Post-stroke dementia is associated with alpha(1)-antichymotrypsin polymorphism.

BACKGROUND AND PURPOSE: Alpha-1-antichymotrypsin (ACT) is an acute phase protein involved in inflammatory reaction, promoting the assembly of beta amyloid protein into filaments and contributing to its resistance to proteolytic digestion. The aim of our study was to determine ACT signal peptide polymorphism (A/T) as a possible risk factor for post-stroke dementia (PSD). METHODS: 142 consecutive ischemic stroke patients and 188 controls were included in this study. Pre-stroke dementia (PRESD) was evaluated using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). The diagnosis of the post-stroke dementia (PSD) was established according to DSM-IV criteria. The ACT gene (A/T) polymorphism was determined by PCR-RFLR. RESULTS: Both ACT-TT genotype and T-allele were significantly more prevalent in patients with PSD than in non-demented stroke patients, controls or patients with PRESD. After adjustment for age, gender, and vascular risk factors, both the ACT-TT genotype and T-allele remained independently associated with PSD. CONCLUSION: Our findings suggest that ACT polymorphism (A/T) is a risk factor for PSD.

Factors associated with pre-stroke dementia: the cracow stroke database.

BACKGROUND: Many stroke patients who fulfilled diagnostic criteria for dementia three months after stroke had a mental deterioration before stroke, implying an underlying neurodegenerative process. The goal of this study was to determine the factors associated with pre-stroke dementia in hospitalised-based population. SUBJECTS AND METHODS: Pre-stroke cognitive decline was evaluated in 250 stroke patients using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Patients with IQCODE score > or=104 were classified as having pre-stroke dementia. Clinical, radiological, and biochemical data of patients with and without pre-stroke dementia were compared. RESULTS: Pre-stroke dementia was found in 12% of 250 stroke patients. Patients with pre-stroke dementia were older, suffered more frequently from ischemic heart disease and diabetes, and had more frequently prior cerebrovascular disease. These patients had significantly more brain atrophy and number of old infarcts on CT than patients without pre-stroke dementia. Serum gamma-globulins levels at admission were significantly higher in patients with pre-stroke dementia. In logistic regression analysis female gender (OR 3.47, CI 95% 1.25-9.64), history of previous stroke (OR 3.46, CI 95 % 1.26-9.51), the number of old infarcts on CT (OR 1.58, CI 95 % 1.08-2.33) and serum gamma-globulins level (OR 1.19, CI 95 % 1.02-1.40) were independently associated with pre-stroke dementia. CONCLUSIONS: Female gender and previous ischemic stroke are the most important determinants of pre-stroke cognitive decline.

Asymmetrical modulation of interleukin-10 release in patients with intracerebral hemorrhage.

The brain modulates the immune system in an asymmetrical way. Intracerebral hemorrhage triggers IL-6 and IL-10 release into blood. We measured (using ELISA method) serum IL-6 and IL-10 in acute phase of intracerebral hemorrhage in 11 patients with right hemisphere's hematoma and 15 patients with left hemisphere's hematoma. These patients did not differ significantly with respect to their age, size, and location of hematoma. IL-6 level was comparable in patients with left hematoma and patients with right hematoma, but patients with left hematoma had significantly higher level of IL-10 than patients with right hematoma. These results suggest that left and right hemisphere could modulate IL-10 release in different way.

Dexamethasone inhibits TNF-alpha synthesis more effectively in Alzheimer's disease patients than in healthy individuals.

Inflammatory mechanisms are involved in the pathogenesis of Alzheimer's disease (AD). It is postulated that cytokine synthesis is altered in AD patients compared with nondemented subjects. Glucocorticoids play an important role in cytokine synthesis. We assessed the release of tumor necrosis factor-alpha (TNF-alpha), interleukin-10 (IL-10) and interleukin-12 (IL-12) and its regulation by dexamethasone in AD patients in vitro. Cytokine levels were measured using the ELISA method in unstimulated, LPS-stimulated or whole-blood samples incubated with LPS and dexamethasone from 18 AD patients and 12 controls. The cytokine levels spontaneously produced by blood cells after incubation with LPS or LPS and dexamethasone did not differ significantly between groups. Dexamathasone inhibited TNF-alpha synthesis by LPS-stimulated blood cells more effectively in AD patients than in controls. These results suggest that cytokine synthesis in AD patients could be regulated by glucocorticoids in a different way than in nondemented subjects.

Is mannitol safe for patients with intracerebral hemorrhages? Renal considerations.

OBJECTIVES: Mannitol, a drug widely used to decrease intracranial pressure, can cause renal failure. The goal of this study is to determine the renal safety of mannitol therapy in patients with intraparenchymal hemorrhages. MATERIAL AND METHODS: 51 patients with intracerebral hemorrhages were treated with mannitol according to guideline of American Heart Association. Serum urea and creatinine levels were measured before mannitol administration and on the 2nd, 5th and 14th day. RESULTS: Transient elevation of urea and creatinine concentration was noticed, however, none of patients developed anuria or oliguria. CONCLUSIONS: Our study points out safety of mannitol therapy under control of osmolality, although control of urea and creatinine concentrations in special group of patients (persons with history of renal failure or diabetes) should be considered.

Intracerebral hemorrhage triggers interleukin-6 and interleukin-10 release in blood.

BACKGROUND AND PURPOSE: Acute brain insult can cause systemic anti-inflammatory response, including anti-inflammatory cytokine release. The goal of this study was to determine the serum level of interleukin-6, interleukin-10, and interleukin-13 in patients with intracerebral hemorrhage and to correlate cytokine concentrations with stroke severity. METHODS: Thirty patients with intraparenchymal hemorrhage and 16 control subjects were included. Serum samples were collected on the second day of hemorrhagic stroke. Cytokine level was measured with the enzyme-linked immunosorbent assay method. RESULTS: Increased serum levels of interleukin-6 and interleukin-10 were detected in stroke patients. Interleukin-6 and interleukin-10 levels were significantly correlated with Glasgow Coma Scale score. In addition, interleukin-6 level correlated with blood volume and mass effect. CONCLUSIONS: Intracerebral hemorrhage is associated with systemic release of anti-inflammatory cytokines.

Incidence of pre- and poststroke dementia: cracow stroke registry.

BACKGROUND AND PURPOSE: Dementia after stroke may be caused by vascular lesion, but preexisting degenerative changes can also influence its development. After stroke, the patients with coexisting Alzheimer-type pathology need appropriate treatment. The aim of the study was to evaluate the frequency of prestroke and new- onset dementia in stroke patients. METHODS: We evaluated prestroke dementia in 250 patients with ischemic or hemorrhagic stroke using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Poststroke dementia was assessed in 220 patients 3 months after stroke by means of the neuropsychological tests and/or IQCODE. The DSM-IV definition of dementia was used. RESULTS: Dementia after stroke was found in 31.4% of stroke patients. Twelve percent of stroke patients had a significant impairment of cognitive functions detected by the IQCODE on admission suggesting prestroke dementia. When we excluded the patients with recurrent stroke, the incidence of pre- and poststroke dementia was 9.3 and 21.2%, respectively. CONCLUSION: About one tenth of stroke patients have preexisting dementia.