ISSN:1350-7540    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Cluster headache, one of the most severe pain syndromes in humans, is usually described as a vascular headache. However, the striking circadian rhythmicity of this strictly unilateral pain syndrome cannot readily be explained by the vascular hypothesis. Recent studies using positron emission tomography suggest that a central nervous system dysfunction in the region of the hypothalamus is theprimum movensin the pathophysiology of cluster headache. From a physiological viewpoint, therefore, cluster headache should be described as a neurovascular headache, thus placing equal emphasis on its fundamental pathophysiology and clinical expression. Curr Opin Neurol 11:199–203. © 1998 Lippincott–Raven Publishers

ISSN:1350-7540    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Central neuronal hyperexcitability is proposed to be the putative basis for the physiologic disturbances in migraine. Because there are no structural disturbances in migraine, only physiologic studies can provide insight into the underlying mechanisms. Recently, transcranial magnetic stimulation has been developed as a valuable research tool and can be used to study brain function noninvasively. This article is a review of the studies done in migraine using transcranial magnetic stimulation. Curr Opin Neurol 11:205–209. © 1998 Lippincott–Raven Publishers

ISSN:1350-7540    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Familial hemiplegic migraine (FHM) has been related to mutations in a brain calcium channel gene among Chr19p linked FHM families. Subsequent genetic Studies in different FHM families showed that additional causative genes must reside in other regions of the genome, including the long arm of Chromosome 1. Parallel discoveries in mouse mutants involving ion channel genes have also accelerated our understanding of the spectrum and functional significance of the CNS‐related ion channel disorders. These studies have clear implications for migraine, epilepsy, and ataxia. An association study has suggested that other ‘susceptibility’ genes like the dopamine DRD2 receptor will be important in characterizing the genetic components of the larger, heterogeneous group of migraine disorders. Curr Opin Neurol 11:211–216 © 1998 Lippincott–Raven Publishers

ISSN:1350-7540    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Over the past 8 years an increasing awareness of the role of mutant ion channels in episodic diseases of humans has emerged. The importance of these discoveries is now being extended to a growing list of membrane excitability disorders of the nervous system. Molecular characterization of episodic diseases that are rare and monogenic will ultimately shed light on more common and complex disorders, such as epilepsy and migraine. Curr Opin Neurol 11:217–226. © 1998 Lippincott–Raven Publishers

ISSN:1350-7540    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Although spreading depression has been known for over 50 years, recent research into this interesting experimental phenomenon provides evidence for an integrative role of spreading depression in brain pathophysiology. Spreading depression activates neurophysiological pathways that may have widespread consequences on brain function, but depends on the basal energy state of the brain. Curr Opin Neurol 11:227–231. © 1998 Lippincott–Raven Publishers

ISSN:1350-7540    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:1350-7540    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

In many neurologic diseases, activated leukocytes enter the nervous system and initiate a chronic inflammatory process. Understanding how the cellular and humoral responses are associated with pathogenesis is essential for the formulation of a unifying model of central and peripheral nervous system inflammation. Based on such a model, immunotherapeutic strategies and protocols can be designed. Curr Opin Neurol 11:235–240. © 1998 Lippincott–Raven Publishers

ISSN:1350-7540    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Central nervous system vasculitis occurs in a variety of clinical settings. Some exhibit a distinct age preference; others a tissue tropism. Most frequently encountered are giant cell arteritis (temporal arteritis) and vasculitis secondary to infections. The central nervous system may be involved in the antineutrophil cytoplasmic antibody‐associated systemic vasculitides and occasionally neurologic abnormalities appear as a presenting manifestation of disease. Isolated angiitis of the central nervous system, a rare form of vasculitis that is restricted to the central nervous system, must be distinguished from other causes of central nervous system inflammation and from noninflammatory vascular disease. We are learning a great deal about the cellular mechanisms of vascular inflammation in general. Some manifestations of the clinical disease result from histologic features of the infiltrate and the size of affected vessel. However, the local consequences of inflammation, such as increased coagulation and altered vasomotor tone, as well as the systemic consequences, such as activation of the central noradrenergic systems, trigeminovascular system, and hypothalamic pituitary adrenal axis, contribute both to pathogenesis of disease and to recovery. Curr Opin Neurol 11:241–246. © 1998 Lippincott–Raven Publishers

ISSN:1350-7540    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The aetiology of neurological involvement in systemic lupus erythematosus (SLE) still remains largely uncertain, but there are some recent reports of retrovirus activity linked to human and mouse models of SLE. Antiribosomal P antibodies appear specific to SLE and tend to be associated with psychiatric disease, but not exclusively so. The role of antiphospholipid antibodies in the pathogenesis of SLE may not be solely to cause thrombotic events, but also to act directly on neuronal tissue. The importance of another group of antibodies, those against Beta 2 glycoprotein I, a phospholipid binding protein, is now being recognized. Amongst the many neurological manifestations of SLE, cognitive impairment is becoming increasingly recognized and appears not to be simply a response to chronic disease or its treatment. Of the newer imaging techniques applied to SLE, positron emission tomography has proved inconsistent and somewhat disappointing but single photon emission computed tomography in active disease appears more sensitive compared to MRI, although it still remains a nonspecific technique. The treatment of SLE remains disappointing and no controlled trials for neurological disease have been published to date but a number of experimental approaches do offer hope for the future. Curr Opin Neurol 11: 247–251 © 1998 Lippincott–Raven Publishers

ISSN:1350-7540    

出版商:OVID    

年代:1998

数据来源: OVID