Neurological And Communicative Disorders And Stroke Research Articles

Electrophysiological study to detect serial changes and prognosis in patients of Guillain Barre syndrome from North-West Rajasthan, India

Background: The Guillain Barre syndrome (GBS) is the commonest cause of acute flaccid paralysis in much of the world, after the introduction of vaccine for poliomyelitis. Electrophysiological study may play an important role in further investigation of the pathogenesis and assessment of prognosis. This study was undertaken to see any changes in electrophysiological pattern at one month follow up and prognosis of patients with Guillain Barre syndrome. Methods: The study included 28 patients of Guillain Barre syndrome admitted between the period of July 2014 to June 2015 in the department of medicine and neurology, SP Medical College and AG Hospitals, Bikaner, India. The clinical diagnosis was based on criteria proposed by the national institute of neurological, and communicative disorders and stroke (NINCDS). Each patient was assessed both clinically (including disability score) and electrophysiologically at the time of presentation and at one month±seven days of follow up. Results: GBS was more common in early decades. Male to female ratio was 4.6:1. On electrophysiological study mixed pattern was most common (42.86%) followed by axonal (32.14%) and demyelinating (25%) patients. Mean disability score at the time of presentation was maximum for axonal pattern and the same group had minimum score at one month follow up indicating better recovery. Sequential electrophysiological changes were seen in this study. Axonal pattern had better recovery (77.78%) than demyelinating and mixed was worst with 16.67% mortality. Conclusions: Mixed pattern is predominant pattern on electrophysiological studies. Axonal pattern has better recovery. Secondary changes of electrophysiological finding in some of our cases suggest that primary demyelinating and mixed subtype could, be misinterpreted as primary axonal pathology without timely serial studies.

Imaging biomarkers for amyloid: a new generation of probes and what lies ahead

Since the original 1984 criteria for Alzheimer's disease (AD), put forth by a work group jointly established by the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) and the Alzheimer's Disease and Related Disorders Association (ADRDA) (McKhannet al., 1984), important advances have occurred in our ability to detect AD pathophysiology, with the incorporation of biomarkers – defined as anatomic, biochemical, or physiologic parameters that providein vivoevidence of AD neuropathology (Cummings, 2011) – that can improve the certainty of AD diagnosis. Use of imaging biomarkers such as positron emission tomography (PET) with amyloid ligands, particularly in asymptomatic and pre-dementia stages of AD, however, has been the subject of debate (Duboiset al., 2013), with arguments both for and against the biomarker driven diagnosis of AD.

Depressive, functional status, and neuropsychiatric symptom trajectories before an Alzheimer's disease diagnosis

Objectives: This short report relied on multiyear data from the National Alzheimer's Coordinating Center – Uniform Data Set (NACC-UDS) to examine whether significant changes occurred in functional status, neuropsychiatric symptoms, and depressive symptoms in the years before receiving an Alzheimer's disease (AD) diagnosis.Method: The secondary analysis used a retrospective cohort design. The NACC-UDS is a publicly accessible, longitudinal database that includes standardized data on neuropsychiatric symptoms, functional status, and depressive symptoms for Alzheimer's Disease Center (ADC) participants in the USA based on their annual visits from 2005 to 2011. ADC participants were considered diagnosed with AD if a follow-up data form indicated an affirmative response to whether the ADC participant had ‘probable AD (National Institute of Neurological and Communicative Disorders and Stroke (NINCDS)/Alzheimer's Disease and Related Disorders Association (ADRDA))’ or ‘possible AD (NINCDS/ADRDA).’ This yielded an analytic sample of 2478 individuals (139 with an eventual probable AD diagnosis, 109 individuals with an eventual possible AD diagnosis, and 2230 without any AD diagnosis) representing a total of 11,358 visits/points of data. Results: Multilevel linear models revealed significant decreases (p < 0.05) in functional status prior to a probable or possible AD diagnosis and significant increases in depressive symptoms prior to a probable AD diagnosis.Discussion: Changes in functional and depressive symptoms were partly independent of cognitive decline. The longitudinal results lend additional support to conceptual and empirical models of pre-diagnosis declines in AD.

Mortality in mechanically ventilated patients of Guillain Barré Syndrome

Background:The mortality of patients with Guillain Barré syndrome (GBS) has varied widely with rates between 1-18%. Death results from pneumonia, sepsis, adult respiratory distress syndrome (ARDS) and less frequently due to autonomic dysfunction or pulmonary embolism. There are only few studies which have used a large sample and have in detail analyzed the circumstances relating to death and the prognostic factors for the same in a cohort, including only mechanically ventilated patients.Objective:The objective of our study was to analyze the circumstances and factors related to mortality in mechanically ventilated patients of GBS.Materials and Methods:Case records of patients of GBS, satisfying National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria, and requiring mechanical ventilation from 1984 to 2007, were analyzed.Results:A total of 273 GBS patients were managed with ventilatory support (190 men and 83 women) during the period. Besides symmetrical paralysis in all patients, bulbar palsy was present in 186 (68.1%), sensory involvement in 88 (32.2%) and symptomatic autonomic dysfunction in 72 (26.4%) patients. The mortality was 12.1%. The factors determining mortality were elderly age group (P=0.03), autonomic dysfunction (P=0.03), pulmonary complications (P=0.001), hypokalemia (P=0.001) and bleeding (P=0.001) from any site. Logistic regression analysis showed the risk of mortality was 4.69 times more when pneumonia was present, 2.44 times more when hypokalemia was present, and 3.14 times more when dysautonomia was present. The odds ratio for age was 0.97 indicating that a higher age was associated with a higher risk of mortality.Conclusions:Ventilator associated pulmonary complications, bleeding and hypokalemia especially in elderly patients require optimal surveillance and aggressive therapy at the earliest for reducing the mortality in this group of GBS patients.

Prognosis of patients with Guillain-Barré syndrome requiring mechanical ventilation

Severe Guillain-Barré syndrome (GBS) is associated with significant morbidity and also mortality. Identification of modifiable risk factors may help in reducing the morbidity and mortality. To study the prognostic factors in a selected cohort of mechanically ventilated GBS patients. Case records of GBS patients requiring mechanical ventilation admitted between 1997 and 2007 were analyzed. All patients satisfied the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria for GBS. Primary outcome parameters included mortality and GBS disability (Hughes) scale score at discharge. During the study period, 173 (118 men and 55 women; mean age of 33.5 ± 21 years) GBS patients were mechanically ventilated. A history of antecedent events was present in 83 (48%) patients. In addition to motor weakness, In all facial palsy was present in 106 (61%), bulbar palsy in 91 (53%), sensory involvement in 74 (43%), and symptomatic autonomic dysfunction in 27 (16%). The overall mortality was 10.4%. On univariate analysis the risk factors for mortality included elderly age (P = 0.014), autonomic dysfunction (P = 0.002), pulmonary complications (P = 0.011), hypokalemia (P = 0.011), and bleeding (P = 0.026). All these factors were significant in multivariate analysis except for bleeding from any site and hypokalemia. In univariate analysis factors associated with Hughes scale score ≤ 3 at discharge included younger age (P = 0.02), presence of bulbar symptoms (P = 0.03) and less severe weakness at admission (P = 0.02), slower evolution of disease over more than 3 days (P = 0.01), electrodiagnostic evidence of demyelinating neuropathy (P = 0.00), and absence of sepsis (P = 0.01), hyperkalemia (P = 0.0001), and anemia (P = 0.02). In multivariate analysis age was the only significant factor. Early identification of modifiable risk factors, such as pulmonary involvement, autonomic dysfunction, hypokalemia, sepsis, bleeding, and nutritional complications, may reduce the mortality and morbidity associated with GBS.

Temporal profile of pain and other sensory manifestations in Guillain-Barre′ syndrome during ten days of hospitalization

Focused studies on sensory manifestations, especially pain and paresthesia in Guillain-Barre' (GB) syndrome are few and far between. To study the sensory manifestations in GB syndrome during 10 days of hospitalization with clinico-electrophysiological correlation. The study included 60 non-consecutive patients with GB syndrome, fulfilling National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria for GB syndrome. Data especially related to clinical and electrophysiological evidence of sensory involvement were analyzed. Pain was assessed using a) visual analogue paraesthesias (Vapar), b) visual analogue for pain (Vap) and c) verbal rating scale for pain (Verp). Sensory symptoms were widely prevalent: paraesthesia in 45 (75%) patients and pain in 30 (50%) patients. Impairment of different sensory modalities included: pain in 8 (13.3%), joint position sense in 14 (23.3%), and vibration in 11 (18.3%). Electrophysiological evidence of abnormal sensory nerve conduction was noted in 35 (58.3%) patients. Pain assessment using Vapar, Vap and Verp for from Day 1 to Day 10 of hospitalization revealed that from Day 7 onwards the degree and frequency of sensory symptoms and signs decreased. On comparing various clinico-electrophysiological parameters among patients of GB syndrome with and without pain and paresthesia. Presence of respiratory distress correlated with pain and paresthesia (P=0.02). Sensory manifestations in GB syndrome are often under-recognized and under-emphasized. This study analyzed the evolution and the profile of pain and paresthesia in GB syndrome during hospitalization. Knowledge, especially about evolution of pain and paresthesia during hospitalization might improve understanding and patient care.

ChemInform Abstract: Synthesis and Anticonvulsant Activity of Imidooxy Derivatives.

Previous results of anticonvulsant activity in several imidooxy carboxylates related to (aminooxy)acetic acid in young chicks, prompted an in-depth reinvestigation of these analogues in mice. A series of 22 succinimidooxy, phthalimidooxy, and naphthalimidooxy carboxylates were synthesized and evaluated for anticonvulsant activity by the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS). Methyl (succinimidooxy)acetate (2d), ethyl (succinimidooxy)acetate (2e), methyl (phthalimidooxy)acetate (3d), ethyl (phthalimidooxy)acetate (3e), and ethyl 2-(phthalimidooxy)propionate (3g), which were initially found to be active as anticonvulsants in young chicks were uniformly inactive in the Phase I seizure tests involving maximal electroshock (MES), pentylenetetrazol (scMet), or neurologic toxicity toxicity (Tox). Several newer analogues, ethyl (succinimidooxy)formate (2c) and methyl 3-(phthalimidooxy)-2-methylacrylate (4h) were found to be active in the scMet (3a) or both (4h) evaluations. Most interesting was the anticonvulsant results of N-(benzyloxy)-2-azaspiro[4,4] nonane-1,3-dione (5b), which displayed anti-MES activity and a protective index (TD50/ED50) of greater than 4.5.

The Relationship Between Inflammatory Markers and Post Stroke Cognitive Impairment

To determine whether there is a relationship between inflammatory markers (serum C-reactive protein (CRP) and cytokines) and post stroke cognitive impairment (PSCI). This was a cross-sectional observational study. Patients were recruited from 4 sources: (1) the acute stroke unit of a general hospital, (2) an outpatient stroke prevention clinic, (3) a stroke rehabilitation unit in a specialized geriatric hospital, or (4) a stroke rehabilitation unit of a rehabilitation hospital. Patients meeting National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) and World Health Organization Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (WHO-MONICA) project criteria for stroke were invited to participate in this study within the first 5 to 31 days post stroke. Patients with subarachnoid or intracranial hemorrhage, decreased level of consciousness, severe aphasia or dysarthria, or a significant acute medical, neurological, or psychiatric illness were excluded. Clinical assessments included the Mini-Mental State Examination (MMSE) for cognition, the National Institutes of Health Stroke Scale (NIHSS) for stroke severity, and the Center for Epidemiological Studies-Depression Scale (CES-D) for depressive symptoms. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum concentrations of CRP, interleukin 6 (IL-6), and interferon gamma (IFN-gamma). A total of 48 patients with ischemic stroke (age [mean +/- SD] 71.6 +/- 13.2 years, 54.2% male, MMSE 26.4 +/- 3.8, NIHSS 6.8 +/- 4.0) were recruited within their first month post stroke. Backward stepwise elimination linear regression showed that higher concentrations of serum CRP (beta(CRP) = -0.46, p( CRP) = 0.002) predicted lower post stroke global cognition ([MMSE], F1,44 = 11.31, P = .002), with age (P = .92), level of education (P = .22), infarct side (P = 0.49), IL-6 (P = 0.36), and IFN-gamma (P = .57) removed from the final model. A post stroke inflammatory response may be important in subacute, PSCI.

Guillain-Barré syndrome in south-west Stockholm, 1973-1991, 1. Quality of registered hospital diagnoses and incidence.

We describe the incidence and explore the quality of registered diagnosis for Guillain-Barré syndrome (GBS) in a population-based retrospective study in South-West Stockholm (SWS), Sweden, during the period 1973-1991. We used data on registered hospital discharges and open-care visits, and from medical records. Medical records were available for 83 (80.6%) of 103 patients with registered GBS diagnosis at discharge from hospitals. For 69 (83.1%) of such patients, the information from the hospital record fulfilled the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) clinical criteria for GBS. One out-patient presented with suspected GBS. In contrast, none of 40 patients discharged with diagnosis of unspecific polyneuropathy fulfilled the above mentioned criteria. During the period 1973-1991, the mean annual incidence of GBS per 100,000 was 1.74, 95% CI 1.41-2.12, from register data and 1.49, 95% CI 1.19-1.85, after excluding those not fulfilling criteria for GBS. The age-adjusted incidence after validation was higher for men, 1.64, 95% CI 1.19-2.21, than for women, 1.46, 95% CI 1.05-1.99. An increasing incidence with age was found, presenting the age-specific curve a bimodal shape. The results of this study confirm that hospital discharge diagnostic data in Sweden can be used for purposes of epidemiological research and surveillance for GBS, and show that the incidence of GBS in SWS compares to those described in other populations.

Aortic Atherosclerotic Disease and Stroke

In the 1940s, most strokes were attributed to cerebral vasospasm, a mechanism that is not given a great deal of credence today. It was not until the early 1950s that Harvard neurologist C. Miller Fisher1 stressed the importance of carotid artery atherosclerosis as a major cause of cerebral infarction. Later that decade, the importance of atrial fibrillation as a cause of cerebral embolism began to be stressed,2 and the presence of a left atrial thrombus was first seen on angiocardiography in 1965.3 Despite the established importance of these 2 causes of stroke, carotid disease and atrial fibrillation, nearly half of strokes were listed as “of undetermined cause” in a large stroke registry as recently as 1989.4 In this series, 40% of 1273 cerebral infarctions in the Stroke Databank of the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) were thought to be cryptogenic (from the Latin crypticus , meaning secret or mysterious). The clinical syndrome in those patients, as well as the angiographic and computed tomographic (CT) findings, could be reclassified as embolic; however, because no source of embolus could be identified, the authors kept these strokes in the undetermined cause category. In 1990, a third leading cause of embolic stroke was identified on transesophageal echocardiography (TEE), namely severe atherosclerotic plaques in the aortic arch.5 The 3 patients described in that initial report were a 68-year-old woman with dysarthria and an embolus to the foot, a 77-year-old woman with a cerebellar infarction after cardiac catheterization, and a 70-year-old man with staggering, diplopia, and a visual field cut. All 3 had severe plaque in the aortic arch on TEE. In addition, freely mobile projections were seen superimposed on the plaques, making it seem likely that these findings were the reason for the patients’ embolic …

Incidence and clinical features of acute inflammatory polyradiculoneuropathy in Lombardy, Italy, 1996.

To assess the annual incidence of typical Guillain-Barré syndrome (GBS) and its main variants (atypical GBS) in a well-defined population from a large area. A population-based prospective survey of GBS was undertaken during the calendar year 1996 in Lombardy, Italy (population 8,891,652). Typical and atypical GBS was diagnosed using the National Institutes of Neurological and Communicative Disorders and Stroke (NINCDS) and Ropper criteria. Eligible cases were hospital inpatients traced through a regional registry, the hospital discharge diagnoses, and an ongoing case-control study. Diagnostic and demographic findings were collected for each case. Complete clinical and laboratory features were available for 80% of cases. A total of 138 patients (males 74; females 64) aged 2-91 years fulfilled the diagnostic criteria for typical GBS (128) or atypical GBS (10). GBS variants included Miller-Fisher syndrome (four cases), cranial polyneuritis (three cases), pure motor GBS (two cases), and sensory loss with areflexia (one case). The crude annual incidence of GBS was 1.55 per 100,000 (typical GBS 1.43; atypical GBS 0.11; male 1.67; female 1.43; age <35 years, 0.79; 35-54 years, 1.33; 55-74 years, 3.22; 75+ years, 4.67). The overall rate was 1.58 when age- and sex-adjusted to the 1996 Italian population. Previous infections were reported for 37% of patients. The electrophysiological findings indicated demyelination in 51%, primary axonopathy in 14%, and mixed myelin and axon involvement in 27%. The incidence of typical GBS is comparable with that in other reports using the NINCDS diagnostic criteria. Atypical GBS accounts for a limited number of cases.

Defining dementia: clinical criteria for the diagnosis of vascular dementia

The recognition of cerebrovascular disease (CVD) as a contributing factor and a cause of dementia has led to the development of clinical criteria for vascular dementia (VaD). Due to high specificity, the consensus criteria developed by the National Institute for Neurological and Communicative Disorders and Stroke (NINDS)-Association Internationale pour la Recherche et l'Enseignement en Neurosciences (AIREN) have been used in controlled clinical trials to select patients with pure VaD. VaD is predominantly a subcortical frontal form of dementia with prominent executive dysfunction. In contrast, the criteria of the NINCDS-Alzheimer's Disease and Related Disorders Association (ADRDA) emphasize memory loss as the main feature to distinguish Alzheimer's disease (AD) from VaD and from other forms of dementia. Moreover, CVD may precipitate the clinical expression of AD. Although no criteria have been created specifically for patients having AD with CVD, the ischemic score, the Informant Questionnaire on Cognitive Decline in the Elderly and a history of prestroke mild cognitive impairment (MCI) may be useful for identifying patients with this mixed form of dementia.

Serial brain MRI at 3-6 month intervals as a surrogate marker for Alzheimer's disease.

A surrogate marker is needed for Alzheimer's disease (AD) both to aid diagnosis and to assess interventions. Despite widespread use, brain imaging markers have largely been confounded by overlap with "normal" ageing. 39 elderly subjects completed up to four serial volumetric brain MRI scans with intervals from 2.5 months to 7 months. By National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria, five subjects had probable AD, two possible AD and 32 were negative for AD, although this group included memory-impaired subjects. Total brain and ventricular volumes were measured for each scan, and rates of change for each interval calculated. The rate of change in ventricle-to-brain ratio was 15.6% per year (standard deviation (SD) 2.8%) for probable AD compared with 4.3% per year (SD 1.1%) for negative AD (p<0.001). There was no significant difference between these groups' mean ventricle-to-brain ratios measured at a single time point (p=0.25). Rates of change in brain or ventricular volume over time also differed between the two groups (p<0.001). Power calculations reveal that to detect a 20% reduction in the excess rate of atrophy of a probable AD cohort in just 6 months, with 90% power, 135 subjects would be required in each arm of a randomized placebo controlled trial. For a 30% reduction in the excess rate of atrophy, 61 subjects would be required. Rate of change analysis makes serial brain MRI a valuable surrogate marker for Alzheimer's disease. Since only 6 months or less is required between scans, this procedure has both clinical relevance and potential for monitoring interventions.

Elevation of β-Amyloid Peptide 2–42 in Sporadic and Familial Alzheimer's Disease and Its Generation in PS1 Knockout Cells

Urea-based beta-amyloid (Abeta) SDS-polyacrylamide gel electrophoresis and immunoblots were used to analyze the generation of Abeta peptides in conditioned medium from primary mouse neurons and a neuroglioma cell line, as well as in human cerebrospinal fluid. A comparable and highly conserved pattern of Abeta peptides, namely, 1-40/42 and carboxyl-terminal-truncated 1-37, 1-38, and 1-39, was found. Besides Abeta1-42, we also observed a consistent elevation of amino-terminal-truncated Abeta2-42 in a detergent-soluble pool in brains of subjects with Alzheimer's disease. Abeta2-42 was also specifically elevated in cerebrospinal fluid samples of Alzheimer's disease patients. To decipher the contribution of potential different gamma-secretases (presenilins (PSs)) in generating the amino-terminal- and carboxyl-terminal-truncated Abeta peptides, we overexpressed beta-amyloid precursor protein (APP)-trafficking mutants in PS1+/+ and PS1-/- neurons. As compared with APP-WT (primary neurons from control or PS1-deficient mice infected with Semliki Forest virus), PS1-/- neurons and PS1+/+ neurons overexpressing APP-Deltact (a slow-internalizing mutant) show a decrease of all secreted Abeta peptide species, as expected, because this mutant is processed mainly by alpha-secretase. This drop is even more pronounced for the APP-KK construct (APP mutant carrying an endoplasmic reticulum retention motif). Surprisingly, Abeta2-42 is significantly less affected in PS1-/- neurons and in neurons transfected with the endocytosis-deficient APP-Deltact construct. Our data confirm that PS1 is closely involved in the production of Abeta1-40/42 and the carboxyl-terminal-truncated Abeta1-37, Abeta1-38, and Abeta1-39, but the amino-terminal-truncated and carboxyl-terminal-elongated Abeta2-42 seems to be less affected by PS1 deficiency. Moreover, our results indicate that the latter Abeta peptide species could be generated by a beta(Asp/Ala)-secretase activity.

Synthesis and anticonvulsant activity of imidooxy derivatives

Previous results of anticonvulsant activity in several imidooxy carboxylates related to (aminooxy)acetic acid in young chicks, prompted an in-depth reinvestigation of these analogues in mice. A series of 22 succinimidooxy, phthalimidooxy, and naphthalimidooxy carboxylates were synthesized and evaluated for anticonvulsant activity by the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS). Methyl (succinimidooxy)acetate (2d), ethyl (succinimidooxy)acetate (2e), methyl (phthalimidooxy)acetate (3d), ethyl (phthalimidooxy)acetate (3e), and ethyl 2-(phthalimidooxy)propionate (3g), which were initially found to be active as anticonvulsants in young chicks were uniformly inactive in the Phase I seizure tests involving maximal electroshock (MES), pentylenetetrazol (scMet), or neurologic toxicity toxicity (Tox). Several newer analogues, ethyl (succinimidooxy)formate (2c) and methyl 3-(phthalimidooxy)-2-methylacrylate (4h) were found to be active in the scMet (3a) or both (4h) evaluations. Most interesting was the anticonvulsant results of N-(benzyloxy)-2-azaspiro[4,4] nonane-1,3-dione (5b), which displayed anti-MES activity and a protective index (TD50/ED50) of greater than 4.5.

Interrater reliability of Alzheimer's disease diagnosis

To determine interrater reliability of dementia diagnosis, 4 physicians experienced in the evaluation of dementia patients applied 3 sets of diagnostic criteria to each of 62 patients, based on a standardized set of medical record information. All patients had undergone similar examinations and follow-up to establish the initial clinical diagnosis (76% had autopsy). Raters were blind to the diagnosis and to follow-up information after the initial evaluation period. This paper presents interrater agreement (kappa values) for a diagnosis of Alzheimer's disease using the American Psychiatric Association diagnostic criteria from the Diagnostic and Statistical Manual (DSM-III), the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria for the clinical diagnosis of Alzheimer's disease, and the Eisdorfer and Cohen Research Diagnostic Criteria (ECRDC) for primary neuronal degeneration. The NINCDS showed somewhat higher average interrater reliability (kappa = 0.64) than the DSM-III (kappa = 0.55) and considerably higher interrater reliability than the ECRDC (kappa = 0.37). One rater displayed conspicuously lower levels of interrater reliability than the other 3, especially in DSM-III and ECRDC. This study indicates that interrater reliability of DSM-III and NINCDS criteria are comparable. Documentation of interrater reliability and, if necessary, training to improve reliability is an important consideration in research where different observers are diagnosing dementing illnesses.

Guillain-Barré syndrome: diagnostic criteria, epidemiology, clinical course and prognosis.

Thirty-four patients were identified with Guillain-Barré syndrome (GBS) on review of 266 neuropathy cases admitted to a Copenhagen county hospital from June 1977 to January 1984. The age-adjusted incidence rate of GBS is 2.0 x 10(-5) years-1. The natural history of the disease, antecedent events, symptoms and signs, autonomic dysfunction, sequelae, CSF findings and mortality are described. Six cancer patients with GBS differed significantly from the non-cancer patients in a more protracted disease course and failure to improve. The National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria for the diagnosis of GBS are discussed, and it is concluded that the criteria, although useful in comparative studies, are too restrictive when used in clinical practice.

The Neurological Information Network.

The Neurological Information Network (NIN) of the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) was a loosely structured assemblage of a variety of information-transfer activities that existed for approximately 20 years, starting in the early 1960s. These activities included the Neurosciences Research Program at the Massachusetts Institute of Technology, the Parkinson's Disease Information Center at Columbia University, the Brain Information Service at UCLA, the Information Center for Hearing, Speech, and Disorders of Human Communication at the Johns Hopkins Medical Institutions, the Clinical Neurology Information Center at the University of Nebraska, the Cerebrovascular Disease Abstracts generated at the Mayo Foundation and appearing in the journal Stroke, and Epilepsy Abstracts published by Excerpta Medica. The article discusses primarily the sociopolitical factors that govern the creation and life of activities of the type enumerated.

Criteria for the clinical diagnosis of Alzheimer's disease. Excerpts from the NINCDS-ADRDA Work Group report.

A Work Group on the Diagnosis of Alzheimer's Disease was established by the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) and the Alzheimer's Disease and Related Disorders Association (ADRDA).The need for this report was suggested by the National Advisory Council of the NINCDS. The report has been reviewed by workshop participants, representatives of the National Advisory Neurological and Communicative Disorders and Stroke Council, representatives of the ADRDA, and designated reviewers representing professional societies concerned with the diagnosis of Alzheimer's disease. Based on a consensus of the participants, criteria were developed to serve as a clinical basis for diagnosis. These criteria should be useful also for comparative studies of the patients in different kinds of investigations, including case control studies, therapeutic trials, evaluation of new diagnostic laboratory tests, and clinicopathologic correlations. The criteria are not yet fully operational because of insufficient knowledge about the disease. The criteria are compatible with definitions in the current Diagnostic and Statistical Manual of Mental Disorders (DSM III) and in the International Classification of Diseases.The following excerpts from the NINCDS‐ADRDA Work Group report are reproduced with permission for the interest of our readership. An accompanying editorial in this issue (page 1) comments further on the value of these criteria.—Editor

NINCDS faces 'exploding' field of neuroscience

It started with Plato, or perhaps even earlier. And, ever since, philosophers have discussed who are, how think, how remember, and most important, what the organ that permits all this really is. Until about 15 years ago, says Murray Goldstein, DO, MPH, director of the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS), these indeed were fundamentally philosophical questions. Today, many of these questions are still unanswered. But, says Goldstein, we have the tools in neuroscience by which can begin to dissect [them] into researchable problems. He says—and the growing number of publications seem to attest—that this area has captured the attention of the scientific community, both new and established, and is expanding on all frontiers. With the proliferation of research discoveries about speech, language, hearing, and the functions and dysfunctions of the brain and other parts of the nervous system, it's extraordinarily difficult