ABSTRACT
Arteriovenous malformations (AVMs) are the most dangerous congenital vascular malformations. Intracranial AVMs occur in about 0.1 percent of the population and account for 1 to 2 percent of all strokes. The angioarchitecture of AVMs consists of direct arterial to venous connections without an intervening capillary network. The main symptom reported by half of all patients with arteriovenous malformations is an episodic headache. The headache is associated with nausea and vomiting and due to this resembles the hemicrania or cluster headache attacks. Although cerebral angiography is considered as the gold standard for the diagnosis, planned treatment and after treatment observation, AVMs are usually identified with advanced visual imaging techniques such as magnetic resonance imaging, computed tomography, and computed angiotomography. The treatment options consist of surgery, radiosurgery and endovascular embolization. We report a case of a 68-year-old man with giant intracranial arteriovenous malformation and right-sided hemicrania.
Subject(s)
Headache/etiology , Intracranial Arteriovenous Malformations/diagnosis , Intracranial Arteriovenous Malformations/therapy , Aged , Cerebral Angiography , Diagnosis, Differential , Embolization, Therapeutic , Humans , Intracranial Arteriovenous Malformations/complications , Male , Nausea/etiology , Tomography, Spiral Computed , Vision Disorders/etiology , Vomiting/etiologyABSTRACT
Early effects of cadmium (Cd) on the structure and function of the kidney were studied in an experimental model using rats intoxicated with Cd at the levels of 5 and 50 mg Cd/l drinking water. The effect of Cd was evaluated histopathologically and biochemically. Damage to the cellular structures was assessed on the basis of histoenzymatic analyses of the activity and localization of indicator enzymes (succinate dehydrogenase, lactate dehydrogenase, glucose-6-phosphatase, Mg(2+)-dependent adenosine triphosphatase and acid phosphatase). The histochemical observations indicate that Cd causes damage to the organization and function of the nephron. Several structures, i.e. endoplasmic reticulum, mitochondrion, lysosome, cellular and intracellular membrane, as well as their biological functions, i.e. aerobic and anaerobic respiration, transport functions and biochemical processes taking place in the endoplasmic reticulum, were affected. The cytotoxic action of Cd occurs mainly in the tubules and partially also in the glomeruli. The results clearly indicate that Cd damages kidney structurally and functionally even at a relatively low level (5 mg/l) corresponding to human environmental exposure, and they confirm our previous hypothesis that the threshold for the kidney effects of Cd is less than 4.08+/-0.33 microg/g kidney wet weight and higher than 2.40+/-0.15 microg/g. The target for Cd action in the kidney is the tubules (proximal convoluted tubules and straight tubules), and disturbance in their function is the main toxic effect of Cd. Renal glomeruli are also injured, but only partially, whereas in other parts of the nephron the damage is slight. The results, together with observations reported in the first paper of the study, incline us to conclude that humans environmentally exposed to Cd are at risk of tubular damage.
