|
1. |
Editorial |
|
The Neurologist,
Volume 6,
Issue 1,
2000,
Page 1-1
Preview
|
PDF (389KB)
|
|
ISSN:1074-7931
出版商:OVID
年代:2000
数据来源: OVID
|
2. |
NEUROMUSCULAR COMPLICATIONS OF CRITICAL ILLNESS |
|
The Neurologist,
Volume 6,
Issue 1,
2000,
Page 2-11
Shawn,
Bird Mark,
Preview
|
PDF (6809KB)
|
|
摘要:
BACKGROUNDNeuromuscular weakness is common in the setting of critical illness. Over the past two decades, it has been recognized that polyneuropathy or myopathy may develop de novo as a complication of the underlying illness, sepsis, or the medical therapies. This weakness complicates recovery and often contributes to prolonged ventilator dependence.REVIEW SUMMARYThe neuromuscular complications of critical illness include critical illness polyneuropathy, an acute myopathy, and prolonged pharmacologic neuromuscular blockade. As a complication of critical illness and the systemic inflammatory response syndrome (usually produced by sepsis), an axonal sensory‐motor polyneuropathy may be seen. A myopathy, often called acute quadriplegic myopathy, may develop in a similar setting, often in association with the use of corticosteroids and/or nondepolarizing neuromuscular‐blocking agents (NMBAs). Weakness in this latter disorder may result from electrical inexcitability of muscle due to altered membrane sodium channels with reduced sodium currents and loss of myosin thick filament. Some patients, particularly those with abnormal renal or hepatic function, may have prolonged weakness for as long as one week after the use of NMBAs. This large, heterogeneous group of patients are difficult to evaluate due to the limitations imposed by the critical care setting and may have critical illness polyneuropathy, acute quadriplegic myopathy, or both.CONCLUSIONSNeuromuscular weakness may occur in association with a combination of risk factors, including sepsis and multiorgan failure (systemic inflammatory response syndrome), high‐dose corticosteroids, and NMBAs. This may take the form of an axonal polyneuropathy, an acute myopathy, or both.
ISSN:1074-7931
出版商:OVID
年代:2000
数据来源: OVID
|
3. |
AN UPDATE ON SICKLE CELL DISEASE |
|
The Neurologist,
Volume 6,
Issue 1,
2000,
Page 12-17
Robert,
Preview
|
PDF (4109KB)
|
|
摘要:
BACKGROUNDNeurological complications, especially stroke, are important causes of morbidity and mortality in sickle cell disease (SCD). The neurologist is often called in consultation.REVIEW SUMMARYRecent new information has better established the epidemiology of stroke in SCD and demonstrated that high incidence rates are seen in early childhood and later in life as well. Secondary prevention of recurrent stroke in children is accomplished with chronic transfusion, and there is little experience with other preventive treatments. Primary prevention is now feasible for children using screening with transcranial Doppler. There are data from a randomized controlled clinical trial that indicates that children with high velocities on transcranial Doppler (>200 cm/sec time averaged mean in the middle cerebral or intracranial internal carotid arteries) have a very significant reduction in stroke with chronic transfusion. Hydroxyurea and bone marrow transplantation may in the future be used for stroke prevention, but there are no data at present. There is no primary stroke prevention strategy for adults and prevention of recurrent stroke has not been well studied. Transfusion is an option, as well as empiric use of antiplatelet agents, warfarin, or surgery, but there are virtually no data on risk/benefit for these treatments in adults. All SCD patients with intracranial hemorrhage should be considered for angiography to look for surgically correctable lesions.CONCLUSIONThe neurologist should bear in mind that, although stroke is common in SCD, other etiologies and causes for neurological dysfunction may be present and should be considered in patients with SCD who present with neurological symptoms.(THE NEUROLOGIST 6:12‐17, 2000)
ISSN:1074-7931
出版商:OVID
年代:2000
数据来源: OVID
|
4. |
THE NONMOTOR PROBLEMS OF PARKINSON'S DISEASE |
|
The Neurologist,
Volume 6,
Issue 1,
2000,
Page 18-27
Joseph,
Friedman Hubert,
Preview
|
PDF (7109KB)
|
|
摘要:
BACKGROUNDAlthough the motor symptoms of Parkinson's disease (PD) dominate the clinical picture, the nonmotor complaints are often more disabling for the Parkinson patient.REVIEW SUMMARYBehavioral, psychiatric, and cognitive changes occur commonly and are frequent causes for concern. Depression affects up to half of Parkinson patients and can worsen their motor function. Drug‐induced psychoses can range from benign visual hallucinations to paranoid delusions. Dementia, classically described as subcortical, usually occurs in the elderly PD patient and is often clinically distinct from the cortical dementia of Alzheimer's disease although pathological descriptions overlap. A parkinsonian personality has been noted by psychoanalysts and movement disorder experts characterized as rigid and compulsive yet cautious and apprehensive with a subordinate behavior. Sleep disturbances associated with PD include insomnia, sleep fragmentation, daytime somnolence, vivid dreams, rapid eye movement behavior disorder, and restless legs syndrome. Sensory symptoms, including pain, may occur, as do symptoms of autonomic dysfunction including postural syncope. Problems with bladder and bowel control and sexual dysfunction are common and often distressing to both the patients and their partners. Fatigue, akathisia, seborrheic dermatitis, and scoliosis are conditions intrinsic to or aggravated by PD. Most of these problems are amenable to pharmacologic and nonpharmacologic treatments.CONCLUSIONHelping patients with PD cope with these difficulties is just as important as manipulating therapy to provide control of their motor symptoms.(THE NEUROLOGIST 6:18‐27, 2000)
ISSN:1074-7931
出版商:OVID
年代:2000
数据来源: OVID
|
5. |
POSITRON EMISSION TOMOGRAPHY AND SINGLE PHOTON EMISSION COMPUTED TOMOGRAPHY IMAGING IN ALZHEIMER'S DISEASE |
|
The Neurologist,
Volume 6,
Issue 1,
2000,
Page 28-43
Marc,
Preview
|
PDF (12517KB)
|
|
摘要:
BACKGROUNDPositron emission tomography (PET) and single photon emission computed tomography (SPECT) are imaging modalities that can be used for in vivo evaluation of brain function in health and in disease. This review focuses on research into the underlying neurobiology of Alzheimer's disease (AD) using these modalities between 1995 and 1998. By binding radioactive molecules to water, neurotransmitters, or products of intermediary metabolism and imaging the distribution of radioactivity within the brain, PET and SPECT images can provide information on neural/synaptic function, the status of neurotransmitter systems, or specific metabolic processes within the brain under controlled conditions.REVIEW SUMMARYPET studies during the review period evaluated a wide range of metabolic, neurotransmitter, and genetic abnormalities thought to be involved in the etiology and pathogenesis of AD and AD‐associated cognitive symptoms. Several large SPECT studies measured the sensitivity and specificity of imaging as part of the evaluation of dementia. Few studies evaluated management of AD.CONCLUSIONSRecent PET and SPECT research focused primarily on 1) identifying the important neuropathological processes underlying AD or AD symptoms in vivo and 2) finding a biological marker for preclinical diagnosis. This knowledge is essential for developing and testing novel therapies to enhance AD therapy.(THE NEUROLOGIST 6:28‐43, 2000)
ISSN:1074-7931
出版商:OVID
年代:2000
数据来源: OVID
|
6. |
TUBERCULOUS MENINGITIS AND NEUROCYSTICERCOSIS: CLINICAL, LABORATORY, AND RADIOLOGICAL FEATURES |
|
The Neurologist,
Volume 6,
Issue 1,
2000,
Page 44-57
John,
Pierpont Jose,
Laguna Joachim,
Preview
|
PDF (8692KB)
|
|
摘要:
BACKGROUNDThe important clinical, laboratory, and radiological features of tuberculous meningitis (TBM) and neu‐rocysticercosis are presented in this report through retrospective analysis, case reports, and review of the literature.REVIEW SUMMARYPatients with TBM most often present with fever, stiff neck, and headache. They may present with or without tuberculomas in the central nervous system. The best laboratory data for TBM includes a positive cerebrospinal fluid culture, a positive polymerase chain reaction, or a meningeal biopsy demonstratingMycobacterium tuberculosiswith a positive culture. On the other hand, neurocysticercosis usually presents with seizures, with <2% of the patients having fever. The most sensitive test for neurocysticercosis is a cerebrospinal fluid enzyme‐linked immunoelectrotransfer blot. The most consistent neuroimaging differences between tuberculomas and neurocysticercosis lesions are seen on T2‐weighted magnetic resonance imaging scans. Tuberculomas have hypointense centers (composed of macrophages, fibrosis, and lipids) and hyperintense borders, whereas active neurocysticercosis lesions most often have hyperintense centers (composed of clear or turbid fluid) and hypointense borders.CONCLUSIONSThis review will help neurologists recognize the important clinical, laboratory, and radiological aspects of tuberculous meningitis and neurocysticercosis. It is important to initiate therapy early for TBM based on the available clinical data. Both of these central nervous system infections can be difficult to diagnose, and a high clinical suspicion is necessary for early diagnosis.(THE NEUROLOGIST 6:44‐57, 2000)
ISSN:1074-7931
出版商:OVID
年代:2000
数据来源: OVID
|
7. |
MOST COMMONLY ASKED QUESTIONS ABOUT CAROTID ANGIOPLASTY AND STENTING |
|
The Neurologist,
Volume 6,
Issue 1,
2000,
Page 58-62
Christopher,
Preview
|
PDF (3352KB)
|
|
ISSN:1074-7931
出版商:OVID
年代:2000
数据来源: OVID
|
8. |
TESTING OF THE CEREBRAL VESSELS |
|
The Neurologist,
Volume 6,
Issue 1,
2000,
Page 63-64
Catherine,
Preview
|
PDF (1419KB)
|
|
ISSN:1074-7931
出版商:OVID
年代:2000
数据来源: OVID
|
9. |
List of Reviewers |
|
The Neurologist,
Volume 6,
Issue 1,
2000,
Page 65-65
&NA;,
Preview
|
PDF (319KB)
|
|
ISSN:1074-7931
出版商:OVID
年代:2000
数据来源: OVID
|
|