Risk factors in patients with perimesencephalic hemorrhage.

BACKGROUND AND PURPOSE: Smoking and hypertension are risk factors for aneurysmal subarachnoid hemorrhage (aSAH), whilst excessive alcohol consumption is less consistently linked with aSAH. Perimesencephalic hemorrhage (PMH) is a benign subset of non-aneurysmal subarachnoid hemorrhage. The exact cause of PMH is unknown, and its risk factor profile may help to elucidate the pathogenesis. The influence of smoking, hypertension and excessive alcohol consumption on the occurrence of PMH was studied. METHODS: Seventy-nine patients admitted with a PMH to the University Medical Center Utrecht were studied. As controls 574 persons were selected from five different general practices in the referral region of the University Medical Center Utrecht. All participants filled in a questionnaire about smoking habits, the presence of hypertension and alcohol consumption before their hemorrhage. Odds ratios (ORs) with corresponding 95% confidence intervals (CIs) were calculated to assess the association of risk factors and PMH, and multivariable logistic regression was used to adjust for possible confounding by age and sex. RESULTS: Adjusted ORs for the occurrence of PMH were 1.7 (95% CI 1.0-2.8) for smoking cigarettes, cigars, pipes or any combination of these, 1.1 (95% CI 0.6-2.0) for hypertension and 1.1 (95% CI 0.5-2.1) for excessive alcohol consumption. CONCLUSIONS: Similar to aSAH, smoking is a risk factor for PMH and excessive alcohol consumption is not. In contrast to aSAH, hypertension is not a risk factor for PMH. This implies that the pathophysiological mechanisms causing PMH might be slightly different from those causing aSAH.

Comparison of patient and proxy responses on risk factors for stroke.

BACKGROUND: For studies on chronic risk factors and trigger (i.e. acute risk) factors, stroke researchers often have to rely on proxies. The reliability of proxy responses regarding trigger factors for stroke is unknown. METHODS: Thirty patients with stroke and their proxies were interviewed about chronic risk factors and trigger factors. We assessed the completeness of proxy-derived data by calculating the level of non-response and the level of agreement using Cohen kappa statistics. RESULTS: For most chronic risk factors and trigger factors, the response rate to whether or not exposure had taken place in the past year was 87% or higher. If couples agreed on exposure, patient and proxy could also provide a comparable estimate of the average frequency of exposure. Although the non-response on last time of exposure was higher, proxies who could answer provide a reasonably good estimate for most trigger factors. CONCLUSIONS: Proxies provide reliable information on exposure to chronic risk factors and trigger factors for stroke. For exposure and average frequency of exposure, non-response is low and the level of agreement is high for most chronic risk factors; for last time of exposure non-response is higher, but proxies who could respond provided reliable estimates of last time of exposure to most trigger factors.

Intake of 13C-4 creatine enables simultaneous assessment of creatine and phosphocreatine pools in human skeletal muscle by 13C MR spectroscopy.

The feasibility of a novel method for the noninvasive and local assessment of creatine (Cr) and phosphocreatine (PCr) dynamics in human skeletal muscle based on (13)C magnetic resonance (MR) spectroscopy is presented. A high dose of Cr, labeled at the guanidino C-4 position with (13)C 11% enrichment, was administered orally to a human subject for 5 days. Using a surface coil, (13)C MR spectra of the lower leg were acquired on a 1.5T MR system at regular time intervals during and after Cr supplementation. An almost twofold increase in the intensities of the resolved PCr and Cr (13)C-4 signals was observed during this period. The slow decrease in these signals to normal values after supplementation reflects the slow daily turnover of Cr. The PCr/Cr ratio did not appear to change over the whole measurement period. During exercise of the leg, reversible changes in PCr and Cr signals were observed, reflecting conversion by the Cr kinase reaction.

An unbiased and efficient computerised tomography method to quantify muscle and adipose tissue volume in neuromuscular patients.

The objective was to evaluate the applicability and reliability of an unbiased stereological computerised tomography (CT) method for estimating total human body (HB), skeletal muscle (SM) and adipose tissue (AT) volumes in groups of neuromuscular patients. In 10 neuromuscular patients HB, SM and AT volumes were estimated using systematic sampling on equidistant CT sections throughout the total body axis using a counting grid with systematically ordered intersection points. Each intersection point hitting HB, SM or AT represented a known volume dependent on intersection point distance and sum of section thickness and gap. Random and systematic intra- and interobserver errors for volume estimates were below 0.035. These errors were negligible to the coefficient of variation of the group mean, being 0.190 for HB, 0.323 for SM and 0.471 for AT. Even in the presence of intrafascicular and intramuscular fat in neuromuscular patients, unbiased and reliable quantification of HB, SM and AT is possible.

Calcium regulation and muscle disease.

Changes in intracellular Ca2+-concentration play an important role in the excitation-contraction-relaxation cycle of skeletal muscle. In this review we describe various inheritable muscle diseases to highlight the role of Ca2+-regulatory mechanisms. Upon excitation the ryanodine receptor releases Ca2+ in the cytosol. During and after contraction the sarcoplasmic reticulum (SR) Ca2+ATPase (SERCA) pumps Ca2+ back in the SR resulting in relaxation. An abnormal change in the intracellular Ca2+-concentration results in defective muscle contraction and/or relaxation, which is the cause of various muscle diseases. Malignant hyperthermia (MH) and central core disease (CCD) are both caused by mutations in the ryanodine receptor but show different clinical phenotypes. In MH an acute increase of Ca2+ results in excessive muscle contraction causing rigidity, while in CCD a chronic rise of cytosolic Ca2+ is seen, leading to mitochondrial damage, disorganization of myofibrils and muscle weakness. In Brody disease and also in mitochondrial myopathies, SERCA functions sub optimal causing a prolonged physiological Ca2+-elevation leading to slowing of relaxation. Defective actin-myosin interactions, as in nemaline myopathy and also in mitochondrial myopathies due to ATP-shortage, cause Ca2+-hyposensitivity and slowness of contraction. Information of Ca2+-kinetics in these inherited muscular diseases improves our understanding of the role of calcium in the physiology and pathophysiology of the skeletal muscle cell.