摘要:

BACKGROUNDEncephalitis is the second most common type of infection of the central nervous system and continues to be an important cause of mortality and morbidity.REVIEW SUMMARYIn a patient who is suspected of having encephalitis, one must distinguish between encephalitis and encephalopathy and between infectious encephalitis and acute disseminated encephalomyelitis. Once infectious encephalitis has been diagnosed, one should determine whether the patient has herpes simplex encephalitis, because treatment with antiviral drugs such as acyclovir greatly improve outcome. Most cases of infectious encephalitis are due to viruses, but bacteria, fungi, and parasites also can be the cause, especially in immunosuppressed individuals. The rapid determination of the cause of infectious encephalitis remains difficult, but newer assays to detect IgM antibody to the infectious agent in CSF or serum and polymerase chain reaction assays for nucleic acid fragments of the infectious agent in CSF are enabling faster and more accurate diagnoses. Antimicrobial drugs now are available for many of the infectious agents and some DNA viruses, but excellent treatment of the patient's symptoms remains very important.CONCLUSIONSThis review provides an approach to diagnosing possible encephalitis through asking and answering several key questions. Recent advances in methods of determining the cause of the encephalitis and better antimicrobial drugs improve the likelihood of successful treatment.(THE NEUROLOGIST 6:145‐159, 2000)

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BACKGROUNDHyperlipidemia is associated with coronary heart disease (CHD) and stroke and is a widespread problem. There is emerging evidence that cholesterol‐modifying agents can reduce the risk of stroke, making this a topic of interest for neurologists.REVIEW SUMMARYReducing cholesterol with agents other than 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors (statins) has not been shown to lessen the incidence of ischemic stroke. Primary prevention using statin agents has not been beneficial in reducing the risk of stroke, but it does reduce CHD. In patients who have CHD, the use of statins has been associated with decreased incidence of ischemic stroke. The mechanisms of stroke reduction may include lipid‐lowering or anti‐atherothrombotic effects. Statins generally are safe and well tolerated. Dosing and side effects are reviewed.CONCLUSIONSStatin agents should be prescribed by neurologists for stroke prevention in patients who have a history of CHD. Statin use could reasonably be recommended in ischemic stroke patients who have vascular risk factors. Age and cholesterol levels should be carefully considered before starting a statin in the care of stroke patients.(THE NEUROLOGIST 6:160‐170, 2000)

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BACKGROUNDControversy exists regarding the timing of surgery and the surgical strategy for patients who have cerebellar infarction.REVIEW SUMMARYCerebellar infarction with mass effect (pseudotumoral cerebellar infarction) has a higher prevalence than previously noted. Not all of these patients require surgical intervention. Surgery is likely to be beneficial for patients who deteriorate clinically and who have radiologic evidence of hydrocephalus or brainstem compression. Bias in patient selection has not clarified the issue of isolated ventricular drainage or suboccipital craniotomy in these patients. Half of the obtunded or comatose patients who had cerebellar infarction and were treated either by isolated ventricular drainage or suboccipital craniotomy made meaningful recovery.CONCLUSIONSSurgical intervention is indicated for patients who have cerebellar infarction with mass effect and who have deteriorated clinically. Either isolated ventricular drainage or suboccipital craniotomy may be beneficial for these patients.(THE NEUROLOGIST 6:172‐176, 2000)

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BACKGROUNDParoxysmal dyskinesias are a heterogenous group of disorders that are characterized by the sudden onset of a variety of abnormal movements out of a background of normal motor activity.REVIEW SUMMARYParoxysmal dyskinesias can be classified into four basic varieties: paroxysmal kinesigenic dyskinesia, paroxysmal nonkinesigenic dyskinesia, paroxysmal exertion‐induced dyskinesia, and paroxysmal hypnogenic dyskinesia. Most cases are idiopathic and familial, but sporadic cases and symptomatic cases as a result of a number of different causes are well described. The familial cases are inherited in an autosomal dominant fashion, and the gene loci for some have been described. These disorders may belong to an ever‐increasing family of episodic neurological disorders that are caused by a dysfunction of ion channels (channelopathies).CONCLUSIONSParoxysmal dyskinesias can be idiopathic or symptomatic. The identification of distinct genetic loci will lead to a new genetic classification and to a better understanding of the idiopathic disorders.(THE NEUROLOGIST 6:177‐185, 2000)

ISSN:1074-7931    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BACKGROUNDEasy fatigability and weakness of muscles are the salient clinical features of disorders that affect the neuromuscular junction (NMJ). Congenital myasthenic syndromes (CMSs) are a heterogeneous group of inherited diseases of the NMJ, and each individual condition is seen infrequently. However, as a group, the incidence of these conditions is frequent enough that they should be considered in the differential diagnosis of patients who present with myasthenic symptoms, especially when the onset is from infancy or childhood.REVIEW SUMMARYThe congenital myasthenic syndromes result from inherited disorders of the structure and/or function of the pre‐ and postsynaptic structures. The symptoms of fatigue and weakness result from compromise of the safety factor in neuromuscular transmission. We review the physiological basis of the safety factor of neuromuscular transmission and the clinical features, electrodiagnostic findings, diagnosis, and treatment of the common congenital myasthenic syndromes. Weakness of ocular and facial muscles beginning from infancy and childhood is the most common clinical presentation.Repetitive nerve stimulation studies and single‐fiber electromyography demonstrate abnormalities that are consistent with dysfunction of the NMJ. The advances in molecular biology, microelectrode recordings, and ultrastructural studies have elucidated the genetic basis of most of these syndromes and their pathophysiology.Anticholinesterase agents, such as pyridostigmine, help to improve the symptoms in patients who have defects in acetylcholine resynthesis or packaging or myasthenic syndromes secondary to deficiency of acetylcholine receptors. Patients who have slow channel syndrome respond to guanidine.CONCLUSIONSUnderstanding of the molecular genetics and pathogenesis of congenital myasthenic syndromes have led to improved accuracy in diagnosis of and therapy for these disorders.(THE NEUROLOGIST 6:186‐196, 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