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Biomedical subjects

M Segatore

Publications and source records attributed to M Segatore.

At least 19 recordsLinked to original sources
PubMed1999

Corticosteroids and traumatic brain injury: status at the end of the decade of the brain.

Although high dose glucocorticosteroid therapy has become the standard of care for hyperacute management of non-penetrating spinal cord injury, it does not enjoy the same prestigious status in traumatic brain injury (TBI). A Brain Trauma Foundation standard concluded that steroids fail to improve outcome and lower intracranial pressure in severe TBI, but in the absence of interventions able to improve the functional outcome, glucocorticosteroid use continues into the present day. This paper summarizes the pathobiology of TBI and provides a methodological critique of the major studies of steroids in TBI. Given the growing appreciation of the complexity and heterogeneity of brain injury, corticosteroid use may find a rational place in management. Alone or in combination with other agents, corticosteroids may have a role in the treatment of severe injury, which so far has remained intractable to all manner of intervention.

Brain↗
PubMed1998

The delirious cardiac surgical patient: theoretical aspects and principles of management.

Delirium, an etiologically nonspecific disorder of consciousness characterized by prominent deficits in attention, cognition, and perception, affects more than one-third of adult cardiac surgical patients. Despite the frequency of occurrence and the increased morbidity and mortality associated with it, the diagnosis is commonly late or missed, and management is less than optimal. This article addresses the recognition and management of delirium. Nurses who develop an index of suspicion for the diagnosis and acquire the diagnostic and interventional skills required to address this cerebral complication of cardiac surgery may well decrease its incidence and severity.

Antipsychotic Agents↗
PubMed1997

Neuroprotection after spinal cord injury: state of the science.

Advances in the basic and clinical sciences are improving our ability to alter the course of injury that occurs after acute spinal cord trauma. Methylprednisolone, naloxone, GM-1 ganglioside, tirilazad mesylate and other agents have been or are currently being subjected to rigorous testing to determine their ability to protect compromised but viable cellular elements and improve the functional outcome of survivors. The authors summarize mechanisms of secondary (spinal cord) injury, discuss derivative pharmacotherapy, review clinical trial findings and raise issues related to future research. Special attention is directed to the Maryland studies of GM-1 ganglioside and the National Acute Spinal Cord Injury trials. Preliminary work regarding the roles of excitatory amino acids, endogenous opioid peptides, calcium channel blockers and nerve growth factors in secondary injury are also outlined.

Humans↗
PubMed1996

Understanding central post-stroke pain.

Almost a century ago, two French neurologists described an unusual pain syndrome following stroke. This so-called "thalamic" pain of Dejerine-Roussy exists today, affecting approximately 30,000 survivors of stroke in the United States (US) alone. Lesions involving the neospinothalamocortical tract are thought to cause thalamic pain, but the exact pathogenesis is unclear. Pharmacotherapeutic and surgical approaches offer pain relief in selected patients. Although definitive relief of central post-stroke pain (CPSP) may not be achievable for all at this time, intelligent and informed examination of the full range of options offers every sufferer a real potential for relief and mastery of pain. It is hoped that information provided herein will foster "intelligent caring" and facilitate informed decision making by consumers and caregivers alike.

Analgesics↗
PubMed1995

The skeleton after spinal cord injury. Part 1. Theoretical aspects.

Sublesional osteoporosis occurs after acute spinal cord injury (SCI), preferentially weakening the skeleton below the level of the neurological lesion. Although its pathogenesis is unclear, it resembles post-menopausal, high turnover osteoporosis. Physical and pharmacologic therapies are currently being tested for their ability to prevent early loss and restore lost bone. Although treatment strategies hold promise, preservation of skeletal strength after injury may ultimately rest on lifestyle decisions made early in life. If skeletal strength is to be maintained after SCI, ways must be found to optimize skeletal strength prior to injury, arrest early losses, and stabilize, if not restore, lost bone over time.

Female↗
PubMed1995

Thrombolysis after stroke hope for the future.

Over the past two decades, several prospective, randomized clinical trials have shown that thrombolytic therapy of acute myocardial infarction (AMI) decreases morbidity and mortality. The generally positive results have been tempered by a small, but clinically significant risk of potentially lethal intracerebral haemorrhage. Given that the pathogenesis of thrombotic stroke is similar to AMI, interest has recently turned to the use of the same drugs to "cure" stroke. The purpose of this paper is to develop a comprehensive position regarding neuroscience nursing roles concerning this new therapy. The importance of proactive public educational programmes and rapid and accurate patient identification derive directly from the pathogenesis of thrombotic stroke, and the pharmacology of the thrombolytic agents. Guidelines for drug preparation and administration and patient monitoring during treatment are developed from tested cardiovascular models.

Cerebrovascular Disorders↗
PubMed1995

The pharmacotherapy of spinal spasticity: a decade of progress. II. Therapeutics.

Spinal spasticity is the term used to describe the increase in muscle tone which often develops following spinal cord injury (SCI). A review of spasticity and approaches to its treatment has been presented in a previous article. The purpose of this paper is to discuss the pharmacologic agents that are currently used to treat spinal spasticity. These medications can be classified as centrally and peripherally acting agents. The following review is therefore organized into two sections, according to the site of drug action.

Humans↗
PubMed1994

Understanding chronic pain after spinal cord injury.

Survivors of spinal cord injury (SCI) have a range of sensory experiences following the trauma. Acute pain commonly accompanies the injury and recedes as healing occurs. Following the initial event, most spinal cord-injured individuals experience phantom sensations and many suffer chronic pain. In extreme cases, chronic pain can become the most disabling sequela, leading to chemical dependency, severe depression and even suicide. Pain arising from injury to peripheral and central neural structures possesses unique characteristics that distinguish it from persisting acute pain and phantom sensations. Ironically, it is experienced in regions of the body that are anesthetic or possess diminished or altered sensation as a consequence of the injury. The qualitative features of the pain have been linked to structural and functional alterations that have been documented in peripheral and central neural structures following SCI. An understanding of these unique relationships provides direction for future research.

Adult↗
PubMed1994

Development and preliminary testing of the neurological assessment instrument.

The purpose of this study was to test a neurological assessment instrument (NAI), used to assess neurological function in adults with acute brain lesions. Instrument items were designed to reflect different aspects of neurological function and assess consciousness along the arousal/awareness continuum as described by Plum and Posner. Content of the NAI was validated by 10 neuroscience expert physicians, nurses and speech pathologists. Reliability was tested with one pair of raters on 39 neurologically stable patients with acute brain lesions. Based on preliminary findings, the critical preliminary steps have been taken towards establishing a reliable and valid instrument with the potential of improving the assessment of neurological function in patients with acute brain lesions.

Adolescent↗
PubMed1993

Illiteracy: implications for nursing education.

Possession of an internally consistent body of knowledge from which principles and practice can be derived is the pre-eminent characteristic of professional groups. Active, enquiring minds are required as nursing struggles to develop such a base. Yet, recent evidence, such as the 1992 report of the Economic Council of Canada, suggests a pervasive decline in basic language competencies. The illiteracy of candidates entering professional schools of nursing is creating problems for students, faculty and the profession, with ramifications for public safety and professional growth. This article describes problems and proposes action that can, and must, be taken to remedy the situation.

Canada↗
PubMed1993

Assessment and management of galactorrhea.

Galactorrhea, inappropriate lactation, is a relatively common clinical sign encountered by primary health care providers. However, this physical sign is not synonymous with life-threatening breast or intracranial malignancy; rather, it may be physiologic, drug-induced or idiopathic. Given the 20 percent prevalence of pituitary adenomas in women with galactorrhea, the primary health care provider must rule out, in every case, intracranial causes for galactorrhea. This article reviews relevant physiopathology and develops an assessment and diagnostic protocol, which includes indications for urgent referral. It concludes with summaries of treatment modalities, outlining the role of the primary care provider throughout the diagnostic and treatment processes.

Adult↗
PubMed1993

Hyponatremia after aneurysmal subarachnoid hemorrhage.

Hyponatremia frequently complicates the clinical course for patients with aneurysmal subarachnoid hemorrhage (SAH). Although commonly attributed to the syndrome of inappropriate antidiuretic hormone (SIADH), emerging evidence suggests a range of pathological conditions may produce the abnormality. Effective management requires an approach to data collection which avoids suppositions about etiology, as incorrect assumptions may result in selection of interventions leading to further clinical deterioration. Adherence to comprehensive monitoring and management protocols ensures rapid detection and efficient management of this common problem after SAH.

Humans↗
PubMed1993

Posttraumatic seizures: consensus and controversies.

Seizures after traumatic brain injury may cause acute deterioration in level of consciousness, signal the presence of significant intracranial pathology, herald potentially lethal status epilepticus and carry some risk for the development of a chronic disorder. Specific implications of immediate, early and late seizures are different and vary across age groups. While there is a consensus to manage status epilepticus aggressively, and some agreement to treat a seizure once it has begun, no such unanimity exists about management of patients who have one or more seizures after injury. This article identifies controversies about seizures that occur after traumatic brain injury in paediatric and adult populations. It concludes with a summary of research imperatives for the future.

Brain Injuries↗
PubMed1993

Methylprednisolone after spinal cord injury.

The assumption that maximal spinal cord injury occurs at the moment of trauma is being challenged by emerging evidence that cellular injury continues after the acute event. Efforts are now being made to alter the course of secondary injury in order to improve the functional outcome of survivors. Methylprednisolone has been studied in two clinical trials--the National Acute Spinal Cord Injury Studies (NASCIS I, NASCIS II)--to determine its ability to protect compromised but viable cellular elements, and thus improve outcome. The purpose of this paper is threefold: (1) to explore the putative mechanisms of secondary spinal cord injury, (2) to examine the role of methylprednisolone in spinal cord injury, and (3) to discuss the findings and clinical implications of NASCIS I and NASCIS II.

Humans↗
PubMed1992

Fever after traumatic brain injury.

Fever or pyrexia is a common clinical phenomenon. Among survivors of traumatic brain injury, it may appear immediately after injury, signal the presence of infection or reflect dysfunction of the thermoregulatory system. Management of pyrexia must be distinguished from measures that seek to identify and remove the putative cause of fever. Guidelines for decision making regarding the nursing management of patients with fever are presented. Given the potential benefit of fever, the ability of most patients to tolerate temperature elevations and the adverse effects, costs and discomforts associated with therapy, our habit of automatically reducing temperature should be examined.

Adult↗