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The purpose of this study has been to describe the microanatomy of the recurrent artery of Heubner (RAH) in detail, to deepen anatomical knowledge and aid neurosurgeons in their work. The material was obtained from cadavers (ages 31-75 years) at routine autopsy. A total of 70 human brains (39 male and 31 female) were examined. People who died due to neurological disorders were not included in the study. Right after dissection, the arteries were perfused with acrylic paint emulsion, through the Circle of Willis or electively through the RAH. Brains were fixed in a 10% solution of formaldehyde, sectioned and placed in methyl salicylate for tissue transparency. To obtain corrosion-casts, the vessels were perfused with polyvinyl chloride or Mercox CL-2R resin and corroded using concentrated potassium chloride. The obtained material was analyzed using a stereoscopic light microscope. The RAH was present in 138 hemispheres with a mean of 1.99 RAH per hemisphere (275 RAH in total). The mean RAH length was 25.2 mm and the mean RAH diameter, in its place of origin, was 1 mm. Two to 30 branches (mean=9.4) originated from the stem of the RAH. The number of RAHs showed a negative correlation to the number of arteries from the medial group of lenticulo-striate arteries (LSA) (R=-0.62; p < 0.0001) which branch off the middle cerebral artery (MCA). This study further supports the RAH embryologic theory by Abbie. The RAH, in its extra- and intracerebral course, may join with the middle group of the LSA or directly with the MCA.

The aim of this study was to present review of the pterygomandibular space with some referrals to clinical practice, specially to the methods of lower teeth anesthesia.Pterygomandibular space is a clinically important region which is commonly missing in anatomical textbooks. More attention should be paid to it both from theoretical and practical point of view, especially in teaching the students of first year of dental studies.

Carpal tunnel syndrome (CTS) is the most common and widely known of the entrapment neuropathies in which the body's peripheral nerves are compressed. Common symptoms of CTS involve the hand and result from compression of the median nerve within the carpal tunnel. In general, CTS develops when the tissues around the median nerve irritate or compress on the nerve along its course through the carpal tunnel, however often it is very difficult to determine cause of CTS. Proper treatment (conservative or surgical) usually can relieve the symptoms and restore normal use of the wrist and hand.

Homocysteine is known risk factor for the development of atherosclerosis, but its contribution to the different etiologies of ischaemic stroke remains unclear.Comparison of homocysteine, folic acid and vitamin 812 plasma concentrations in patients with ischaemic stroke due to large vessel disease (LVD), small vessel disease (SVD) and in controls.We studied 71 patients with ischaemic stroke (including 30 patients with LVD and 41 patients with SVD) as well as 30 control subjects. Aetiology of ischaemic stroke was established according to the TOAST criteria using computed tomography of the head, EKG, carotid ultrasound and echocardiography. In patients being 3-12 months after stroke we registered age, sex and the presence of common risk factors for stroke. The serum concentrations of homocysteine, folic acid, and vitamin 812 were measured in venous blood samples drawn after the overnight fasting.Serum homocysteine concentrations were similar in patients with LVD, SVD, and in controls (19.5 +/- 8.9, 18.6 +/- 6.6, and 16.8 +/- 6.4 micromol/l, respectively) (p = 0.36, ANOVA). Vitamin 812 concentrations did not differ significantly among patients with LVD, SVD, and in controls (377 +/- 143, 414 +/- 179, and 412 +/- 173 pg/ml, respectively) (p = 0.66, ANOVA). Patients with LVD, SVD, and controls were also similar regarding the concentrations of folic acid (7.1 +/- 4.0, 6.4 +/- 2.7, and 7.6 +/- 4.0 ng/ml, respectively) (p = 0.38, ANOVA).Serum concentrations of homocysteine, vitamin 812, and folic acid are similar in patients with stroke due to LVD, SVD, and in control subjects.

of the study was to compare hemostatic markers of endothelial injury in patients with ischaemic stroke caused by large vessel disease (LVD) or small vessel disease (SVD).We studied 30 patients with LVD and 41 patients with SVD (recruited out of 585 patients with ischaemic stroke) as well as 30 control subjects. Etiology of ischaemic stroke was established according to the TOAST criteria. In patients being 3-12 months after stroke we registered age, sex and the presence of common risk factors for stroke. We measured serum concentration of fibrinogen and plasminogen activator inhibitor 1 (PAI-1), activity of von Willebrand factor (vWF) and the level of beta-thromboglobulin (beta-TG).The concentration of fibrinogen was greater in patients with LVD (3.56 +/-0.88 g/L) when compared to patients with SVD (2.78 +/-0.69 g/L, pO.0005). Activity of vWF was higher in all stroke survivors (155.8+/-53.9%) when compared to controls (124.8+/-43.3%; p0.01). It was also higher in patients with LVD (179.9+/-53.6%) than in patients with SVD (139.3+/-48. 1%; pO.01). The level of /-TG in patients with LVD [192.0 (69.7-222.1) UI/mL] was higher than in patients with SVD [90.6 (56.6-165.8) UI/mL; p0.05] and higher than in controls [108.7 (49.0-166.5) Ul/mL, p0.05]. The concentration of PAl-1 was similar among all studied groups.Stroke patients with LVD are characterized by higher concentration of fibrinogen, higher activity of vWF and higher levels of (Beta-TG) than patients with SVD. PAI-1 concentration is similar in both groups. Our results confirm the need for reanalysis of risk factors and pathomechanism of each cause of stroke separately.

Controversies concerning the significance of lipid abnormalities in stroke come mostly from the researches that studied lipid profile without considering stroke aetiologies. We investigated the prevalence of LDL phenotype B and other lipid abnormalities in stroke survivors with large vessel disease (LVD) or small vessel disease (SVD) (TOAST criteria) and in control subjects (CS).We studied 30 patients with LVD and 41 patients with SVD screened out of 585 stroke patients and 30 CS who fulfilled the following exclusion criteria: cardiac disorders, renal or hepatic failure, diabetes mellitus, or treatment with lipid-lowering agents. At least 3 months after stroke, the concentrations of total cholesterol (TC), HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), triglycerides (TGs), apolipoprotein E (apoE), and lipoprotein (a) [lp(a)] were measured and LDL phenotypes and apoE isoforms were identified.Patients with LVD had significantly higher concentrations of LDL-C than CS (p0.05). They had higher concentrations of TGs and lower concentrations of HDL-C than patients with SVD and CS (p0.05). LDL phenotype B was more frequent in patients with LVD (63.3%) than in patients with SVD (39.0%) or in CS (16.7%) (p0.05). The concentration of apoE was higher in patients with LVD than in patients with SVD or in CS (p0.05). The percentage of patients with increased level of lp(a) (i.e.,30 mg/ml) was greater in patients with LVD (36.7%) than in CS (10%) (p0.05).Patients with stroke due to LVD, but not SVD, have high prevalence of atherogenic lipid abnormalities, including increased frequency of LDL phenotype B and higher percentage of increased lp(a) level, like patients with other atherogenic diseases.

The significance of lipid abnormalities as the risk factor for stroke remains uncertain. The aim of this study was to compare the concentrations of lipoprotein (a) [lp(a)] in stroke patients with large and small vessel disease. We studied 71 patients being 3 to 12 months after ischemic stroke (including 30 subjects with large vessel disease and 41 subjects with small vessel disease) and 30 controls. We excluded patients with stroke of cardioembolic, rare or uncertain etiology, subjects with diabetes, with history of myocardial infarction, arrhythmia, valvular heart disease, hypo- or hyperthyreoidism, hepatic or renal insufficiency, and treated with statins or fibrates. We assessed basal lipid fractions and nephelometrically measured the concentration of lp(a). The concentrations of total and LDL-cholesterol were similar in studied groups. Patients with large vessel disease had lower levels of HDL-cholesterol and higher levels of triglycerides than patients with small vessel disease and than controls. Median concentrations of lp(a) were similar in all studied groups (8.4 mg/dl in all stroke patients; 10.85 mg/dl in large vessel disease; 7.7 mg/dl in small vessel disease and 6.3 mg/dl in controls; p = n.s.). The percentage of subjects with increased lp(a) concentrations (i.e.30 mg/dl) was greater in large vessel disease (36.7%) than in small vessel disease (12.2%; p0.05) and in controls (10%; p0.05). The concentrations of basal lipid fractions were similar in subjects with normal and with increased concentration of lp(a), both in stroke patients and in controls.

Microalbuminuria is a frequent finding in several acute clinical conditions and predicts poor outcome; its role in acute ischemic stroke, however, is unknown. This study was designed to investigate the prevalence and predictive power of microalbuminuria in acute stroke patients and to establish the relationship between microalbuminuria and the patients’ clinical status. We studied 60 patients admitted within 24 h of their first ischemic stroke, 50 patients with a history of ischemic stroke, and 30 control subjects without known cerebrovascular diseases. Neurological deficit was assessed by the Scandinavian Stroke Scale (SSS) on admission and on days 1, 7, 14, and 30. Urinary albumin excretion was measured using immunonephelometric method, with 24-hour collections performed on day 2. Outcome was assessed by 30-day, 90-day and 1-year mortality. Microalbuminuria was found in 46.7% of patients with acute stroke, 16% of subjects with a history of stroke, and 16.7% of controls. On admission, acute stroke patients with microalbuminuria had more severe neurological deficit (median of SSS score on admission was 28 vs. 40, and on day 1, 22 vs. 39, both p < 0.05; Mann-Whitney U test) and more often had a decreased level of consciousness (32 vs. 10%, p < 0.05; Fisher exact test). Mortality was higher in the group of patients with microalbuminuria in acute stroke (21 vs. 3% after 30 days, 39 vs. 6% after 90 days and 50 vs. 9% after 1 year, p < 0.05 for all differences; Fisher exact test). In logistic regression analysis, microalbuminuria was found to be an independent predictor of 1-year mortality after ischemic stroke (OR = 6.0; p = 0.022; 95% CI = 1.3–27.7).

The aim of the study was to investigate glucose derangement and its short- and long-term prognostic significance in nondiabetic ischemic stroke patients. The study involved 262 consecutive patients, mean age: 70.1±12.4 years, with a supratentorial ischemic stroke. The following data were collected: patients characteristics, risk factors, comorbidities, and stroke severity assessed by the Scandinavian Stroke Scale (SSS). Serum glucose levels were measured on admission, on the next, 2nd, 3rd, 5th, 7th and 14th day after stroke onset. The outcome measures on day 30 were mortality and capacity to perform daily activities: the Barthel Index and Rankin Scale. The 1-year survival was estimated by the Kaplan–Meier method. Cox proportional hazards regression was used to assess predictors of 1-year mortality in nondiabetics. Diabetes mellitus was found in 24.8% of patients and transient hyperglycemia in 36.3% of patients. Patients with transient hyperglycemia scored lower on SSS in the subsequent days of assessment than patients with either diabetes mellitus or normoglycemia. They had larger ischemic lesions on computer tomography (CT) than diabetics and had higher 30-day mortality than normoglycemics (p