Recurrent Cerebral Stroke Research Articles

Determining the etiology of cerebral stroke: from the most prevalent to rare causes

Cerebral stroke remains the leading cause of death and disability worldwide as well as in Ukraine. After a cerebral stroke, there is an increased risk of a new cerebral stroke (9‒15 % within 1 year), and about a quarter of all cerebral stroke are recurrent. Up to 80 % of recurrent cerebral stroke can be avoided through lifestyle modifications (healthy diet, sufficient amount of physical activity, normalization of body weight, cessation of smoking and alcohol abuse) and control of chronic diseases such as hypertension, diabetes, hyperlipidemia and atrial fibrillation. The key to effective secondary prevention is determining the etiology of cerebral stroke, which requires a primary examination in all cases and a number of additional tests as needed. The most common causes of ischemic cerebral stroke are cardiogenic embolism, atherosclerosis of the large cerebral arteries (macroangiopathy), and brain small vessels disease (microangiopathy), but approximately 1/3 of cerebral stroke have other, rear, determined cause or the cause remains unknown despite the appropriate workup (cryptogenic cerebral stroke). In the review, we discuss modern approaches to ischemic cerebral stroke classification and determination of their etiology, from the most prevalent to the rarest causes. A careful search for the cause of cerebral stroke is particularly important in young patients (aged 18 to 50 years) with a high life expectancy. We have reviewed in detail the possibilities of screening for subclinical atrial fibrillation by long-term cardiac monitoring with implantable devices and the diagnosis of monogenetic causes of cerebral stroke, with a particular focus on Fabry disease, for which there is an effective treatment.

SUN-437 PODOCYTOPATHY IN TYPE 2 DIABETES MELLITUS: A CASE REPORT AND REVIEW OF LITERATURES

The association of Per-hilar FSGS with type 2 diabetes is not uncommon and represent a form of podocytopathy. Several reports have shown various primary glomerulonephritis can be superimposed on diabetic nephropathy. The appearance of urinary abnormalities or deterioration in renal function inconsistent with natural history of diabetic nephropathy raises the possibility of nondiabetic renal disease and should lead to a more detailed evaluation. The association of podocytopathy in the form of heavy proteinuria, muscle weakness and arteriolopathy suggest mitochondrial cytopathy. Case report: A 60 year-old male patient with type 2 diabetes presented with high serum creatinine 3.5 mg/dl, heavy proteinuria 13.6 gm/day, serum albumin 1.07 gm/dl, high serum cholesterol 288 mg/dl, anemia of chronic disease HB 8 gm/l, recurrent cerebral stroke, generalized muscle pain and atrophy in the upper and lower muscle girdle, intermittent air hunger, poor oral nutrition and generalized anasarca with poor response to diuretic therapy, GFR was 16 ml/min. Renal biopsy was done and revealed per-hilar FSGS [Figure 1.A], mesangial sclerosis [Figure 1.B]. Electron microscopy revealed podocyte foot process effacement [Figure 1.C] and occasional mitochondria displaying abnormal internal structure specially in tubular cells [Figure 1.D]. Carotid doppler showed atherosclerosis with 50% stenosis on the right side and 60% on the left side. In view of refractory anasarca not responding to high dose of diuretic, regular ultrafiltration was initiated. Improvement of the fluid overload was achieved but patient still suffer muscle pain, weakness, and intermittent air hunger. Which improved after L-carnitin was added to improve the mitochondrial metabolism. - - we report a rare case of podocytopathy associated with advanced diabetic nephropathy in type II DM that suggesting acquired mitochondrial cytopathy.

Secondary pallidonigral degeneration mimicking recurrent acute stroke in clinical presentation and magnetic resonance imaging: a case report

BackgroundSecondary pallidonigral transneuronal degeneration after a remote primary cerebral infarct can mimic recurrent stroke at clinical presentation. We describe a patient with secondary pallidonigral degeneration following a previous putaminal infarct, which was diagnosed through diffusion-weighted (DWI) and T2-weighted imaging (T2WI).Case presentationA 64-year-old man complained of an acute relapse of right-lower-limb weakness following a cerebral infarction 2 months before presentation. Recurrent cerebral stroke was initially diagnosed in the emergency room. DWI of the brain revealed a subacute to chronic infarct in the left putamen and new acute cytotoxic edema in the left substantia nigra (SN) and globus pallidus while T2WI also showed hyperintensity in the same regions. The SN was outside the aforementioned middle cerebral arterial territory, which includes the putamen. These findings are compatible with the diagnosis of acute pallidonigral injury secondary to striatal infarction. The patient had fully recovered from his right-lower-limb weakness after 1 month.ConclusionsSecondary pallidonigral degeneration may mimic recurrent stroke. DWI along with T2WI facilitates elucidation of this clinicopathological entity, and thus unnecessary treatment can be avoided.

Recurrent cerebral stroke in a thalassemic patient

Hematol Oncol Stem Cell Ther 1(2) April 2008 hemoncstem.edmgr.com 136 T halassemia major (TM) is a congenital hemot lytic disorder caused by decreased production of globin chains. It is known that there is a hight er than normal incidence of thromboembolic events in TM. Silent infarctions have also been documented. hromboembolic events occur at a signiicantly higher incidence statistically in the presence of other hypert coagulability factors, and prophylactic antithrombotic therapy has been suggested in these patients. Several etiologic factors may play a role in the pathogenesis of the hypercoagulable state in thalassemia. We report a case of TM associated with a methylenetetrahydrofot late reductase (MTHFR) mutation in which recurrent cerebral stroke was noted during follow up.