1,721,020 research outputs found
Vascular Dementia
No full textAlthough vascular dementia (VaD) represents the second most common cause of dementia after
Alzheimer’s disease (AD) in the elderly, and is referred to as the ‘‘silent epidemic of the twenty‐first century,’’
there is still a controversy on terminology, classification, and diagnostic criteria of VaD. The diagnosis of
VaD resides on diagnostic clinical criteria determining (1) a cognitive impairment, (2) the presence
of cerebrovascular disease, and (3) specifically in poststroke or multi‐infarct dementia, a temporal relationship
between these. The search for a reliable biochemical test helping in the diagnosis of VaD is so far not
available. Several vascular risk factors have a role in the development of VaD and their identification and
treatment are among the major aspects of VaD management. A new line of research in this field is the study
of genetic factors underlying vascular cognitive impairment which are: (1) genes predisposing to cerebrovascular
disease, and (2) genes that influence brain tissue responses to cerebrovascular lesions. Evidence in
favor of a coexistence of vascular and degenerative components in the pathogenesis of dementia in an
elderly population comes from neuropathological and epidemiological studies. There is now a great debate
whether VaD and AD are more than common coexisting unrelated pathologies or, instead, represent
different results of synergistic pathological mechanisms. Current available medications for the treatment
of VaD include acetylcholinesterase inhibitors for mild to moderate cases, and memantine, an NMDAreceptor
antagonist. However, therapeutic preventive approaches aiming at reducing incident VaD by
targeting patients at risk of cerebrovascular disease (primary prevention), or acting on patients after a
stroke (secondary prevention) to prevent stroke recurrence and the progression of brain changes associated
with cognitive impairment are the mandatory strategies
Vascular cognitive disorder. A biological and clinical overview
No full textAlthough vascular dementia (VaD) represents the second most common cause of dementia after Alzheimer's disease (AD) in the elderly, and is referred as the "silent epidemic of the twenty-first century", there is still a controversy on terminology, classification and diagnostic criteria of VaD. The diagnosis of VaD resides in clinical criteria determining a cognitive impairment, the presence of cerebrovascular disease and, only in the case of post-stroke dementia or multi-infarct dementia, a temporal relationship between these. The search for a reliable biochemical tests helping in the diagnosis of VaD is so far not available. Several vascular risk factors have a role in the development of VaD and their identification and treatment are among the major aspects of management of VaD. A new line of research in this field is the study of genetic factors underlying vascular cognitive impairment which are: (1) genes predisposing to cerebrovascular disease, and (2) genes that influence brain tissue responses to cerebrovascular lesions. Evidence in favour of a coexistence of vascular and degenerative components in the pathogenesis of dementia in an elderly population comes from neuropathological and epidemiological studies. There is now a great debate whether VaD and AD are more than common coexisting unrelated pathologies and, instead, represent different results of synergistic pathological mechanisms. Preventive approaches aiming at reducing incident VaD by targeting patients at risk of cerebrovascular disease (primary prevention), or acting on patients after a stroke (secondary prevention) to prevent stroke recurrence and the progression of brain changes associated with cognitive impairment are mandatory therapeutic strategies
Intrathecal IgM production at clinical onset correlates with a more severe disease course in multiple sclerosis
No full textApraxia of eyelid closure in autopsy-confirmed vascular progressive supranuclear palsy
No full textVascular progressive supranuclear palsy (PSP) is a rare condition that may mimic idiopathic PSP and is caused by diffuse subcortical ischemic white matter lesions. Among clinical signs distinguishing neurodegenerative from vascular PSP, the type of supranuclear impairment of lid motility may be of diagnostic value. We describe the clinical features and the neuropathological findings of a 71-year-old man diagnosed with vascular PSP and discuss the pathophysiology of apraxia of eyelid closure
A short review of cognitive and functional neuroimaging studies of cholinergic drugs: implications for therapeutic potentials
No full textIn the last 20 years a cholinergic dysfunction has been the major working hypothesis for the pharmachology of memory disorders. Cholinergic antagonists and lesions impair and different classes of cholinomimetics (i.e. acetylcholine precursors, cholinergic agonists and acetylcholinesterase inhibitors) enhance attention and memory in experiment animals, healthy human subjects and Alzheimer disease patients. In addition, acetylcholinesterase inhibitors improve different cognitive (i.e. visuospatial and verbal) functions in a variety of unrelated disorders such as dementia with Lewy bodies, Parkinson disease, multiple sclerosis, schizoaffective disorders, iatrogenic memory loss, traumatic brain injury, hyperactivity attention disorder and, as we recently reported, vascular dementia and mild cognitive impairment. In animals, different cholinomimetics dose-dependently increased regional cerebral metabolic rates for glucose (rCMRglc) and regional blood flow (rCBF), two indices of neuronal function, more markedly in subcortical regions (i.e. thalamus, hippocampus and visual system nuclei). In both healthy human subjects and Alzheimer disease patients acetylcholinesterase inhibitors increased rCMRglc and rCBF in subcortical and cortical brain regions at rest but attenuated rCBF increases during cognitive performances. Hence, acetylcholinesterase inhibitors may enhance cognition and rCMRglc by acting primarily on subcortical regions that are involved in attentional (i.e. thalamus) and memory (i.e. hippocampus) processes; such an effect probably is not specific for Alzheimer disease and can be beneficial in patients suffering from a wide array of neuropsychiatric disorders
Serotonin syndrome and rhabdomyolysis induced by concomitant use of triptans, fluoxetine and hypericum
No full textWe describe a 28-year-old woman affected by migraine without aura according to the ICHD-2
criteria who manifested with seizures as presenting symptom of a serotonin syndrome characterized
by mild and transient fever and subtle postural hand tremor. Few days later she developed an acute
rhabdomyolysis with associated increased D-dimer and liver enzymes. The condition was
precipitated by triptans use. Chronic therapy with fluoxetine, taken to treat an eating disorder, and
the use of a self-prescribed herbal medication containing hypericum predisposed to a serotonergic
hyperstimulation. This case report calls attention on the importance to avoid multidrug regimens for
the prevention of serotonin syndrome that can present with atypical symptoms and may worsen with
severe acute rhabdomyolysis
- …
