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Frontiers in Aging Neuroscience 2013Vascular cognitive impairment (VCI) [vascular cognitive disorder (VCD), vascular dementia] describes a continuum of cognitive disorders ranging from mild cognitive...
Vascular cognitive impairment (VCI) [vascular cognitive disorder (VCD), vascular dementia] describes a continuum of cognitive disorders ranging from mild cognitive impairment (MCI) to dementia, in which vascular brain injury involving regions important for memory, cognition and behavior plays an important role. Clinical diagnostic criteria show moderate sensitivity (ca 50%) and variable specificity (range 64-98%). In Western clinical series, VaD is suggested in 8-10% of cognitively impaired elderly subjects. Its prevalence in autopsy series varies from 0.03 to 58%, with means of 8 to 15% (in Japan 22-35%). Major types of sporadic VaD are multi-infarct encephalopathy, small vessel and strategic infarct type dementias, subcortical arteriosclerotic leukoencephalopathy (SAE) (Binswanger), multilacunar state, mixed cortico-subcortical type, granular cortical atrophy (rare), postischemic encephalopathy, and a mixture of cerebrovascular lesions (CVLs). They result from systemic, cardiac and local large or small vessel disease (SVD); their pathogenesis is multifactorial. Hereditary forms of VaD caused by gene mutations are rare. Cognitive decline is commonly associated with widespread small ischemic vascular lesions involving subcortical brain areas (basal ganglia and hemispheral white matter). The lesions affect neuronal networks involved in cognition, memory, and behavior (thalamo-cortical, striato-subfrontal, cortico-subcortical, limbic systems). CVLs often coexist with Alzheimer-type lesions and other pathologies; 25-80% of elderly demented show mixed pathologies. The lesion pattern of "pure" VaD differs from that in mixed dementia (AD + CVLs) suggesting different pathogenesis of both phenotypes. Minor CVLs, except for severe amyloid angiopathy, appear not essential for cognitive impairment in full-blown AD, while both mild AD-type pathology and SVD may interact synergistically in promoting dementia. However, in a large percentage of non-demented elderly individuals, both AD-related and vascular brain pathologies have been reported. Despite recent suggestions for staging and grading CVLs in specific brain areas, due to the high variability of CVLs associated with cognitive impairment, no validated neuropathological criteria are currently available for VaD and mixed dementia. Further clinico-pathological studies and harmonization of neuropathological procedures are needed to validate the diagnostic criteria for VaD and mixed dementia in order to clarify the impact of CVLs and other coexistent pathologies on cognitive impairment as a basis for further successful therapeutic options.
PubMed: 23596414
DOI: 10.3389/fnagi.2013.00017 -
Sao Paulo Medical Journal = Revista... 2013CONTEXT Coagulase-negative staphylococci are common colonizers of the human skin and have become increasingly recognized as agents of clinically significant nosocomial... (Review)
Review
CONTEXT Coagulase-negative staphylococci are common colonizers of the human skin and have become increasingly recognized as agents of clinically significant nosocomial infections. CASE REPORT The case of a 79-year-old male patient with multi-infarct dementia who presented systemic inflammatory response syndrome is reported. This was attributed to bacteremia due to Staphylococcus cohnii ssp. urealyticus, which was grown on blood cultures originating from an infected pressure ulcer. The few cases of Staphylococcus cohnii infection reported in the literature consist of bacteremia relating to catheters, surgical prostheses, acute cholecystitis, brain abscess, endocarditis, pneumonia, urinary tract infection and septic arthritis, generally presenting a multiresistant profile, with nearly 90% resistance to methicillin. CONCLUSIONS The reported case is, to our knowledge, the first case of true bacteremia due to Staphylococcus cohnii subsp. urealyticus caused by an infected pressure ulcer. It shows that this species may be underdiagnosed and should be considered in the differential diagnosis for community-acquired skin infections.
Topics: Aged; Bacteremia; Coagulase; Cross Infection; Diagnosis, Differential; Humans; Male; Pressure Ulcer; Staphylococcal Infections; Staphylococcus
PubMed: 23538597
DOI: 10.1590/s1516-31802013000100010 -
PloS One 2013A growing body of evidence suggests a link between early childhood trauma, post-traumatic stress disorder (PTSD) and higher risk for dementia in old age. The aim of the...
A growing body of evidence suggests a link between early childhood trauma, post-traumatic stress disorder (PTSD) and higher risk for dementia in old age. The aim of the present study was to investigate the association between childhood trauma exposure, PTSD and neurocognitive function in a unique cohort of former indentured Swiss child laborers in their late adulthood. To the best of our knowledge this is the first study ever conducted on former indentured child laborers and the first to investigate the relationship between childhood versus adulthood trauma and cognitive function. According to PTSD symptoms and whether they experienced childhood trauma (CT) or adulthood trauma (AT), participants (n = 96) were categorized as belonging to one of four groups: CT/PTSD+, CT/PTSD-, AT/PTSD+, AT/PTSD-. Information on cognitive function was assessed using the Structured Interview for Diagnosis of Dementia of Alzheimer Type, Multi-infarct Dementia and Dementia of other Etiology according to ICD-10 and DSM-III-R, the Mini-Mental State Examination, and a vocabulary test. Depressive symptoms were investigated as a potential mediator for neurocognitive functioning. Individuals screening positively for PTSD symptoms performed worse on all cognitive tasks compared to healthy individuals, independent of whether they reported childhood or adulthood adversity. When controlling for depressive symptoms, the relationship between PTSD symptoms and poor cognitive function became stronger. Overall, results tentatively indicate that PTSD is accompanied by cognitive deficits which appear to be independent of earlier childhood adversity. Our findings suggest that cognitive deficits in old age may be partly a consequence of PTSD or at least be aggravated by it. However, several study limitations need to considered. Consideration of cognitive deficits when treating PTSD patients and victims of lifespan trauma (even without a diagnosis of a psychiatric condition) is crucial. Furthermore, early intervention may prevent long-term deficits in memory function and development of dementia in adulthood.
Topics: Aged; Aged, 80 and over; Analysis of Variance; Child; Cognition; Employment; Female; Humans; Male; Middle Aged; Risk; Stress Disorders, Post-Traumatic
PubMed: 23469076
DOI: 10.1371/journal.pone.0057826 -
Brain Pathology (Zurich, Switzerland) Sep 2013We quantified vascular changes in the frontal lobe and basal ganglia of four inherited small vessel diseases (SVDs) including cerebral autosomal dominant arteriopathy...
We quantified vascular changes in the frontal lobe and basal ganglia of four inherited small vessel diseases (SVDs) including cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), pontine autosomal dominant microangiopathy and leukoencephalopathy (PADMAL), hereditary multi-infarct dementia of Swedish type (Swedish hMID), and hereditary endotheliopathy with retinopathy, nephropathy, and stroke (HERNS). Vascular pathology was most severe in CADASIL, and varied with marginally greater severity in the basal ganglia compared to the frontal lobe. The overall sclerotic index values in frontal lobe were in the order CADASIL ≥ HERNS > PADMAL > Swedish hMID > sporadic SVD, and in basal ganglia CADASIL > HERNS > Swedish hMID > PADMAL> sporadic SVD. The subcortical white matter was almost always more affected than any gray matter. We observed glucose transporter-1 (GLUT-1) protein immunoreactivities were most affected in the white matter indicating capillary degeneration whereas collagen IV (COL4) immunostaining was increased in PADMAL cases in all regions and tissue types. Overall, GLUT-1 : COL4 ratios were higher in the basal ganglia indicating modifications in capillary density compared to the frontal lobe. Our study shows that the extent of microvascular degeneration varies in these genetic disorders exhibiting common end-stage pathologies but is the most aggressive in CADASIL.
Topics: Actins; Age Factors; Aged; Aged, 80 and over; Analysis of Variance; Blood Vessels; Brain; CADASIL; Cerebral Small Vessel Diseases; Female; Humans; Male; Middle Aged; Phenotype; Postmortem Changes; Severity of Illness Index
PubMed: 23387519
DOI: 10.1111/bpa.12041 -
Journal of the Neurological Sciences Dec 2012We describe an extraordinarily protracted case of varicella zoster virus (VZV) multifocal vasculopathy in a man who presented initially with ischemic optic neuropathy...
We describe an extraordinarily protracted case of varicella zoster virus (VZV) multifocal vasculopathy in a man who presented initially with ischemic optic neuropathy and then suffered 4 episodes of stroke manifesting as multi-infarct dementia over a 2-year period. Brain magnetic resonance imaging (MRI) and angiography (MRA) revealed cortical and subcortical infarctions as well as vasculitic occlusion and stenosis. The patient was treated with corticosteroids and later with cyclophosphamide. More than 2 years after the onset of neurological disease, two cerebrospinal fluid (CSF) examinations revealed the presence of anti-VZV IgG antibody with reduced serum-to-CSF ratios of anti-VZV IgG compared with ratios for total IgG and albumin, indicative of intrathecal synthesis of anti-VZV IgG. After definitive diagnosis, immunosuppressive drugs were discontinued and he was treated with intravenous acyclovir; both mental status and gait improved and no further episodes of neurological dysfunction ensued. The favorable outcome in this patient indicates that VZV vasculopathy can be treated successfully even after 26 months. VZV must be considered as a possible cause of neurological disease in any patient with idiopathic multifocal vasculopathy.
Topics: Acyclovir; Aged; Antiviral Agents; Apraxias; Basal Ganglia Cerebrovascular Disease; Cyclophosphamide; Dementia, Multi-Infarct; Disease Progression; Drug Therapy, Combination; Dysarthria; Encephalitis, Varicella Zoster; Gait Disorders, Neurologic; Humans; Magnetic Resonance Angiography; Male; Memory Disorders; Prednisone; Pupil Disorders; Recovery of Function; Thalamus; Valacyclovir; Valine; Vertebrobasilar Insufficiency; Vision Disorders
PubMed: 22935406
DOI: 10.1016/j.jns.2012.07.059 -
Actas Espanolas de Psiquiatria 2012Cerebrovascular disease is a cause of late-onset psychosis in the elderly more frequent, accompanied or not, multi-infarct dementia. In many cases the patient has...
Cerebrovascular disease is a cause of late-onset psychosis in the elderly more frequent, accompanied or not, multi-infarct dementia. In many cases the patient has adequate preservation of cognitive functions or in any case, no criteria for dementia. In those that do, is in vascular dementia where psychotic symptoms are more frequent, occurring in over half cases, compared to one third of patients with Alzheimer disease. A case of a 92 year-old woman with no somatic background -except for a bilateral progressive hearing loss-, who debuted at this age with psychotic delusions structured injury and auditory hallucinations. The CT scan showed signs of cortico-subcortical atrophy. Neuropsychological examinations showed some cognitive impairment but no clinical criteria for dementia. Was refractory to first-line atypical antipsychotics, remitting symptoms after administration of low doses of clozapine. We discuss the clinical features of this psychosis, as well as its therapeutic approach.
Topics: Aged, 80 and over; Cerebrovascular Disorders; Female; Humans; Psychotic Disorders
PubMed: 22851482
DOI: No ID Found -
Neurologia (Barcelona, Spain) May 2015A review of current criteria for the diagnosis of categories related with vascular cognitive impairment, in particular the nomenclature, diagnostic criteria, and... (Review)
Review
OBJECTIVE
A review of current criteria for the diagnosis of categories related with vascular cognitive impairment, in particular the nomenclature, diagnostic criteria, and differential clinical-radiological findings.
DEVELOPMENT
The criteria for the diagnosis of vascular cognitive impairment have evolved, but available criteria were designed basically for differentiating between vascular dementia and dementia due to Alzheimer disease, and for research purposes. Nevertheless, in clinical practice precise elements are required for: 1) Clinical diagnosis of dementia and mild cognitive impairment; 2) Clinical and neuroimaging criteria for identification of the various cerebrovascular lesions associated with cognitive dysfunction, and 3) A formulation of the aetiogenic-pathogenic relationship between cognitive impairment and cerebrovascular lesions. For this reason, a review was carried out on the diagnostic elements of vascular cognitive impairment categories, classification, and their most relevant characteristics. It highlights the characteristic for the diagnosis of multi-infarction dementia, strategic single infarct dementia, small vessel disease with dementia, mixed dementia, and vascular mild cognitive impairment.
CONCLUSIONS
Standardisation is required, by a multidisciplinary expert team, as regards nomenclature and criteria for the diagnosis of the full spectrum associated with vascular cognitive impairment and especially for vascular dementia and its categories.
Topics: Alzheimer Disease; Brain; Cognitive Dysfunction; Dementia, Vascular; Diagnosis, Differential; Humans; Neuroimaging; Stroke
PubMed: 22739039
DOI: 10.1016/j.nrl.2011.12.014 -
Experimental Gerontology Nov 2012The diagnosis of vascular dementia (VaD) describes a group of various vessel disorders with different types of vascular lesions that finally contribute to the... (Review)
Review
The diagnosis of vascular dementia (VaD) describes a group of various vessel disorders with different types of vascular lesions that finally contribute to the development of dementia. Most common forms of VaD in the elderly brain are subcortical vascular encephalopathy, strategic infarct dementia, and the multi infarct encephalopathy. Hereditary forms of VaD are rare. Most common is the cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Sporadic forms of VaD are caused by degenerative vessel disorders such as atherosclerosis, small vessel disease (SVD) including small vessel arteriosclerosis, arteriolosclerosis, and lipohyalinosis, and cerebral amyloid angiopathy (CAA). Less frequently inflammatory vessel disorders and tumor-associated vessel lesions (e.g. angiocentric T-cell or angiotropic large cell lymphoma) can cause symptoms of dementia. Here, we review and discuss the impact of vessel disorders to distinct vascular brain tissue lesions and to the development of dementia in elderly individuals. The impact of coexisting neurodegenerative pathology in the elderly brain to VaD as well as the correlation between SVD and CAA expansion in the brain parenchyma with that of Alzheimer's disease (AD)-related pathology is highlighted. We conclude that "pure" VaD is rare and most frequently caused by infarctions. However, there is a significant contribution of vascular lesions and vessel pathology to the development of dementia that may go beyond tissue damage due to vascular lesions. Insufficient blood blow and alterations of the perivascular drainage mechanisms of the brain may also lead to a reduced protein clearance from extracellular space and subsequent increase of proteins in the brain parenchyma, such as the amyloid β-protein, and foster, thereby, the development of AD-related neurodegeneration. As such, it seems to be important for clinical practice to consider treatment of potentially coexisting AD pathology in cognitively impaired patients with vascular lesions.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Arteriosclerosis; Blood Vessels; Brain; Cerebral Amyloid Angiopathy; Dementia, Vascular; Female; Humans; Male; Middle Aged
PubMed: 22705146
DOI: 10.1016/j.exger.2012.05.023 -
Journal of Neuro-oncology Sep 2012Ginkgo biloba has been reported to improve cognitive function in older adults and patients with Alzheimer's disease and multi-infarct dementia. We conducted an...
UNLABELLED
Ginkgo biloba has been reported to improve cognitive function in older adults and patients with Alzheimer's disease and multi-infarct dementia. We conducted an open-label phase II study of this botanical product in symptomatic irradiated brain tumor survivors. Eligibility criteria included: life expectancy ≥30 weeks, partial or whole brain radiation ≥6 months before enrollment, no imaging evidence of tumor progression in previous 3 months, or stable or decreasing steroid dose, and no brain tumor treatment planned while on study. The Ginkgo biloba dose was 120 mg/day (40 mg t.i.d.) for 24 weeks followed by a 6-week washout period. Assessments performed at baseline, 12, 24 (end of treatment), and 30 weeks (end of washout) included KPS, Functional Assessment of Cancer Therapy-Brain (FACT-Br), Profile of Mood States, Mini-Mental Status Exam, Trail Making Test Parts A (TMT-A) and B (TMT-B), Digit Span Test, Modified Rey Osterrieth Complex Figure (ROCF), California Verbal Learning Test Part II, and the F-A-S Test.
RESULTS
Of the 34 patients enrolled on study, 23 (68 %) completed 12 weeks of treatment and 19 (56 %) completed 24 weeks of treatment. There were significant improvements at 24 weeks in: executive function (TMT-B) (p = 0.007), attention/concentration (TMT-A) (p = 0.002), and non-verbal memory (ROCF-immediate/delayed recall) (p = 0.001/0.002), mood (p = 0.002), FACT-Br subscale (p = 0.001), and the FACT physical subscale (p = 0.003).
CONCLUSIONS
Some improvement in quality of life and cognitive function were noted with Ginkgo biloba. However, treatment with Ginkgo biloba was associated with a high dropout rate.
Topics: Adult; Aged; Aged, 80 and over; Analysis of Variance; Brain Neoplasms; Cognition Disorders; Female; Follow-Up Studies; Ginkgo biloba; Humans; Male; Middle Aged; Mood Disorders; Neuropsychological Tests; Phytotherapy; Plant Preparations; Quality of Life; Severity of Illness Index; Time Factors
PubMed: 22700031
DOI: 10.1007/s11060-012-0901-9 -
Psychogeriatrics : the Official Journal... Jun 2011The homeostasis of neuronal cells is maintained by the cerebral circulation and blood-brain barrier. Circulating bone marrow-derived immature cells, including... (Review)
Review
The homeostasis of neuronal cells is maintained by the cerebral circulation and blood-brain barrier. Circulating bone marrow-derived immature cells, including CD34-positive (CD34+) cells, have been implicated in homeostasis of the cerebral microvasculature. Decreased levels of circulating CD34+ cells, associated with ageing and/or cardiovascular risk factors, correlate with poor clinical outcomes in patients with cerebrovascular and cardiovascular diseases. Clinical trials with local transplantation of bone marrow-derived immature cells for patients with limb ischaemia, including Buerger's disease and arteriosclerosis obliterans, have been shown to improve impaired microcirculation. In the present review, current findings about the correlation between circulating immature cells and microcirculation are reviewed, and the possibility of novel cell-based therapy in patients with vascular dementia is discussed.
Topics: Age Factors; Aged; Animals; Antigens, CD34; Blood-Brain Barrier; Brain; Brain Ischemia; Cardiovascular Diseases; Dementia, Multi-Infarct; Dementia, Vascular; Hematopoietic Stem Cell Transplantation; Humans; Microcirculation; Neovascularization, Physiologic; Neurogenesis
PubMed: 21707859
DOI: 10.1111/j.1479-8301.2010.00343.x