American Academy Of Neurology Criteria Research Articles

Epidemiologic variability of chronic inflammatory demyelinating polyneuropathy with different diagnostic criteria: Study of a UK population

Epidemiologic data on chronic inflammatory demyelinating polyneuropathy (CIDP) is limited, and previous studies have shown variable results. The frequencies of CIDP subtypes remain unknown. Variations due to use of different diagnostic criteria have not been studied. We examined the prevalence and incidence of CIDP in Leicestershire and Rutland, UK (population 963,600). Prevalence day was 1 May 2008. The prevalence of CIDP fulfilling the 2006 clinical and electrophysiologic European Federation of Neurological Societies/Peripheral Nerve Society (EFNS/PNS) criteria was 4.77 per 100,000 (95% confidence interval [CI] 3.49-6.37). Using the 1991 American Academy of Neurology (AAN) criteria, the prevalence was 1.97 per 100,000 in this population (95% CI 1.19-3.08). Lewis-Sumner syndrome was diagnosed in 15.2% of patients, and 23.9% had pure sensory onset. Over 40% required no immunotherapy, and 84.6% of those treated responded. More than 80% of the AAN criteria-negative but EFNS/PNS criteria-positive patients were responsive to treatment. Both sets of criteria were equally likely to identify patients who required therapy. The mean annual incidence rate over the 3 years preceding the prevalence day was 0.70 per 100,000/year using EFNS/PNS criteria (95% CI 0.43-1.08), and 0.35 per 100,000/year using AAN criteria (95% CI 0.17-0.64). We conclude that the AAN criteria may underestimate prevalence and incidence of the disease. The EFNS/PNS criteria provide higher diagnostic sensitivity and are of greater clinical relevance, and they also offer a useful breakdown of the epidemiologic data for CIDP subtypes.

Detecting HIV Associated Neurocognitive Disorders in Adolescents: What Is the Best Screening Tool?

PurposeTo examine the ability of the HIV-Dementia Scale (HDS) and Mini Mental State Exam (MMSE) to detect encephalopathy in adolescents living with human immunodeficiency virus (HIV) and/or acquired immunodeficency syndrome (AIDS). MethodThe study was based on chart review (N = 71) from 1999 to 2006, extracting data from psychological testing, disease classification, and demographic variables. HDS and MMSE scores were independent. Diagnosis of encephalopathy used American Academy of Neurology Criteria. Receiver Operating Characteristic Curves were plotted. ResultsSix patients had encephalopathy. The HDS identified five of these cases (83% sensitivity, 76% specificity). The MMSE identified three cases (50% sensitivity, 92% specificity). ConclusionBased on the study results, the HDS appears to be clinically useful.

Supplementary tests for confirmation of brain death

In 1959, the concept of brain death (BD) or irreversible coma was described by Mollaret and Goulon (1959). The first guideline (the Harvard criteria) for deciding BD was established in 1968 (Ad Hoc Committee of the Harvard Medical School, 1968). This concept has been accepted worldwide although its fundamental meaning is not exactly globally uniform yet. Some countries (e.g., the US) view BD as “whole brain death”, while others (e.g., the UK) as brain-stem death. The guidelines for the diagnosis of BD also differ among countries, even among hospitals in the same country. The American Academy of Neurology (AAN) published its guidelines in 1995 (The Quality Standards Subcommittee of the American Academy of Neurology, 1995). This dilemma about the “real” death of physiological or physical basis among the leading neurological hospitals is debating (Greer et al., 2008). Surprisingly, adherence to AAN guidelines is variable among those top hospitals. The role of confirmatory tests differs among countries too. In some countries (e.g., France and the Netherlands), the confirmatory tests are mandatory, while in others (e.g., the US and the UK) they are facultative (Haupt and Rudolf, 1999). According to the AAN guidelines, the confirmatory tests are only required when specific components of the clinical testing cannot be reliably evaluated. Electroencephalography (EEG), evoked potentials (EP), cerebral angiography, transcranial Doppler (TCD), magnetic resonance angiography (MRA), computed tomographic angiography (CTA), and single photon emission computed tomographic (SPECT) brain scintigraphy are the most common confirmatory tests, but none of them is “ideal” for the diagnosis of BD. The EEG, EP, and TCD can be performed at bedside. They are non-invasive, not time-consuming, and easy to carry out. The limitations of them are listed in this article, and the combination for more accurate diagnosis seems promising (The Quality Standards Subcommittee of the American Academy of Neurology, 1995). As the clinical diagnosis of BD is made, more neurons die over time physiologically. It is reasonable that the sensitivity increases over time in the second examination. However, it is hard to decide which combination is the best without multiple comparisons, confidence interval or inter-quintile range (IQR) in those non-parametrical groups. The sensitivity of TCD to confirm BD varied among studies. In AAN guidelines, the sensitivity and specificity is 91% and 100%, respectively (Sloan et al., 2004). In Cuba, using TCD to confirm the BD is allowed by law. By exclusion of specific conditions (e.g., large craniotomy, external ventricular drains), TCD is sensitive and the receiver operating characteristic (ROC) is reliable in our results (Kuo et al., 2006). The time-lag between clinical BD and performing TCD is a key to increase the sensitivity, so are EEG and short latency somatosensory evoked potentials (SLSEP). It is difficult to decide which combination is more simply by a P value without more information (Luo et al., 2008). The timing of each test, the younger age, and the sample size may affect the outcome. If EEG, TCD, and SLSEP are carried out in sequence, the sensitivity may be different by the “time-lag” period. In general, more studies are still needed to verify which combination of confirmatory test is the best in the future. Some physicians view BD as a particular condition in which life support should be legitimately forgone and organs could be retrieved from consenting patients (Zamperetti et al., 2004). In a recent neuropathologic study (Wijdicks and Pfeifer, 2008), 41 patients who fulfilled AAN criteria of BD were examined, but no distinctive neuropathologic features were seen. According to this study, neuronal loss was widespread in the brain, but total brain necrosis (called “respirator brain”) was not observed. In order to make accurate diagnosis and facilitate legal organ donation, we hope world neurologists to draw up new global evidence-based consensus including specific recommendations to avoid too many tests for the confirmation of BD.

Assessment: Botulinum neurotoxin for the treatment of movement disorders (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology.

To perform an evidence-based review of the safety and efficacy of botulinum neurotoxin (BoNT) in the treatment of movement disorders. A literature search was performed including MEDLINE and Current Contents for therapeutic articles relevant to BoNT and selected movement disorders. Authors reviewed, abstracted, and classified articles based on American Academy of Neurology criteria (Class I-IV). The highest quality literature available for the respective indications was as follows: blepharospasm (two Class II studies); hemifacial spasm (one Class II and one Class III study); cervical dystonia (seven Class I studies); focal upper extremity dystonia (one Class I and three Class II studies); focal lower extremity dystonia (one Class II study); laryngeal dystonia (one Class I study); motor tics (one Class II study); and upper extremity essential tremor (two Class II studies). Botulinum neurotoxin should be offered as a treatment option for the treatment of cervical dystonia (Level A), may be offered for blepharospasm, focal upper extremity dystonia, adductor laryngeal dystonia, and upper extremity essential tremor (Level B), and may be considered for hemifacial spasm, focal lower limb dystonia, and motor tics (Level C). While clinicians' practice may suggest stronger recommendations in some of these indications, evidence-based conclusions are limited by the availability of data.

Assessment: Botulinum neurotoxin for the treatment of spasticity (an evidence-based review): [RETIRED

To perform an evidence-based review of the safety and efficacy of botulinum neurotoxin (BoNT) in the treatment of adult and childhood spasticity. A literature search was performed including MEDLINE and Current Contents for therapeutic articles relevant to BoNT and spasticity. Authors reviewed, abstracted, and classified articles based on American Academy of Neurology criteria (Class I-IV). The highest quality literature available for the respective indications was as follows: adult spasticity (14 Class I studies); spastic equinus and adductor spasticity in pediatric cerebral palsy (six Class I studies). Botulinum neurotoxin should be offered as a treatment option for the treatment of spasticity in adults and children (Level A).

Diferencias del patrón electrofisiológico en las variantes de presentación de la polineuropatía desmielinizante inflamatoria crónica

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a mixed (predominantly motor) neuropathy, with an autoimmune aetiology and different forms of clinical presentation including the idiopathic form and one related to concurrent diseases. Neurophysiological studies play a decisive role in its diagnosis.To evaluate the differences in the electrophysiological patterns in the two forms of presentation of the disease, based on the variables that were analysed by studying nerve conduction and the F wave.The study involved 27 patients with a diagnosis of probable CIDP, according to American Academy of Neurology criteria from 1991. Of all the patients included in the study group, 17 presented primary CIDP and in 10 cases it was related to other diseases, such as diabetes mellitus, adenocarcinoma, multiple sclerosis and human immunodeficiency virus infection. Motor and sensory nerve conduction studies were performed, as well as F wave studies of the nerves in the four limbs. Statistical methods were applied to compare the neurophysiological variables in the two groups of patients.Significant differences were found to exist between the two groups. The sensory study was more affected in patients with primary CIDP, whereas the motor and F wave study were affected to a greater extent in patients with secondary CIDP; these cases displayed a predominantly axonomyelinic pattern, with greater involvement of the proximal motor segment.The different variant forms of presentation of CIDP display distinct electrophysiological behaviours.

Botulinum Neurotoxin for Spasticity

This evidence-based review is a report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology (AAN). Using the AAN criteria for the classification of evidence, the authors reviewed the literature on “the safety and efficacy of botulinum neurotoxin (BoNT) in the treatment of adult and childhood spasticity.” For the treatment of spasticity in adults, they found 14 Class I trials (11 for upper- and 3 for lower-extremity spasticity), most of which showed that BoNT reduced …

The value of sensory electrophysiology in chronic inflammatory demyelinating polyneuropathy

Objective The purpose of this study was to evaluate the usefulness of sensory nerve conduction studies in comparison and in combination with motor conductions in diagnosing chronic inflammatory demyelinating polyneuropathy (CIDP). Methods We retrospectively compared the electrophysiology of 20 patients with CIDP to that of 20 controls with axonal polyneuropathy, and 20 controls with myopathy. Five sensory abnormality patterns were evaluated. Results The “abnormal radial normal sural” (“ARNS”) pattern showed a sensitivity of 25% for CIDP and specificity of 100% versus axonal neuropathies ( p = 0.047). The “abnormal sural normal radial” (“ASNR”) pattern had a sensitivity of 75% for axonal neuropathy with a specificity of 80% versus CIDP ( p = 0.0012). Presence of ARNS or absence of ASNR patterns showed equivalent or superior sensitivity and specificity to most individual motor demyelinating defects for CIDP. Presence of ARNS or absence of ASNR patterns, integrated within three different sets of electrodiagnostic criteria for CIDP, increased sensitivity in all without significantly altering specificity. Effects were most remarkable with the American Academy of Neurology criteria (1991), which showed significantly improved sensitivity (50–85%; p = 0.041), with preserved specificity of 100%. Conclusions The use of sensory abnormality patterns appears justified in comparison and combination with motor defects in diagnosing CIDP. Significance Sensory studies may be useful in contributing to the electrodiagnosis of CIDP and their inclusion in existing electrodiagnostic criteria deserves consideration.

Classifications and treatment responses in chronic immune-mediated demyelinating polyneuropathy

Chronic immune-mediated demyelinating polyneuropathy (CIP) represents a heterogeneous pool of motor, sensory, sensorimotor, symmetric, or asymmetric syndromes. To evaluate published diagnostic classifications and characterize predictors of treatment response. One hundred two of 158 patients with a working diagnosis of CIP were included and clinically characterized because they had electrophysiologic and/or histologic evidence of demyelination. The biostatistical profile of patients with symmetric clinical manifestation was analyzed using three proposed classifications (American Academy of Neurology [AAN] criteria, modified AAN criteria, European Federation of Neurological Societies/Peripheral Nerve Society [EFNS/PNS] criteria). Treatment responses to IV immunoglobulins (IVIg) and their positive predictors were investigated. Sensitivities (0.52 [AAN] vs 0.83 [modified AAN] vs 0.95 [EFNS/PNS]) and negative predictive values (0.68 vs 0.85 vs 0.92) differed markedly, whereas specificities (0.94 vs 0.90 vs 0.96) and positive predictive values (0.89 vs 0.89 vs 0.97) were similar. In CIP patients treated with IVIg, a positive response was found in 62 of 76 (82%). Patients with a monophasic or relapsing-remitting course or a more than twofold CSF protein increase had the highest probability to respond to IVIg, most evident when using the modified AAN criteria. The European Federation of Neurological Societies/Peripheral Nerve Society criteria for chronic inflammatory demyelinating polyneuropathy improve treatment of patients with chronic immune-mediated demyelinating polyneuropathy, particularly with respect to diagnostic issues. To predict IV immunoglobulin treatment response, the modified American Academy of Neurology criteria are the most valuable classification provided an increased CSF protein level.

Neuropathologic confirmation of definitional criteria for human immunodeficiency virus–associated neurocognitive disorders

Research findings have suggested a need for modifications to the original nomenclature for human immunodeficiency virus (HIV)-associated neurocognitive disorders issued in 1991 by the American Academy of Neurology (AAN). The HIV Neurobehavioral Research Center (HNRC) proposed a diagnostic scheme that departs from the AAN 1991 criteria primarily in the inclusion of an asymptomatic neurocognitive impairment (ANI) category that relies on cognitive disturbances as a necessary criterion for diagnosis, without requiring declines in daily functioning, motor, or other behavioral abnormalities. In order to test the predictive validity of these two nomenclatures, the authors compared the correspondence between antemortem neurocognitive diagnoses resulting from AAN and HNRC criteria to a neuropathological diagnosis of HIV encephalitis (HIVE) made at autopsy. Agreement between the two sets of definitional criteria was 79% regarding the classification of cases as either neurocognitively normal or impaired, and 54% with regard to specific neurocognitive diagnoses. When pathological evidence of HIVE was considered as the external indicator of HIV-related brain involvement, 64% of cases were correctly classified by AAN criteria, compared to 72% by HNRC criteria. HNRC criteria had better positive predictive power (95% versus 88%), sensitivity (67% versus 56%), and specificity (92% versus 83%). Three cases with HIVE and were correctly identified by HNRC criteria for ANI but called normal by AAN criteria, supporting inclusion of an asymptomatic neurocognitive condition. The modifications to the AAN 1991 criteria proposed by the HNRC and others in the field have served as a point of departure for a recently revised consensus nomenclature.

Associations of cigarette smoking with viral immune and cognitive function in human immunodeficiency virus–seropositive women

Cigarette smoking alters the immune system and may improve cognitive deficits in neuropsychiatric disorders. Smoking prevalence is high in human immunodeficiency virus (HIV)-infected patients; however, its effect on HIV-associated cognitive impairment remains unknown in the era of antiretroviral treatment. The authors examined associations of smoking with viral immune profile and cognitive function in a cohort of HIV-seropositive women. This observational cross-sectional study included 56 women (36 HIV-seropositive and 20 HIV-seronegative) surveyed with a tobacco questionnaire: the Fagerström Test for Nicotine Dependency. Viral immune status was obtained 6 to 12 months before questioned. Neurocognitive testing (NP) assessed verbal memory, frontal/executive function, psychomotor speed, and motor speed. A reference group of HIV-seronegative women was used to calculate standardized z-scores. Cognitive impairment was classified using a modified American Academy of Neurology criteria, adding an asymptomatic group based on NP tests. Statistics included parametric and nonparametric tests. HIV-seropositive women were more likely to report a history of smoking (P = 0.028). Among them, current smoking correlated with higher plasma viral load (P = 0.048), and history of smoking correlated with lower CD4 cell count (P = 0.027). The authors observed no associations between cognitive impairment and either current or past history of smoking and no differences in neurocognitive domain scores between HIV-seropositive and -seronegative women or between those with and without a history of smoking. However, restricting analysis to HIV-seropositives showed a significant better performance on the frontal/executive domain in those with history of smoking. In summary, history of smoking correlated with better frontal/executive cognitive domain performance in HIV-seropositive women and with worse viral immune profile.

Prevalence of human immunodeficiency virus–associated cognitive impairment in a group of Hispanic women at risk for neurological impairment

Human immunodeficiency virus (HIV)-associated cognitive impairment, a significant cause of morbidity, affects up to 30% of HIV-infected people. Its prevalence doubled as patients began to live longer after the introduction of highly active retroviral therapy. Women are now one of the fastest growing groups with acquired immunodeficiency syndrome (AIDS) in the United States and Puerto Rico, but relatively little is known about the prevalence and characteristics of cognitive dysfunction in HIV-infected women. In this study the authors investigated its prevalence in a group of HIV-1-seropositive Hispanic women in Puerto Rico. Forty-nine women with a nadir CD4 cell count of < or = 500 cells/mm3 were enrolled. Cognitive impairment was defined according to the American Academy of Neurology criteria for HIV dementia as modified to identify an "asymptomatic cognitively impaired" group. Observed prevalence was compared with prevalence in other populations in United States, Europe, and Australia. Differences in clinical markers and neuropsychological test performance among the cohort stratified by cognitive impairment were tested. Cognitive impairment was observed in 77.6% (38/49) of cases; asymptomatic cognitive impairment in 32.7% (16/49); minor cognitive motor disorders in 16.3% (8/49); and HIV-associated dementia (HAD) in 28.6% (14/49). Cognitive impairment did not correlate with age, CD4 cell count, viral load, or treatment modality. The cross-sectional prevalence of HIV-associated cognitive impairment was 77.6% (28.6% for HAD). These findings should enhance awareness of the prevalence of HIV-associated cognitive impairment, both clinically apparent and "asymptomatic," in Hispanic women and lead to improvements in areas such as education and compliance and to reevaluation of treatment interventions.

Standard regression-based methods for measuring recovery after sport-related concussion

Clinical decision making about an athlete's return to competition after concussion is hampered by a lack of systematic methods to measure recovery. We applied standard regression-based methods to statistically measure individual rates of impairment at several time points after concussion in college football players. Postconcussive symptoms, cognitive functioning, and balance were assessed in 94 players with concussion (based on American Academy of Neurology Criteria) and 56 noninjured controls during preseason baseline testing, and immediately, 3 hr, and 1, 2, 3, 5, and 7 days postinjury. Ninety-five percent of injured players exhibited acute concussion symptoms and impairment on cognitive or balance testing immediately after injury, which diminished to 4% who reported elevated symptoms on postinjury day 7. In addition, a small but clinically significant percentage of players who reported being symptom free by day 2 continued to be classified as impaired on the basis of objective balance and cognitive testing. These data suggest that neuropsychological testing may be of incremental utility to subjective symptom checklists in identifying the residual effects of sport-related concussion. The implementation of neuropsychological testing to detect subtle cognitive impairment is most useful once postconcussive symptoms have resolved. This management model is also supported by practical and other methodological considerations.

Evaluation of HIV RNA and markers of immune activation as predictors of HIV-associated dementia

To evaluate whether baseline levels of plasma and CSF HIV RNA, tumor necrosis factor alpha (TNFalpha), monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase-2 (MMP-2), or macrophage colony stimulating factor (M-CSF) are predictors of incident HIV-associated dementia (HIVD) in a cohort with advanced HIV infection. A total of 203 nondemented subjects with CD4 lymphocyte counts less than 200/muL, or <300/microL but with cognitive impairment, underwent semiannual neurologic, cognitive, functional, and laboratory assessments. HIVD and minor cognitive motor disorder (MCMD) were defined using American Academy of Neurology criteria. The cumulative incidence of HIVD was estimated using Kaplan-Meier curves. Cox proportional hazards regression models were used to examine the associations between biologic variables and time to HIVD, adjusting for age, sex, years of education, duration of HIV infection, type of antiretroviral use, premorbid IQ score, and presence of MCMD. After a median follow-up time of 20.7 months, 74 (36%) subjects reached the HIVD endpoint. The dementia was mild in 70% of cases. The cumulative incidence of HIVD was 20% at 1 year and 33% at 2 years. Highly active antiretroviral therapy (HAART) was used by 73% of subjects at baseline. A plasma HIV RNA level was undetectable in 23% of subjects and a CSF HIV RNA level was undetectable in 48% of subjects. In adjusted analyses, neither plasma nor CSF HIV RNA levels (log10) were associated with time to HIVD; log10 levels of plasma TNFalpha (HR 3.07, p = 0.03) and CSF MCP-1 (HR = 3.36, p = 0.06) tended to be associated with time to HIVD. The lack of association between baseline plasma and CSF HIV RNA levels and incident dementia suggests highly active antiretroviral therapy may be affecting CNS viral dynamics, leading to lower HIV RNA levels, and therefore weakening the utility of baseline HIV RNA levels as predictors of HIV-associated dementia.

Atypical electrophysiologic findings in chronic inflammatory demyelinating polyneuropathy (CIDP) – diagnosis confirmed by nerve biopsy

Objectives. – Numerous sets of electrophysiological criteria of chronic inflammatory demyelinating polyneuropathy (CIDP) have been proposed, among which the criteria established by an ad hoc subcommittee of the American Academy of Neurology (AAN) in 1991 (Neurology 41 (1991) 617) are the most widely used. As they seemed rather restrictive, the Inflammatory Neuropathy Cause and Treatment (INCAT) group (Ann. Neurol. 50 (2001) 195) proposed modifications of these electrophysiological criteria. However, even using these criteria, some cases of CIDP may not be recognized. In such cases, nerve biopsy has proven useful for confirmation of the diagnosis by demonstrating specific abnormalities. The objective of the study was to determine the profile of electrophysiological abnormalities in patients with atypical electrophysiologic criteria of CIDP and the diagnostic value of multiple A waves and a low median to sural amplitude ratio. Patients and methods. – Over a period of 3 years, we classified 44 patients into two categories: those presenting the strict AAN and/or INCAT criteria and those who we regarded as cases of CIDP not meeting these criteria. All patients benefited from one or more clinical and electrophysiological examination. Extensive biological workup and genetic study when appropriate excluded other causes of neuropathy. Nerve biopsies were taken from all patients and samples were included in paraffin and epon for systematic light, teasing and electron microscopic examination. Results and conclusion. – Out of 44 patients, 36 fulfilled the INCAT or AAN criteria. In eight other patients, the diagnosis of CIDP was suspected on clinical and EMG examinations and confirmed by nerve biopsy. In these cases, the electrophysiological exploration showed some abnormalities such as multiple A waves in four out of eight patients or an abnormal pattern of the sensory responses of the median and sural nerves in four out of eight patients that were more indicative of an initial demyelinating process. Six of our patients received immunomodulatory treatment, and five responded favorably.

Acute effects and recovery time following concussion in collegiate football players: the NCAA Concussion Study.

Lack of empirical data on recovery time following sport-related concussion hampers clinical decision making about return to play after injury. To prospectively measure immediate effects and natural recovery course relating to symptoms, cognitive functioning, and postural stability following sport-related concussion. Prospective cohort study of 1631 football players from 15 US colleges. All players underwent preseason baseline testing on concussion assessment measures in 1999, 2000, and 2001. Ninety-four players with concussion (based on American Academy of Neurology criteria) and 56 noninjured controls underwent assessment of symptoms, cognitive functioning, and postural stability immediately, 3 hours, and 1, 2, 3, 5, 7, and 90 days after injury. Scores on the Graded Symptom Checklist (GSC), Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and a neuropsychological test battery. No player with concussion was excluded from participation; 79 players with concussion (84%) completed the protocol through day 90. Players with concussion exhibited more severe symptoms (mean GSC score 20.93 [95% confidence interval [CI], 15.65-26.21] points higher than that of controls), cognitive impairment (mean SAC score 2.94 [95% CI, 1.50-4.38] points lower than that of controls), and balance problems (mean BESS score 5.81 [95% CI, -0.67 to 12.30] points higher than that of controls) immediately after concussion. On average, symptoms gradually resolved by day 7 (GSC mean difference, 0.33; 95% CI, -1.41 to 2.06), cognitive functioning improved to baseline levels within 5 to 7 days (day 7 SAC mean difference, -0.03; 95% CI, -1.33 to 1.26), and balance deficits dissipated within 3 to 5 days after injury (day 5 BESS mean difference, -0.31; 95% CI, -3.02 to 2.40). Mild impairments in cognitive processing and verbal memory evident on neuropsychological testing 2 days after concussion resolved by day 7. There were no significant differences in symptoms or functional impairments in the concussion and control groups 90 days after concussion. Collegiate football players may require several days for recovery of symptoms, cognitive dysfunction, and postural instability after concussion. Further research is required to determine factors that predict variability in recovery time after concussion. Standardized measurement of postconcussive symptoms, cognitive functioning, and postural stability may enhance clinical management of athletes recovering from concussion.

Proposed revised electrophysiological criteria for chronic inflammatory demyelinating polyradiculoneuropathy.

Electrophysiological criteria for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) were proposed by an Ad Hoc Subcommittee of the American Academy of Neurology (AAN) in 1991. Only 60% of CIDP patients fulfilled these criteria, which therefore appear poorly sensitive. We therefore sought to revise the electrophysiological criteria. We selected 40 CIDP patients and compared them with 35 patients with axonal polyneuropathy, 116 patients with Charcot-Marie-Tooth type 1A (CMT1A) disease, and 66 patients with immunoglobulin M (IgM) monoclonal gammopathy. The proposed electrophysiological criteria identified 90% of the CIDP patients, although 3% of patients with axonal polyneuropathy were falsely identified. For the CIDP patients, sensitivity and specificity were 90% and 97%, respectively. Of the patients with IgM monoclonal gammaglobulin of undetermined significance (MGUS) and CMT1A, 100% fulfilled these new criteria, whereas 90% and 97%, respectively, fulfilled the AAN criteria. These results suggest that the AAN criteria are more appropriate for IgM MGUS and CMT1A patients than for CIDP patients. We therefore propose new electrophysiological criteria for CIDP that appear to have better sensitivity.

Factors associated with incident human immunodeficiency virus-dementia.

Antecedents to human immunodeficiency virus-dementia (HIV-D) are poorly understood. To identify risk factors for HIV-D. Subjects who are positive for HIV who have CD4+ counts either below 200/microL or below 300/microL with evidence of cognitive impairment were enrolled in this study. Neurologic, cognitive, functional, and laboratory assessments were done semiannually for up to 30 months. Human immunodeficiency virus-dementia was diagnosed using American Academy of Neurology criteria for probable HIV-1-associated dementia complex. One hundred forty-six nondemented patients were enrolled, 45 of whom subsequently met criteria for incident HIV-D. In univariate analyses using the Cox proportional hazards regression model, the following variables were significantly associated with time to develop dementia: cognitive: abnormal scores on Timed Gait, Verbal Fluency, Grooved Pegboard, and Digit Symbol tests; attention-memory, psychomotor, and executive function domain scores; and the diagnosis of minor cognitive/motor disorder; neurologic and medical: increased abnormalities on the neurologic examination, extrapyramidal signs, history of HIV-related medical symptoms; functional: higher reported role or physical function difficulties. Depression was also a strong risk factor, along with sex, hematocrit, hemoglobin, and beta2-microglobulin levels. In a multivariate model that used cognitive domain scores, covariates with significant hazard ratios included depression, executive dysfunction, and the presence of minor cognitive/motor disorder. Cognitive deficits, minor cognitive/motor disorder, and depression may be early manifestations of HIV-D.

Clinical confirmation of the American Academy of Neurology algorithm for HIV-1-associated cognitive/motor disorder. The Dana Consortium on Therapy for HIV Dementia and Related Cognitive Disorders.

Our goal was to put into operation the American Academy of Neurology (AAN) algorithm for the definition of minor cognitive/motor disorder and human immunodeficiency virus type 1 (HIV-1)-associated dementia complex (ADC) and examine the neuropsychological, neurologic, psychiatric, and functional deficits in affected subjects. Two hundred seventy-one HIV-positive men and women with CD4 count of < 200 or demonstrated cognitive impairment were recruited from three sites (Columbia University, The Johns Hopkins University, and the University of Rochester) and underwent standardized assessments. Sixty-five subjects met criteria for ADC (cognitive, functional, and neurologic or behavioral), 56 met criteria for minor cognitive/motor disorder, and 150 met criteria for neither. Seventy-eight subjects met neuropsychological and neurologic/behavioral criteria but did not demonstrate functional impairment. Those with ADC performed significantly worse on speeded motor and verbal memory tests and demonstrated more extrapyramidal signs and behavioral symptoms than did the other two groups. Both ADC and minor cognitive/motor disorder were independently predictive of poor physical function, after adjustment for age, gender, years of education, log (CD4 count), hemoglobin, number of HIV diagnoses and medications, and depression. The operationalization of AAN criteria demonstrates that it is rare to have both cognitive and functional impairment without associated neurologic and/or behavioral deficits. Functional impairment in isolation is also rare. Dementia is an independent predictor of physical function.