Valentin Titus Grigorean

Bio: Valentin Titus Grigorean is an academic researcher from Carol Davila University of Medicine and Pharmacy. The author has contributed to research in topics: Medicine & Acute pancreatitis. The author has an hindex of 10, co-authored 40 publications receiving 467 citations. Previous affiliations of Valentin Titus Grigorean include Clinical Emergency Hospital Bucharest.

Vascular dysfunctions following spinal cord injury.

Abstract: The aim of this article is to analyze the vascular dysfunctions occurring after spinal cord injury (SCI). Vascular dysfunctions are common complications of SCI. Cardiovascular disturbances are the leading causes of morbidity and mortality in both acute and chronic stages of SCI. Neuroanatomy and physiology of autonomic nervous system, sympathetic and parasympathetic, is reviewed. SCI implies disruption of descendent pathways from central centers to spinal sympathetic neurons, originating in intermediolateral nuclei of T1-L2 cord segments. Loss of supraspinal control over sympathetic nervous system results in reduced overall sympathetic activity below the level of injury and unopposed parasympathetic outflow through intact vagal nerve. SCI associates significant vascular dysfunction. Spinal shock occurs during the acute phase following SCI and it is a transitory suspension of function and reflexes below the level of the injury. Neurogenic shock, part of spinal shock, consists of severe arterial hypotension and bradycardia. Autonomic dysreflexia appears during the chronic phase, after spinal shock resolution, and it is a life-threatening syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with SCI above the splanchnic sympathetic outflow (T5-T6). Arterial hypotension with orthostatic hypotension occurs in both acute and chronic phases. The etiology is multifactorial. We described a few factors influencing the orthostatic hypotension occurrence in SCI: sympathetic nervous system dysfunction, low plasma catecholamine levels, rennin-angiotensin-aldosterone activity, peripheral alpha-adrenoceptor hyperresponsiveness, impaired function of baroreceptors, hyponatremia and low plasmatic volume, cardiovascular deconditioning, morphologic changes in sympathetic neurons, plasticity within spinal circuits, and motor deficit leading to loss of skeletal muscle pumping activity. Additional associated cardiovascular concerns in SCI, such as deep vein thrombosis and long-term risk for coronary heart disease and systemic atherosclerosis are also described. Proper prophylaxis, including non-pharmacologic and pharmacological strategies, diminishes the occurrence of the vascular dysfunction following SCI. Each vascular disturbance requires a specific treatment.

Cardiac dysfunctions following spinal cord injury

Abstract: The aim of this article is to analyze cardiac dysfunctions occurring after spinal cord injury (SCI). Cardiac dysfunctions are common complications following SCI. Cardiovascular disturbances are the leading causes of morbidity and mortality in both acute and chronic stages of SCI. We reviewed epidemiology of cardiac disturbances after SCI, and neuroanatomy and pathophysiology of autonomic nervous system, sympathetic and parasympathetic. SCI causes disruption of descendent pathways from central control centers to spinal sympathetic neurons, originating into intermediolateral nuclei of T1-L2 spinal cord segments. Loss of supraspinal control over sympathetic nervous system results in reduced overall sympathetic activity below the level of injury and unopposed parasympathetic outflow through intact vagal nerve. SCI associates significant cardiac dysfunction. Impairment of autonomic nervous control system, mostly in patients with cervical or high thoracic SCI, causes cardiac dysrrhythmias, especially bradycardia and, rarely, cardiac arrest, or tachyarrhytmias and hypotension. Specific complication dependent on the period of time after trauma like spinal shock and autonomic dysreflexia are also reviewed. Spinal shock occurs during the acute phase following SCI and is a transitory suspension of function and reflexes below the level of the injury. Neurogenic shock, part of spinal shock, consists of severe bradycardia and hypotension. Autonomic dysreflexia appears during the chronic phase, after spinal shock resolution, and it is a life-threatening syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with SCI above the splanchnic sympathetic outflow (T5-T6). Besides all this, additional cardiac complications, such as cardiac deconditioning and coronary heart disease may also occur. Proper prophylaxis, including nonpharmacologic and pharmacological strategies and cardiac rehabilitation diminish occurrence of the cardiac dysfunction following SCI. Each type of cardiac disturbance requires specific treatment.

Molecular basis of vascular events following spinal cord injury.

Abstract: The aim of this article is to analyze the effects of the molecular basis of vascular events following spinal cord injury and their contribution in pathogenesis. First of all, we reviewed the anatomy of spinal cord vessels. The pathophysiology of spinal cord injuries revealed two types of pathogenic mechanisms. The primary event, the mechanic trauma, results in a disruption of neural and vascular structures into the spinal cord. It is followed by secondary pathogenesis that leads to the progression of the initial lesion. We reviewed vascular responses following spinal cord injury, focusing on both primary and secondary events. The intraparenchymal hemorrhage is a direct consequence of trauma; it has a typical pattem of distribution into the contused spinal cord, inside the gray matter and, it is radially extended into the white matter. The intraparenchymal hemorrhage is restricted to the dorsal columns, into adjacent rostral and caudal spinal segments. Distribution of chronic lesions overlaps the pattern of the early intraparenchymal hemorrhage. We described the mechanisms of action, role, induction and distribution of the heme oxygenase isoenzymes 1 and 2. Posttraumatic inflammatory response contributes to secondary pathogenesis. We analyzed the types of cells participating in the inflammatory response, the moment of appearance after the injury, the decrease in number, and the nature of their actions. The disruption of the blood-spinal cord barrier is biphasic. It exposes the spinal cord to inflammatory cells and to toxic effects of other molecules. Endothelin 1 mediates oxidative stress into the spinal cord through the modulation of spinal cord blood flow. The role of matrix metalloproteinases in blood-spinal cord barrier disruption, inflammation, and angiogenesis are reviewed.

Laparoscopic treatment of abdominal complications following ventriculoperitoneal shunt.

Abstract: The aim of this study is the evaluation of laparoscopic treatment in abdominal complications following ventriculoperitoneal (VP) shunt. Methods: We report a retrospective study including 17 patients with abdominal complications secondary to VP shunt for hydrocephalus, laparoscopically treated in our department, between 2000 and 2007. Results: Patients' age ranged from 1 to 72 years old (mean age 25.8 years old). Male: female ratio was 1.4. Abdominal complications encountered were: shunt disconnection with intraperitoneal distal catheter migration 47.05% (8/17), infections 23.52% (4/17) such as abscesses and peritonitis, pseudocysts 11.76% (2/17), CSF ascites 5.88% (1/17), inguinal hernia 5.88% (1/17), and shunt malfunction due to excessive length of intraperitoneal tube 5.88% (1/17). Free–disease interval varies from 1 day to 21 years, depending on the type of complication, short in peritoneal irritation syndrome and abscesses (days) and long in ascites, pseudocysts(months– years). Laparoscopic treatment was: extraction of the foreign body in shunt disconnection with intraperitoneal distal catheter migration, evacuation, debridement, lavage and drainage for pseudocysts, abscess and peritonitis, shortening of the tube in shunt malfunction due to excessive length of intraperitoneal tube a nd hernioraphy. One diagnostic laparoscopy was performed in a peritoneal irritation syndrome, which found only CSF ascites. There were no conversions to open surgery. The overall mortality was of 5.88% and postoperative morbidity was of 11.76%. In 7 patients operated for abscesses, peritonitis, pseudocysts, and CSF ascites the shunting system was converted in to a ventriculocardiac shunt. Conclusions: Abdominal complication following VP shunt can be successfully performed laparoscopically. Abdominal surgery required, in selected cases, the repositioning of the distal catheter, frequently as a ventriculocardiac shunt. There are abdominal complications with no indication of surgery, like peritoneal irritation syndrome and CSF ascites. Free– disease interval varies from days (peritoneal irritation syndrome, abscesses) to month–years (pseudocyst, ascites), according to type of complication.

Mortality prognostic factors in acute pancreatitis.

Abstract: Background: The aim of the study was to present the biological prognostic factors of mortality in patients with acute pancreatitis. Methods: Several usual laboratory values were monitored: glucose, urea, partial pressure of oxygen, WBC count, hemoglobin, total bilirubin, and cholesterol. A statistical analysis was performed by using ROC curves and AUC interpretation. Results: The overall mortality rate was 21.1% and was different depending on the severity of the disease. Only 2.22% of the patients with a mild disease died, as opposed to 45.63% of the patients with a severe form. All the analyses studied were significantly elevated in the deceased patients. A close correlation between blood glucose, urea, partial pressure of oxygen, WBC, hemoglobin, total bilirubin, and cholesterol and mortality was objectified by measuring the AUC, which was of 97.1%, 95.5%, 93.4%, 92.7%, 87.4%, 82.2%, and 79.0%. Conclusions: The usual, easy to use, fast, and cheap tests were useful in predicting mortality in patients with acute pancreatitis. Our study confirmed that the combination of several factors led to an accurate mortality prediction.

I and i

Abstract: There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality. Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

eMedicine

Abstract: eMedicine创建于1996年，由近万名临床医师作为作者或编辑参与此临床医学知识库的建设，其中编辑均是来自美国哈佛、耶鲁、斯坦福、芝加哥、德克萨斯、加州大学等各分校医学院的教授或副教授。

Autonomic Failure: A Textbook of Clinical Disorders of the Autonomic Nervous System

Abstract: This book provides a series of reviews about pathophysiology, treatment, and, especially, diagnostic testing of clinical syndromes of autonomie failure. The book is organized into sections about integration of sympathetic and parasympathetic function, progressive autonomie failure, and syndromes of autonomie failure. Even cursory examination of the table of contents reveals a lack of consensus about the proper classification for the several conditions involving autonomie failure, reflecting our relative ignorance about pathophysiology in this new discipline in neurology. The chapter authors are well-chosen experts, the quality of writing is generally good, and the chapters fit together well. Several typographical errors are annoying or misleading (eg, description of prazosin as an ot-2 adrenoceptor blocker, page 164). The book is a worthwhile compilation for cardiologists, neurologists, endocrinologiste, and internists who evaluate patients with suspected autonomie failure and need to know the relevant diagnostic tests. Medical students, medical residents, and fellows should benefit from

Chronic complications of spinal cord injury.

Abstract: Spinal cord injury (SCI) is a serious medical condition that causes functional, psychological and socioeconomic disorder. Therefore, patients with SCI experience significant impairments in various aspects of their life. The goals of rehabilitation and other treatment approaches in SCI are to improve functional level, decrease secondary morbidity and enhance health-related quality of life. Acute and long-term secondary medical complications are common in patients with SCI. However, chronic complications especially further negatively impact on patients' functional independence and quality of life. Therefore, prevention, early diagnosis and treatment of chronic secondary complications in patients with SCI is critical for limiting these complications, improving survival, community participation and health-related quality of life. The management of secondary chronic complications of SCI is also important for SCI specialists, families and caregivers as well as patients. In this paper, we review data about common secondary long-term complications after SCI, including respiratory complications, cardiovascular complications, urinary and bowel complications, spasticity, pain syndromes, pressure ulcers, osteoporosis and bone fractures. The purpose of this review is to provide an overview of risk factors, signs, symptoms, prevention and treatment approaches for secondary long-term complications in patients with SCI.

Inflammogenesis of Secondary Spinal Cord Injury

Abstract: Spinal cord injury (SCI) and spinal infarction lead to neurological complications and eventually to paraplegia or quadriplegia. These extremely debilitating conditions are major contributors to morbidity. Our understanding of SCI has certainly increased during the last decade, but remains far from clear. SCI consists of two defined phases: the initial impact causes primary injury, which is followed by a prolonged secondary injury consisting of evolving sub-phases that may last for years. The underlying pathophysiological mechanisms driving this condition are complex. Derangement of the vasculature is a notable feature of the pathology of SCI. In particular, an important component of SCI is the ischemia-reperfusion injury that leads to endothelial dysfunction and changes in vascular permeability. Indeed, together with endothelial cell damage and failure in homeostasis, ischemia reperfusion injury triggers full-blown inflammatory cascades arising from activation of residential innate immune cells (microglia and astrocytes) and infiltrating leukocytes (neutrophils and macrophages). These inflammatory cells release neurotoxins (proinflammatory cytokines and chemokines, free radicals, excitotoxic amino acids, nitric oxide) , all of which partake in axonal and neuronal deficit. Therefore, our review considers the recent advances in SCI mechanisms, whereby it becomes clear that SCI is a heterogeneous condition. Hence, this leads towards evidence of a restorative approach based on monotherapy with multiple targets or combinatorial treatment. Moreover, from evaluation of the existing literature, it appears that there is an urgent requirement for multi-centered, randomized trials for a large patient population. These clinical studies would offer an opportunity in stratifying SCI patients at high risk and selecting appropriate, optimal therapeutic regimens for personalized medicine. Keywords: Inflammation; ischemia-reperfusion injury; spinal cord injury; reactive oxygen species; leukocytes; glia; therapeutics.