摘要:

BACKGROUNDThis study examined causes of elevated serum creatine kinase (hyper‐CK‐emia) and its frequencies in a neurological department. Few data are available about this topic. We retrospectively evaluated the medical records of all inpatients with hyper‐CK‐emia greater than 70 U/L admitted to our department between October 1995 and October 1998.REVIEW SUMMARYAmong 3,601 patients admitted during this period, 426 (12%) (165 women and 261 men, age 21 to 97 years) had hyper‐CK‐emia. The most frequent causes of hyper‐CK‐emia were stroke (21%), trauma (18%), idiopathic hyper‐CK‐emia (14%), and seizures (12%). In 42 patients, two or three causes for hyper‐CK‐emia were found. Depending on the diagnostic group, mean CK ranged between 129 U/L (thyroid dysfunction) and 882 U/L (electrolyte disturbances). A total of 72% of patients had hyper‐CK‐emia up to 200 U/L, and 96% up to 1,000 U/L. Only one patient had CK greater than 5,000 U/L. The oldest patients with hyper‐CK‐emia were those with myocardial infarction, and the youngest were those with multiple sclerosis. Hyper‐CK‐emia occurred more frequently in men than in women.CONCLUSIONSHyper‐CK‐emia was found in 12% of the patients admitted to our neurological department. In the majority of the patients, CK elevations were only mild. The most frequent causes of hyper‐CK‐emia were stroke, trauma, and seizures.(THE NEUROLOGIST 6:309‐314, 2000)

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BACKGROUNDCerebral amyloid angiopathy (CAA) is increasingly recognized as an important cause of lobar intracerebral hemorrhage in the elderly and is the only major form of stroke without effective treatment. It is characterized by deposition of congophilic material in small‐ to medium‐sized blood vessels of the brain and leptomeninges. In the most severe stages of the disease, amyloid deposits cause breakdown of the blood vessel wall with consequent hemorrhage. Presently, definitive diagnosis of CAA‐related hemorrhage requires examination of the brain at autopsy.REVIEW SUMMARYThis article reviews the pathology and pathogenesis of CAA. To aid in identifying patients at risk for CAA, the range of clinical presentations is discussed. Particular attention is devoted to lobar intracerebral hemorrhage, the most common and devastating manifestation of CAA. We review recent developments in the epidemiology of CAA, particularly the lessons learned from studies of the apolipoprotein E genotype. We conclude with a discussion of antemortem diagnosis, the differential diagnosis and management of CAA, and future directions for the development of treatments.CONCLUSIONSCAA will become increasingly common as the population ages. Its presence should be considered in any elderly patient with lobar hemorrhage or dementia. Recognition of CAA is particularly important in the setting of anticoagulant therapy, which places patients with CAA at high risk for intracerebral hemorrhage. Finally, patients with CAA‐related hemorrhage are at high risk for recurrent hemorrhage.(THE NEUROLOGIST 6:315‐325, 2000)

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BACKGROUNDLow back pain is both a common and pervasive problem in society today. The physical pain itself represents only a small fraction of the overall disability. On an individual level, the emotional cost of dealing with chronic pain and the loss of independence can be devastating. On a societal level, the loss of workforce productivity and the need for additional expenditure of diminished health care resources may be staggering.REVIEW SUMMARYThe syndrome of low back pain is reviewed with descriptions of the common symptoms, clinical signs, and pathologic basis of the disease process. The diagnostic value of the clinical examination and various neuroimaging modalities is discussed. Generation of differential diagnoses on the basis of available clinical information is emphasized. Treatment options, including nonoperative and surgical interventions, are evaluated for relative merit and efficacy.CONCLUSIONSLow back pain is a common problem with widespread implications. Management is based on understanding the causative lesion and judicious application of proven therapies.(THE NEUROLOGIST 6:326‐337, 2000)

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BACKGROUNDNew treatment modalities aimed to decrease both mortality and morbidity in patients with stroke are of the greatest necessity. The rationale for the use of glycerol in stroke is that brain edema is one of the most evident effects of ischemia and a common cause of death and morbidity.REVIEW SUMMARYIn this review, we describe the basic mechanisms leading to accumulation of brain edema in stroke, followed by a discussion of the pharmacology of glycerol and its properties on brain hemodynamics and metabolism in both normal and pathologic circumstances. We also discuss all of the available trials in the English literature of glycerol for acute stroke.CONCLUSIONSGlycerol can be used safely to decrease the brain edema associated with ischemic stroke. However, its routine use has not been proven to significantly decrease morbidity or mortality in this setting. It is apparent that the beneficial effects of glycerol in brain ischemia cannot be explained solely on the basis of its hyperosmolar properties.(THE NEUROLOGIST 6:338‐347, 2000)

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BACKGROUNDDiscontinuation syndromes have been noted for various classes of psychotropic medication and have now been observed for selective serotonin reuptake inhibitors (SSRIs) and other new serotonergic antidepressants.REVIEW SUMMARYSSRIs and other new antidepressants are increasingly being used for neurologic disorders as well as for depression and anxiety, which frequently coexist with these illnesses. Recently, a discontinuation syndrome was identified after abrupt and even tapered withdrawal from these agents. The syndrome presents with somatic symptoms of disequilibrium, gastrointestinal symptoms, flu‐like symptoms, disrupted sleep, and sensory disturbances as well as psychological symptoms of irritability, crying spells, and anxiety or agitation. These symptoms, which usually appear within 1 to 3 days after the last dose, are usually mild and transient but can be more severely distressing and debilitating and lead to disruption of social or occupational activities. When intervention is required, the primary strategy entails reinstituting the SSRI and, if appropriate, commencing a slow and gradual tapering schedule. We review the cases of three patients with SSRI discontinuation syndrome who presented to the clinic with neurologic complaints.CONCLUSIONThe primary prevention strategy for discontinuation syndrome is to avoid abrupt discontinuation of antidepressant medication, particularly for agents demonstrating a pharmacologic profile of a short half‐life and no active metabolites. Awareness of SSRI discontinuation syndrome facilitates rapid identification and effective intervention as well as improved prevention through patient education.(THE NEUROLOGIST 6:348‐352, 2000)

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID