-
Journal of the National Medical... Jun 1996There remains nearly a twofold increase in blacks compared with whites for stroke mortality. The death rate from cerebral hemorrhage in blacks approximates twice that of... (Review)
Review
There remains nearly a twofold increase in blacks compared with whites for stroke mortality. The death rate from cerebral hemorrhage in blacks approximates twice that of whites. Subarachnoid hemorrhage is a frequent cause of mortality and morbidity in stroke and is also about twice as frequent in blacks. Lacunar strokes occur more in blacks reflecting increased incidence of hypertension and are leading causes of multi-infarct encephalopathy and dementia. Therefore, the concomitant occurrence of hypertension and stroke is most common in African Americans and requires diagnosis of the type of stroke, which then defines the rationale of blood pressure control. Cerebral vascular changes associated with acute, chronic, and reactive hypertension are operative. When to treat, when not to treat, and the appropriateness of specific antihypertensive agents in acute stroke are relevant. A common misconception is that the increased blood pressure is the cause of the stroke when it is likely the result of the stroke. Lowering the blood pressure in all acute stroke patients with elevated blood pressure may worsen the neurologic deficit. Thus, the judicious control of blood pressure is to be stressed in the concomitant occurrence of hypertension and stroke.
Topics: Antihypertensive Agents; Barbiturates; Black People; Cerebrovascular Disorders; Humans; Hypertension
PubMed: 8691497
DOI: No ID Found -
The Nurse Practitioner Nov 1990Older adults in non-psychiatric acute and long-term care settings need to be screened routinely for cognitive function and mental status by clinicians and health care... (Review)
Review
Older adults in non-psychiatric acute and long-term care settings need to be screened routinely for cognitive function and mental status by clinicians and health care providers. Screening instruments increasingly are being used in order to evaluate programs, implement clinical decisions and conduct research. The purpose, scope and depth of needed assessment guides the selection of the screening instrument. This article critically reviews 11 screening instruments used to assess cognitive function and mental status in older adults: Dementia of the Alzheimer Type Inventory, Brief Cognitive Rating Scale, Blessed Dementia Scale, Cognitive Capacity Screening Examination, Cognitive Levels Scale, FROMAJE, Global Deterioration Scale, Mini-Mental State Exam, Clinical Dementia Rating, Mental Status Questionnaire and the Short Portable Mental Status Questionnaire. Since cognitive impairment is a broad construct, the descriptors used to search the literature were the following: age-associated memory impairment, acute confusional states, Alzheimer's disease, cognition, confusion, delirium, dementia, mental status, multi-infarct dementia, Pick's disease, primary degenerative dementia, pseudodementia and senile dementia of the Alzheimer's type. The Brief Cognitive Rating Scale and the Dementia of the Alzheimer Type Inventory are the only two instruments capable of distinguishing Alzheimer's from other dementias, and the CDR is the only instrument that assesses hobbies.
Topics: Aged; Cognition Disorders; Humans; Mental Status Schedule; Psychiatric Status Rating Scales; Psychometrics
PubMed: 2255423
DOI: No ID Found -
Brain : a Journal of Neurology May 2017
Topics: 3' Untranslated Regions; Collagen Type IV; Dementia, Multi-Infarct; Family Health; Female; Genetic Association Studies; Genetic Predisposition to Disease; HEK293 Cells; Humans; Male; MicroRNAs; Mutation; Sweden; Transfection
PubMed: 28369186
DOI: 10.1093/brain/awx062 -
Journal of Neurology, Neurosurgery, and... Sep 1988An auditory discrimination paradigm was employed to elicit event-related brain potentials in 13 patients with Alzheimer's disease and 14 patients with multi-infarct...
An auditory discrimination paradigm was employed to elicit event-related brain potentials in 13 patients with Alzheimer's disease and 14 patients with multi-infarct dementia. The P300 latency was significantly prolonged in 12 patients with dementia compared with age-matched controls and showed a significant negative correlation with the score of Wechsler Adult Intelligence Scale (WAIS), especially with that of Digit Span subtest. There was no disease specificity. After physostigmine treatment, P300 latency decreased and WAIS score increased in 6 among 10 cases.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Attention; Auditory Perception; Brain; Dementia, Multi-Infarct; Evoked Potentials, Auditory; Female; Humans; Male; Middle Aged; Physostigmine; Pitch Discrimination; Reaction Time; Wechsler Scales
PubMed: 3225596
DOI: 10.1136/jnnp.51.9.1120 -
Annals of the Rheumatic Diseases Aug 1987Four patients with recurrent stroke and multi-infarct dementia are presented in whom the dementia was progressive and severe. Three of the patients developed the...
Four patients with recurrent stroke and multi-infarct dementia are presented in whom the dementia was progressive and severe. Three of the patients developed the dementia during the course of an illness which was punctuated by repeated episodes of cerebral infarction demonstrated by computed tomographic (CT) scans. The fourth patient presented with an illness dominated by progressive and deteriorating higher mental functions, which culminated in a major stroke 18 months later. Three patients fulfilled the American Rheumatism Association (ARA) criteria for the classification of systemic lupus erythematosus, the fourth had a 'lupus-like' disease. All had livedo reticularis, severe migraines, and also demonstrated antibodies to phospholipids. All four patients suffered deep vein thromboses.
Topics: Adult; Autoantibodies; Blood Coagulation Factors; Cardiolipins; Cerebrovascular Disorders; Dementia; Female; Humans; Lupus Coagulation Inhibitor; Lupus Erythematosus, Systemic; Middle Aged; Phospholipids; Radiography; Recurrence
PubMed: 3116954
DOI: 10.1136/ard.46.8.605 -
European Neurology 2006The term 'vascular dementia' (VaD) corresponds to a clinicoradiological syndrome that can be defined with more or less restriction. VaD can result from: (1) cortical or... (Review)
Review
The term 'vascular dementia' (VaD) corresponds to a clinicoradiological syndrome that can be defined with more or less restriction. VaD can result from: (1) cortical or subcortical ischemic lesions related to the occlusion of large vessels, (2) lacunar infarcts with or without white-matter lesions at the subcortical level related to small-vessel diseases, (3) ischemic lesions related to hypoperfusion or anoxic-ischemic encephalopathy or (4) hemorrhagic lesions. The prevention of VaD is based on stroke prevention which implies risk factor manipulation and use of antithrombotic drugs among which the most widely used are antiplatelet drugs. The efficiency of these drugs to prevent cognitive impairment and dementia is not proven. Prospective studies are needed to investigate their potential in patients at risk of VaD: after ischemic stroke, in the presence of cognitive impairment of vascular origin or when MRI shows 'silent' ischemic white-matter lesions and/or infarcts.
Topics: Aged; Aged, 80 and over; Cognition Disorders; Dementia, Multi-Infarct; Dementia, Vascular; Humans; Platelet Aggregation Inhibitors; Risk Factors; Stroke
PubMed: 16534208
DOI: 10.1159/000091981 -
Journal of Neuropathology and... May 2019Pathogenic hemizygous variants in the SH2D1A gene cause X-linked lymphoproliferative (XLP) syndrome, a rare primary immunodeficiency usually associated with fatal...
Pathogenic hemizygous variants in the SH2D1A gene cause X-linked lymphoproliferative (XLP) syndrome, a rare primary immunodeficiency usually associated with fatal Epstein-Barr virus infection. Disease onset is typically in early childhood, and the average life expectancy of affected males is ∼11 years. We describe clinical, radiographic, neuropathologic, and genetic features of a 49-year-old man presenting with central nervous system vasculitis that was reminiscent of adult primary angiitis but which was unresponsive to treatment. The patient had 2 brothers; 1 died of aplastic anemia at age 13 and another died of diffuse large B-cell lymphoma in his sixties. Exome sequencing of the patient and his older brother identified a novel hemizygous variant in SH2D1A (c.35G>T, p.Ser12Ile), which encodes the signaling lymphocyte activation molecule (SLAM)-associated protein (SAP). Molecular modeling and functional analysis showed that this variant had decreased protein stability, similar to other pathogenic missense variants in SH2D1A. The family described in this report highlights the broadly heterogeneous clinical presentations of XLP and the accompanying diagnostic challenges in individuals presenting in adulthood. In addition, this report raises the possibility of a biphasic distribution of XLP cases, some of which may be mistaken for age-related malignancies and autoimmune conditions.
Topics: Amino Acid Sequence; Dementia, Multi-Infarct; Diagnosis, Differential; Humans; Lymphoproliferative Disorders; Male; Middle Aged; Pedigree; Protein Structure, Secondary; Signaling Lymphocytic Activation Molecule Associated Protein
PubMed: 30990878
DOI: 10.1093/jnen/nlz018 -
Brain Pathology (Zurich, Switzerland) Jul 2002Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary cerebrovascular disease leading to cognitive decline... (Review)
Review
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary cerebrovascular disease leading to cognitive decline and dementia. CADASIL usually begins with migraine in about one third of the patients. More severe manifestations, transient ischemic attacks or recurrent strokes, appear between 30 and 50 years of age. CADASIL, however, may be diagnosed well before the first stroke on the basis of characteristic white matter hyperintensities upon magnetic resonance imaging and presence of pathognomonic granular osmiophilic material in arterial walls, including dermal arteries, since the arteriopathy is generalized. Gradual destruction of vascular smooth muscle cells (VSMC) leads to progressive wall thickening and fibrosis and luminal narrowing in small and medium-sized penetrating arteries. The reduced cerebral blood flow finally causes lacunar infarcts, mainly in the basal ganglia and fronto-temporal white matter, which lead to cognitive deficits and dementia of the subcortical vascular type. CADASIL is caused by single missense mutations or small deletions in Notch3 gene encoding a transmembrane receptor Notch3, of which upon ligand binding a nuclear signaling protein is generated by regulated intramembrane proteolysis. Notch signaling is essential during development, regulating cellular differentiation. In adults Notch3 is expressed only in VSMCs and it may promote cell survival by inhibiting apoptosis, but its exact function is unknown. Mutations result in either a gain or loss of one (or rarely, 3) cysteine residue(s) in one of the 34 epidermal growth factor-like repeats in the extracellular amino-terminal region of Notch3. It is as yet unclear which disturbance in the Notch signaling pathway leads to the characteristic vascular pathology of CADASIL.
Topics: Arteries; Brain Infarction; Dementia; Dementia, Multi-Infarct; Diagnosis, Differential; Humans; Ischemic Attack, Transient; Magnetic Resonance Imaging; Migraine Disorders; Mutation, Missense; Myocytes, Smooth Muscle; Proto-Oncogene Proteins; Receptor, Notch3; Receptors, Cell Surface; Receptors, Notch
PubMed: 12146805
DOI: 10.1111/j.1750-3639.2002.tb00451.x -
The Cochrane Database of Systematic... 2003Transcutaneous electrical nerve stimulation (TENS) is the application of an electrical current through electrodes attached to the skin. The commonest clinical... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Transcutaneous electrical nerve stimulation (TENS) is the application of an electrical current through electrodes attached to the skin. The commonest clinical application of TENS is pain control. TENS is also used occasionally for the treatment of a range of neurological and psychiatric conditions including drug and alcohol dependence, headaches, and depression. TENS is rarely used for the treatment of dementia. However, since the early 1990s a number of studies carried out by a group in the Netherlands, and one study carried out by a group in Japan, suggest that TENS applied to the back or head may improve cognition and behaviour in patients with Alzheimer's disease or multi-infarct dementia. It was claimed that applying TENS could benefit patients with dementia by altering the activity of various neurotransmitters, or by increasing brain activity and thereby retarding neural degeneration and stimulating regenerative processes. It is claimed that application of TENS to the head may also alleviate the sleep disorders associated with dementia.
OBJECTIVES
The aim of this review is to determine the effectiveness and safety of transcutaneous electrical nerve stimulation (TENS) in the treatment of dementia. Secondary objectives of this review are to determine whether any effect of treatment of dementia with TENS is influenced by any treatment parameters or patient features, including: the duration of treatment, electrical waveform, current amplitude, pulse duration and frequency and the patient's type or severity of cognitive impairment.
SEARCH STRATEGY
The trials were identified from a search of the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group on 10 December 2002 using the terms TENS, transcutaneous, "transcutaneous electrical nerve stimulation", and "electric stimulation". The CDCIG Specialized Register contains records from all major health care databases and many ongoing trials databases and is regularly updated.
SELECTION CRITERIA
All RCTs in which TENS was used as an intervention for people with dementia were included in this review. This included peripherally applied transcutaneous electrical stimulation as well as transcutaneous electrical stimulation applied to the head (also known as cranial electrical stimulation (CES)).
DATA COLLECTION AND ANALYSIS
All RCTs that fulfilled the inclusion criteria for the review and for which sufficient data were available were included in this meta-analysis. Two reviewers extracted the data from the included trials. All except one of the included trials used similar outcome measures. Data of the same outcome measures were combined for analysis.
MAIN RESULTS
Eight trials were included in the review but only 3 trials could be included in the meta-analysis. Sufficient data to include the other trials in the meta-analysis could not be obtained. From this limited analysis it appears that TENS produced a statistically significant improvement directly after treatment in: delayed recall of 8 words in one trial, face recognition in two trials and motivation in one trial however, no effect of TENS was found on any of the many other neuropsychological and behavioural measures evaluated either directly after TENS treatment or 6 weeks after treatment was completed.
REVIEWER'S CONCLUSIONS
Although a number of studies suggest that TENS may produce short lived improvements in some neuropsychological or behavioural aspects of dementia, the limited presentation and availability of data from these studies does not allow definite conclusions on the possible benefits of this intervention. Since most of the currently published studies are well designed, although the numbers of subjects in each study is small, analysis of the complete original data from these and/or future studies may allow more definitive conclusions to be drawn.
Topics: Aged; Dementia; Humans; Randomized Controlled Trials as Topic; Transcutaneous Electric Nerve Stimulation
PubMed: 12917999
DOI: 10.1002/14651858.CD004032 -
The Western Journal of Medicine Nov 1995
Topics: Aged; Alzheimer Disease; Apolipoproteins E; Brain; Chromosomes, Human, Pair 21; Dementia; Dementia, Multi-Infarct; Dementia, Vascular; Diagnosis, Differential; Humans; Parkinson Disease
PubMed: 8533415
DOI: No ID Found