MID. In the 2 groups CT scans showed equal frequencies of deep infarcts. When divided according to severity of WMLA, 92% of patients in the cortical MID group and 44% of those in the subcortical MID group were found to have at least one cortical infarct on the CT scan. Although cortical and subcortical MID differed in several clinical features, they did not show major differences in the risk factors for stroke, and clearly overlapped each other as regards ischaemic scores and the findings in neurological examinations and CT. Thus, it is still an open question whether cortical MID and subcortical MID, including the lacunar state and Binswanger's disease, are 2 distinct entities or merely represent the expression of biological variation while having the same etiopathogenesis.
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PMID:Types of multi-infarct dementia. 363 Jun 35

A 69-year-old woman with clinical and CT scan evidence of Binswanger's encephalopathy was successfully treated for an accompanying depression with tranylcypromine. The changing clinical and CT findings in this disorder are discussed, as well as the implications for the care and study of elderly depressed patients.
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PMID:Depression in Binswanger's encephalopathy responsive to tranylcypromine: case report. 396 50

Neurofibrillary tangles and dystrophic neurites are characteristic pathological features found in the brains of Alzheimer's disease (AD) patients. A major constituent of these lesions is the cytoskeletal protein tau. This study examined whether the measurement of tau in cerebral spinal fluid (CSF) has value in the diagnosis of AD. Seventy-seven subjects were enrolled in this prospective study: These included AD (N = 24), Neurological Controls (dementing diseases/syndromes, N = 26), Normal Controls (N = 14), and Others (N = 13). CSF was obtained by lumbar puncture, and tau concentrations (pg/mL) were determined using a dual monoclonal antibody microplate immunoassay. The mean tau value for AD subjects (1,430 +/- 739) was significantly different from Neurological Control subjects (790 +/- 579) (p < 0.001) and Normal Control subjects (816 +/- 355) (p < 0.001). Tau values were elevated in two Neurological Control subjects, one with Binswanger's disease (age 75) and one with depression (age 90). Tau values were also elevated in three Normal Control subjects; two were subjects with a family history of AD. Tau concentrations did not correlate significantly with age in AD subjects (r = 0.05, p = 0.82) or in Normal Control subjects (r = -0.49, p = 0.08). Tau also did not correlate with severity of cognitive impairment in AD subjects (r = -0.03, p = 0.91) or duration of AD symptoms (r = 0.16, p = 0.52). Based on these results and others, CSF levels of tau protein may provide a useful biochemical marker to aid in the clinical diagnosis of AD.
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PMID:Tau protein in cerebrospinal fluid as an aid in the diagnosis of Alzheimer's disease. 760 2

Vascular dementia (VAD) is common, and small vessel disease is one of the most frequent etiologies of the disorder. Lacunar state and Binswanger's disease are the two types of VAD associated with small vessel disease. Lacunar state and Binswanger's disease produce a dementia syndrome with characteristics of subcortical dementia including slowing of information processing, impaired memory, and poor sustained attention. Executive dysfunction includes poor word list generation and verbal fluency (design generation), impaired motor programming with perseveration and impersistence, and difficulty with set shifting. Memory loss in subcortical VAD is characterized by poor retrieval and intact recognition. Apathy is ubiquitous in VAD and depression and psychosis are common. Parkinsonism with prominent gait disturbances in conjunction with pyramidal tract signs, dysarthria, pseudobulbar affect, and incontinence are frequent motor manifestations of VAD with small vessel disease. The lesions of subcortical VAD affect the structures--caudate nucleus, globus pallidus, thalamus-and connecting fibers of frontal--subcortical circuits and produce a clinical syndrome similar to that seen in other subcortical diseases.
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PMID:Vascular subcortical dementias: clinical aspects. 808 75

Since the late 1800s, when Alzheimer and Binswanger proposed the concept of "arteriosclerotic brain degeneration," there has been an evolution in thinking regarding cerebrovascular disease (CVD) as a basis for dementia. While later work recognized the importance of specific infarct characteristics including volume, multiplicity, and location, recent studies have found that many factors may work in combination with those characteristics to produce dementia, including white matter disease; vascular risk factors such as diabetes; comorbid illnesses, particularly those that might produce cerebral ischemia or hypoxia; genetic factors; and host characteristics such as older age and fewer years of education. Studies of the prevalence of vascular dementia (VaD) have suggested that CVD is second only to Alzheimer's disease as a basis for dementia in Western countries and the most common basis in certain Asian countries, but those studies may have underestimated the frequency of dementia associated with CVD due to a failure to perform brain imaging and decreased survival among patients with CVD. Few studies of the incidence of VaD have been performed, but they have also consistently demonstrated an elevated risk associated with CVD. While certain methodologic issues have contributed to the debate regarding the importance of CVD as a basis for dementia, including variability in the techniques that have been used to characterize brain lesions, assess cognitive function, and diagnose dementia; difficulties inherent in the determination of a causal role for CVD in dementia; and the potential confounding effects of aphasia and depression in patients with stroke, it is clear that VaD remains an important public health problem.
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PMID:Vascular dementia: a construct in evolution. 896 67

Vascular dementia (VAD) is currently considered to be the second most common cause of dementia in Europe and the USA, second to dementia of the Alzheimer's type (DAT). However, in Asia and many developing countries the incidence of VAD exceeds that of DAT. The positive clinical diagnostic workup for VAD requires six steps: (1) clear-cut quantitative assessment of cognitive deficits utilizing standard neuropsychological tests to establish and quantify the dementia syndrome and rule out pseudo-dementia OF depression; (2) ascertaining the presence of risk factors for stroke; (3) identifying cerebral vascular lesions by neuroimaging (MRI, Iodine or Xenon contrasted CT, PET and SPECT); (4) exclusion of other causes of dementia; (5) differential diagnosis of possible, probable or definite VAD versus DAT and ascertaining when there are mixtures of the two; and (6) temporal identification of causality between onset and progression of the dementia with identified cerebral vascular lesions. There are eight subtypes of VAD: (1) multi-infarct dementias. These are due to large cerebral emboli, and are usually readily identifiable; (2) strategically placed infarctions causing dementia; (3) multiple subcortical lacunar lesions. Patients with these develop VAD at least five to twenty-five times more frequently than those in age-matched general population samples; (4) Binswanger's disease (arteriosclerotic subcortical leuko-encephalopathy). This form is rare. Neuroimaging confirms the diagnosis during life but the diagnosis can not be made by neuroimaging alone; (5) mixtures of two or more of above VAD subtypes; (6) hemorrhagic lesions causing dementia; (7) subcortical dementias due to cerebral autosomally dominant arteriolopathy with subcortical infarcts and leuko-encephalopathy (CADASIL), or to familial amyloid angiopathies and coagulopathies all of which present with multiple subcortical lacunar lesions similar to Binswanger's disease; (8) mixtures of DAT and VAD. The clinical significance of leukoaraiosis and its suspected relationships to VAD remains to be better established. The presence of ischemic infarctions, single or multiple large or multiple small (lacunar) by neuroimaging are necessary for the diagnosis of VAD, but identifying their presence, by neuroimaging alone, does not permit the diagnosis of dementia which can only be established by neuropsychological assessments. VAD is a clinical entity, identifiable in at least 30-70% of patients after strokes but mechanisms responsible for the cognitive impairments are complex. Some of these mechanisms are incompletely understood but provide subjects for important future research.
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PMID:Vascular dementia: still a debatable entity? 898 Dec 95


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