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Functional Neurology Practice for Sale

03-30-2009

Functional Neurology Practice for Sale Alternative Health Solutions is located in Flower Mound, TX, a thriving suburb of the Dallas/Ft. Worth Metroplex, located only 10 miles north of the DFW airport. Flower Mound is a picturesque town, surrounded by lakes and boasting excellent schools— the perfect place for you to live and work. The clinic was founded 11 years ago by Natalie J Engelbart, DC, DACNB, and is considered to be one of the premier practices incorporating functional neurology and clinical nutrition together with chiropractic care. Recently Alternative Health Solutions has been featured in local television shows and magazines, with an emphasis on the quality of care, and how functional neurology sets this clinic apart from other chiropractic practices. Alternative Health Solutions is a cash practice with a strong patient foundation based on wellness care. New patients are mainly referrals from existing patients or from other doctors. Very little advertising has been done. Still, the practice currently has a waiting list for new patients for the next 3 months. Dr Engelbart is offering the purchase of this cash practice to allow her to attend to research and the non- profit organization she has founded. Over the last 11 years Dr. Engelbart has trained 3 other chiropractors and has developed a successful business model to treat patients with the highest quality of service. Her goal is to pass on the experience she has gleaned after founding and operating a thriving n e u r o l o g i c a l l y - i n t e g r a t e d • chiropractic practice to one or two doctors who share her • pas si on for neurology , chiropractic, and success. • Since it is a cash practice, it can remain as such, or be easily converted into a practice that accepts insurance. It is currently located in a 2200 square foot facility with lease option available in December 2009. The lease can be renewed, or the practice can be moved to a different location to better suit the new owner's needs and preferences. The relationship and importance of this clinic to the community demands a comprehensive transition of clinicians. This will be accomplished by incorporating an optimum transition time that will allow for successful continuation of the practice and maximum patient retention. This truly is a remarkable opportunity. The terms for the sale of Alternative Health Solutions are negotiable, and Dr. Engelbart will be happy to discuss particulars, including practice statistics, financials, and transition time. If you are serious about pursuing this opportunity, do not hesitate.

Contact Dr. Engelbart directly by phone: 972.816.1410 or email: DrEngelbart@hotmail.com

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Phantom Limbs Spark Brain Activity

04-10-2009

Patients may be able to feel, intentionally move, and even see their phantom limb, report investigators. Using functional magnetic resonance imaging (fMRI) to assess the experience, researchers found that a supernumerary phantom limb can spark brain activity. Their findings were published online March 20 in the Annals of Neurology.

Seeing the phantom: A functional MRI study of a supernumerary phantom limb
Asaid Khateb, Ph.D 1 2 3 *, Stéphane R. Simon, Ph.D 4, Sebastian Dieguez, MSc 5, François Lazeyras, Ph.D 4, Isabelle Momjian-Mayor, MD 2, Olaf Blanke, Pr. MD 2 5, Theodor Landis, Pr. MD 2 3, Alan J. Pegna, Ph.D 1 2 3, Jean-Marie Annoni, Pr. MD 2 3 *
1Laboratory of Experimental Neuropsychology, Neurology department, Geneva University Hospitals and Faculty of Medicine, Geneva, Switzerland
2Neurology department, Geneva University Hospitals and Faculty of Medicine, Geneva Switzerland
3Geneva Neuroscience Centre, Faculty of Medicine, Geneva Switzerland
4CIBM and Radiology department, Geneva University Hospitals and Faculty of Medicine, Geneva, Switzerland
5Laboratory of Cognitive Neuroscience, Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland

Abstract


Objective.
Supernumerary phantom limb (SPL) is a rare neurological manifestation, where patients with a severe stroke-induced sensorimotor deficit experience the illusory presence of an extra limb that duplicates a real one. The illusion is most often experienced as a somesthetic phantom, but rarer SPLs may be intentionally triggered or seen. Here, we report the case of a left visual, tactile and intentional SPL due to a right subcortical damage, in a non-deluded woman.

Methods.
Using functional magnetic resonance imaging (fMRI), we investigated the multimodal nature of this phantom, which the patient claimed to be able see, use and move intentionally. The patient participated in a series of sensorimotor and motor imagery tasks involving the right, the left plegic, and the SPL's hand.

Results.
Right premotor, and motor regions were engaged when she imagined that she was scratching her left cheek with her left plegic hand, whereas when she performed the same task with the SPL, additional left middle occipital areas were recruited. Moreover, comparison of responses induced by left cheek (subjectively feasible) versus right cheek scratching (reportedly unfeasible movement) with the SPL, revealed significant activation in right somesthesic areas.

Interpretation.

These findings demonstrate that intentional movements of a seen and felt SPL activate premotor and motor areas together with visual and sensory cortex, confirming its multimodal dimension and the reliability of the patient's verbal reports. This observation, interpreted in terms of cortical de-afferentation/disconnection due to subcortical brain damage, constitutes a new but theoretically predictable entity among disorders of bodily awareness. Ann Neurol 2009.


  This group has been quite prolific and has some very interesting articles.
1-50

1.    Abutalebi J, Annoni JM, Zimine I, et al. Language control and lexical competition in bilinguals: an event-related FMRI study. Cereb Cortex 2008;18:1496-505.
2.    Alonso A, Khateb A, Fort P, Jones BE, Muhlethaler M. Differential oscillatory properties of cholinergic and noncholinergic nucleus basalis neurons in guinea pig brain slice. Eur J Neurosci 1996;8:169-82.
3.    Andino SL, Menendez RG, Khateb A, Landis T, Pegna AJ. Electrophysiological correlates of affective blindsight. Neuroimage 2009;44:581-9.
4.    Annoni JM, Khateb A, Gramigna S, et al. Chronic cognitive impairment following laterothalamic infarcts: a study of 9 cases. Arch Neurol 2003;60:1439-43.
5.    Annoni JM, Michel CM, Landis T, Khateb A. [Variability of right hemisphere activation during semantic word processing in aphasic patients: an electrophysiologic study in three patients]. Rev Neurol (Paris) 2002;158:317-31.
6.    Annoni JM, Pertusio FB, Caldara AS, et al. [Neuropsychological test in daily practice]. Rev Med Suisse Romande 2003;123:263-7.
7.    Annoni JM, Ptak R, Caldara-Schnetzer AS, Khateb A, Pollermann BZ. Decoupling of autonomic and cognitive emotional reactions after cerebellar stroke. Ann Neurol 2003;53:654-8.
8.    de Waele C, Serafin M, Khateb A, et al. An in vivo and in vitro study of the vestibular nuclei histaminergic receptors in the guinea pig. Ann N Y Acad Sci 1992;656:550-65.
9.    de Waele C, Serafin M, Khateb A, Yabe T, Vidal PP, Muhlethaler M. Medial vestibular nucleus in the guinea-pig: apamin-induced rhythmic burst firing--an in vitro and in vivo study. Exp Brain Res 1993;95:213-22.
10.    Etzioni S, Yafe A, Khateb S, Weisman-Shomer P, Bengal E, Fry M. Homodimeric MyoD preferentially binds tetraplex structures of regulatory sequences of muscle-specific genes. J Biol Chem 2005;280:26805-12.
11.    Fort P, Khateb A, Pegna A, Muhlethaler M, Jones BE. Noradrenergic modulation of cholinergic nucleus basalis neurons demonstrated by in vitro pharmacological and immunohistochemical evidence in the guinea-pig brain. Eur J Neurosci 1995;7:1502-11.
12.    Fort P, Khateb A, Serafin M, Muhlethaler M, Jones BE. Pharmacological characterization and differentiation of non-cholinergic nucleus basalis neurons in vitro. Neuroreport 1998;9:61-5.
13.    Genetti M, Khateb A, Heinzer S, Michel CM, Pegna AJ. Temporal dynamics of awareness for facial identity revealed with ERP. Brain Cogn 2009;69:296-305.
14.    Gonzalez Andino SL, Grave de Peralta R, Khateb A, Pegna AJ, Thut G, Landis T. A glimpse into your vision. Hum Brain Mapp 2007;28:614-24.
15.    Khateb A, Abutalebi J, Michel CM, Pegna AJ, Lee-Jahnke H, Annoni JM. Language selection in bilinguals: a spatio-temporal analysis of electric brain activity. Int J Psychophysiol 2007;65:201-13.
16.    Khateb A, Ammann J, Annoni JM, Diserens K. Cognition-enhancing effects of donepezil in traumatic brain injury. Eur Neurol 2005;54:39-45.
17.    Khateb A, Annoni JM, Landis T, et al. Spatio-temporal analysis of electric brain activity during semantic and phonological word processing. Int J Psychophysiol 1999;32:215-31.
18.    Khateb A, Fort P, Alonso A, Jones BE, Muhlethaler M. Pharmacological and immunohistochemical evidence for serotonergic modulation of cholinergic nucleus basalis neurons. Eur J Neurosci 1993;5:541-7.
19.    Khateb A, Fort P, Pegna A, Jones BE, Muhlethaler M. Cholinergic nucleus basalis neurons are excited by histamine in vitro. Neuroscience 1995;69:495-506.
20.    Khateb A, Fort P, Serafin M, Jones BE, Muhlethaler M. Rhythmical bursts induced by NMDA in guinea-pig cholinergic nucleus basalis neurones in vitro. J Physiol 1995;487 ( Pt 3):623-38.
21.    Khateb A, Fort P, Williams S, Serafin M, Jones BE, Muhlethaler M. Modulation of cholinergic nucleus basalis neurons by acetylcholine and N-methyl-D-aspartate. Neuroscience 1997;81:47-55.
22.    Khateb A, Fort P, Williams S, Serafin M, Muhlethaler M, Jones BE. GABAergic input to cholinergic nucleus basalis neurons. Neuroscience 1998;86:937-47.
23.    Khateb A, Martory MD, Annoni JM, et al. Transient crossed aphasia evidenced by functional brain imagery. Neuroreport 2004;15:785-90.
24.    Khateb A, Michel CM, Pegna AJ, Landis T, Annoni JM. New insights into the Stroop effect: a spatio-temporal analysis of electric brain activity. Neuroreport 2000;11:1849-55.
25.    Khateb A, Michel CM, Pegna AJ, O'Dochartaigh SD, Landis T, Annoni JM. Processing of semantic categorical and associative relations: an ERP mapping study. Int J Psychophysiol 2003;49:41-55.
26.    Khateb A, Michel CM, Pegna AJ, Thut G, Landis T, Annoni JM. The time course of semantic category processing in the cerebral hemispheres: an electrophysiological study. Brain Res Cogn Brain Res 2001;10:251-64.
27.    Khateb A, Muhlethaler M, Alonso A, Serafin M, Mainville L, Jones BE. Cholinergic nucleus basalis neurons display the capacity for rhythmic bursting activity mediated by low-threshold calcium spikes. Neuroscience 1992;51:489-94.
28.    Khateb A, Pegna AJ, Landis T, et al. Rhyme processing in the brain: an ERP mapping study. Int J Psychophysiol 2007;63:240-50.
29.    Khateb A, Pegna AJ, Michel CM, Custodi MC, Landis T, Annoni JM. Semantic category and rhyming processing in the left and right cerebral hemisphere. Laterality 2000;5:35-53.
30.    Khateb A, Pegna AJ, Michel CM, Landis T, Annoni JM. Dynamics of brain activation during an explicit word and image recognition task: an electrophysiological study. Brain Topogr 2002;14:197-213.
31.    Khateb A, Serafin M, Muhlethaler M. Histamine excites pedunculopontine neurones in guinea pig brainstem slices. Neurosci Lett 1990;112:257-62.
32.    Khateb S, Weisman-Shomer P, Hershco I, Loeb LA, Fry M. Destabilization of tetraplex structures of the fragile X repeat sequence (CGG)n is mediated by homolog-conserved domains in three members of the hnRNP family. Nucleic Acids Res 2004;32:4145-54.
33.    Khateb S, Weisman-Shomer P, Hershco-Shani I, Ludwig AL, Fry M. The tetraplex (CGG)n destabilizing proteins hnRNP A2 and CBF-A enhance the in vivo translation of fragile X premutation mRNA. Nucleic Acids Res 2007;35:5775-88.
34.    Martory MD, Mayer E, Pegna AJ, Annoni JM, Landis T, Khateb A. Pure global acalculia following a left subangular lesion. Neurocase 2003;9:319-28.
35.    Michel CM, Thut G, Morand S, et al. Electric source imaging of human brain functions. Brain Res Brain Res Rev 2001;36:108-18.
36.    Morand S, Thut G, de Peralta RG, et al. Electrophysiological evidence for fast visual processing through the human koniocellular pathway when stimuli move. Cereb Cortex 2000;10:817-25.
37.    Pegna AJ, Caldara-Schnetzer AS, Khateb A. Visual search for facial expressions of emotion is less affected in simultanagnosia. Cortex 2008;44:46-53.
38.    Pegna AJ, Caldara-Schnetzer AS, Perrig SH, et al. Is the right amygdala involved in visuospatial memory? Evidence from MRI volumetric measures. Eur Neurol 2002;47:148-55.
39.    Pegna AJ, Khateb A, Lazeyras F, Seghier ML. Discriminating emotional faces without primary visual cortices involves the right amygdala. Nat Neurosci 2005;8:24-5.
40.    Pegna AJ, Khateb A, Michel CM, Landis T. Visual recognition of faces, objects, and words using degraded stimuli: where and when it occurs. Hum Brain Mapp 2004;22:300-11.
41.    Pegna AJ, Khateb A, Murray MM, Landis T, Michel CM. Neural processing of illusory and real contours revealed by high-density ERP mapping. Neuroreport 2002;13:965-8.
42.    Pegna AJ, Landis T, Khateb A. Electrophysiological evidence for early non-conscious processing of fearful facial expressions. Int J Psychophysiol 2008;70:127-36.
43.    Pegna AJ, Petit L, Caldara-Schnetzer AS, et al. So near yet so far: neglect in far or near space depends on tool use. Ann Neurol 2001;50:820-2.
44.    Seghier M, Lazeyras F, Momjian S, Annoni JM, de Tribolet N, Khateb A. Language representation in a patient with a dominant right hemisphere: fMRI evidence for an intrahemispheric reorganisation. Neuroreport 2001;12:2785-90.
45.    Seghier ML, Lazeyras F, Pegna AJ, Annoni JM, Khateb A. Group analysis and the subject factor in functional magnetic resonance imaging: analysis of fifty right-handed healthy subjects in a semantic language task. Hum Brain Mapp 2008;29:461-77.
46.    Seghier ML, Lazeyras F, Pegna AJ, et al. Variability of fMRI activation during a phonological and semantic language task in healthy subjects. Hum Brain Mapp 2004;23:140-55.
47.    Serafin M, de Waele C, Khateb A, Vidal PP, Muhlethaler M. Medial vestibular nucleus in the guinea-pig. I. Intrinsic membrane properties in brainstem slices. Exp Brain Res 1991;84:417-25.
48.    Serafin M, de Waele C, Khateb A, Vidal PP, Muhlethaler M. Medial vestibular nucleus in the guinea-pig. II. Ionic basis of the intrinsic membrane properties in brainstem slices. Exp Brain Res 1991;84:426-33.
49.    Serafin M, Khateb A, de Waele C, Vidal PP, Muhlethaler M. Low threshold calcium spikes in medial vestibular nuclei neurones in vitro: a role in the generation of the vestibular nystagmus quick phase in vivo? Exp Brain Res 1990;82:187-90.
50.    Serafin M, Khateb A, de Waele C, Vidal PP, Muhlethaler M. Medial vestibular nucleus in the guinea-pig: NMDA-induced oscillations. Exp Brain Res 1992;88:187-92.



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Childhood Sleep Deficits Linked With Later Anxiety, Depression, and Aggression

04-10-2009

Childhood Sleep Deficits Linked With Later Anxiety, Depression, and Aggression

A longitudinal study conducted in a Dutch population examined sleep problems and later difficulties. Sleeping less than others in childhood emerged as the main predictor of subsequent emotional and behavioral problems in young adulthood, according to the study

 

Sleep problems in childhood predict neuropsychological functioning in adolescence

Pediatrics. 2009 Apr;123(4):1171-6

Gregory AM, Caspi A, Moffitt TE, Poulton R.

Psychology Department, Goldsmiths College, University of London, Lewisham Way, New Cross, London SE14 6NW, United Kingdom.

OBJECTIVES: Our goal was to examine the association between parent-rated sleep problems during childhood and neuropsychological functioning during adolescence. PARTICIPANTS AND METHODS: Longitudinal prospective data on an entire birth cohort from Dunedin, New Zealand, were obtained. One thousand thirty-seven children were enrolled in the study (52% male). Parents reported on sleep problems when the study members were 5, 7, and 9 years of age. Neuropsychological functioning was assessed by using 7 tests when the participants were 13 years of age. RESULTS: After adjusting for gender and socioeconomic status, persistent sleep problems during childhood predicted scores on 2 neuropsychological tests: the copy score of the Rey-Osterrieth Complex Figure Test and 2 measures of performance on the Halstead Trail Making Test. These results were substantively replicated when sleep was assessed at the 5- and 9-year (but not 7-year) assessments separately. CONCLUSIONS: Sleep problems during childhood may be associated with certain aspects of neuropsychological functioning during adolescence. This adds to the growing body of literature suggesting that childhood sleep problems may be a risk indicator of later difficulties.

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Essential Tremor and Parkinsonism: Relationships and influence of Alcohol

04-10-2009

A recent study from Madrid, Spain associated with the New York Neurological Institute suggests that drinking 3 units of alcohol a day increases the risk of developing essential tremor.   A study published in the April issue of the Journal of Neurology, Neurosurgery, and Psychiatry warn of the potential cerebellar neurotoxicity of alcohol. 

Population-Based Study of Baseline Ethanol Consumption and Risk of Incident Essential Tremor

Elan D Louis 1*, Julian Benito-Leon 2 and Felix Bermejo-Pareja 2

 

1 Columbia University, United States
2 University Hospital "12 de Octubre", Spain

 

Abstract

Background Recent postmortem studies have demonstrated pathological changes, including Purkinje cell loss, in the cerebellum in essential tremor (ET). Toxic exposures that compromise cerebellar tissue could lower the threshold for developing ET. Ethanol is a well-established cerebellar toxin, resulting in Purkinje cell loss.

Objective To test whether higher baseline ethanol consumption is a risk factor for the subsequent development of incident ET.

Methods Lifetime ethanol consumption was assessed at baseline (1994-1995) in a prospective, population-based study in central Spain of 3,285 elderly participants, 76 of whom developed incident ET by follow-up (1997-1998).

Results In a Cox proportional hazards model adjusting for cigarette pack-years, depressive symptoms and community, the baseline number of drink-years was marginally associated with higher risk of incident ET (relative risk, RR = 1.003, p = 0.059). In an adjusted Cox model, highest baseline drink-year quartile doubled the risk of incident ET (RR = 2.29, p = 0.018) while other quartiles were associated with more modest elevations in risk (RR3rd quartile = 1.82 [p = 0.10], RR2nd quartile = 1.75 [p = 0.10], RR1st quartile = 1.43 [p = 0.34] vs. non-drinkers [RR = 1.00]). With each higher drink-year quartile, risk of incident ET increased an average of 23% (p = 0.01, test for trend).

Conclusions Higher levels of chronic ethanol consumption increased the risk of developing ET. Ethanol is often used for symptomatic relief; studies should explore whether higher consumption levels are a continued source of underlying cerebellar neurotoxicity in patients who already manifest this disease.

 

Another study by the same team also addressed a relationship between essential tremor and Parkinson's disease

J Neurol Neurosurg Psychiatry. 2009;80:423-425

Risk of incident Parkinson's disease and parkinsonism in essential tremor: a population based study

Benito-León J, Louis ED, Bermejo-Pareja F; Neurological Disorders in Central Spain Study Group.

Department of Neurology, University Hospital, Madrid, Spain.

BACKGROUND: A longstanding literature suggests an association between essential tremor (ET) and Parkinson's disease (PD). However, the risk of incident PD has not been quantified in cases of ET compared with controls. OBJECTIVE: To estimate the risk of incident PD in a population based cohort study of 3813 older people (including ET cases and controls) in central Spain. RESULTS: After a median of 3.3 years, 12 (5.8%) of 207 ET cases developed parkinsonism compared with 56 (1.6%) of 3606 controls (adjusted relative risk (RR) 3.47, 95% CI 1.82 to 6.59; p<0.001). Six (3.0%) of 201 ET cases developed incident PD versus 24 (0.7%) of 3574 controls (adjusted RR 4.27, 95% CI 1.72 to 10.61; p = 0.002). CONCLUSIONS: Patients with ET were four times more likely than controls to develop incident PD during prospective follow-up. These data confirm and begin to quantify the link between these two diseases.

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Lifestyle Changes and Colorectal Cancer Expression

04-10-2009

A study published in the April 4, 2009  European Journal of Cancer Prevention suggests that lifestyle changes can prevent more deaths from colorectal cancer than the implementation of screening strategies.  This study shares a paradigm of functional applications in neurology that embrace a patient based paradigm of health.  When patients are taught applications that they might implement themselves they might have maximum benefits and decreased dependency on health care providers.  This study suggests that simple lifestyle modifications involving diet and exercise would lead to a 26% reduction in the number of cases of colorectal cancer in the British population. A decrease in colorectal cancer expression should be associated with a similar decrease in death from the disease.

Predicting the impact of the screening programme for colorectal cancer in the UK

Eur J Cancer Prev. 2009 Feb 20

Parkin DM, Olsen AH, Sasieni P.

Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Wolfson Institute of Preventive Medicine, Cancer Research UK Centre for Epidemiology, Mathematics and Statistics, London, UK.

On the basis of recent trends (up to 2004), future projections of the incidence of colorectal cancer in the UK in the next 24 years are for a continuing decline in rates (age-standardized rates predicted to be about 9% lower). The potential for modification of the predicted burden through the implementation of five preventive interventions, for which national policies or targets have been promulgated, is examined. We estimate that 31.5% of cancers in men and 18.4% in women could be prevented if reasonable targets with respect to diet (reduced consumption of red meat, increased fruit and vegetables), exercise (30 min 5 days a week), alcohol consumption (3 U a day for men, 2 U for women) and weight control were achieved. This estimate assumes a return of the weight profile of the UK population to that present 20 years ago; if the aim were simply to halt the increasing trend in overweight, the preventable fractions would be 28% in men and 14.7% in women. These predictions suggest that realistic lifestyle modifications can result in a substantial reduction in cases of this major cancer. The benefit in terms of avoided deaths is probably greater than that which can be achieved through implementation of the national screening programme, and improvements in treatment.

Another paper that is of interest by the same team was published in the J Med Screen. 2008;15(4):163-74.

The potential for prevention of colorectal cancer in the UK 

Parkin DM, Tappenden P, Olsen AH, Patnick J, Sasieni P.

Cancer Research UK Centre for Epidemiology, Mathematics and Statistics, Wolfson Institute of Preventive Medicine, Charterhouse Square, London EC1M 6BQ, UK.

OBJECTIVES: Screening for colorectal cancer by biennial testing for faecal occult blood is being introduced in the UK from 2007. We examine the likely impact of the programme, in terms of reduced mortality, lives saved and changes in incidence, over the next 20 years. SETTING: Projections of incidence and mortality of colorectal cancer in England, and the policy that has been adopted for screening in England (biennial at ages 60-69 from 2007, then 60-74 in 2010). METHODS: The results are based on the output of a simulation model that has been used to examine cost-effectiveness of screening policy options, with two scenarios regarding compliance with screening; both assume that 20% of the population will never attend for screening, but attendance of those who do is modelled either as a random 60% or 80%, at each screening round. RESULTS: The decrease in mortality rates expected 20 years after introducing screening is 13-17% in men and 12-15% in women (depending on the attendance levels). The model predicts an initial rise in incidence, followed (after six to seven years) by a fall, so that there is little net change in the number of cases detected over a 20-year period. CONCLUSION: Percentage changes in mortality seem modest, but the projected saving in terms of numbers of lives is not negligible--1800-2400 per year by 2025 in England (equivalent numbers are 2200-2700 in all over the UK). Newer screening modalities may improve on these projected results.

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National Public Health Week

04-10-2009

Learn more about how you can get involved in
National Public Health Week at
www.nphw.org.

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Stress and Toxicity in Neuroscience

04-13-2009

Cellular pathways responding to the toxicity of alpha-synuclein, a protein implicated in several neurodegenerative disorders including Parkinson's disease have been revealed (Nat Genet, March 2009).

Astrocytes can activate NOX2 to produce superoxide and that effect can be reversed by antioxidants. It was shown that NOX2 inhibitor, apocynin, can prevent the loss of motor neurons caused by the astrocytes carrying superoxide dismutase 1 gene (SOD1) mutation (Cell Stem Cell, Dec 2008).

Glucocorticoids play an important biphasic role in modulating neural plasticity; low doses enhance neural plasticity and spatial memory behavior, whereas chronic, higher doses produce inhibition. 3 independent measures of mitochondrial function-mitochondrial oxidation, membrane potential, and mitochondrial calcium holding capacity-were regulated by long-term corticosterone (CORT) treatment (PNAS, March 2009).

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Neurotransmitters and Neuromodulators: Handbook of Receptors and Biological Effects, 2nd Edition

04-13-2009


Neurosciences are one of the most dynamically developing fields within life and medical sciences. This is underlined by the 2000 Nobel Prize for Medicine/Physiology that has been awarded for pioneering research in neuroactive substances.

Here are the details of the newest guide to neurotransmitters and neuromodulators found in this second addition.  This text is ideal for the functional neurologist/researcher

Biological effects, production, and application of these substances are of extremely high pharmaceutical and biotechnological interest. Several book reviews for the first edition stated that this handbook offers a unique combination and presentation of data on neurotransmitters and neuromodulators. The second edition is completely updated and extended with new chapters on additional substances and methods.

For more information please click on:
http://www.researchandmarkets.com/product/80df9b/neurotransmitters_and_neuromodulators_handbo

Title Index:

1 Introduction.
1.1 Neuroactive Substances.
1.2 Receptors and Transporters.
1.3 Distribution and Localization of Neurotransmitters and Neuromodulators.
1.4 The Blood-Brain Barrier.
1.5 Volume Transmission and Wiring Transmission.

2 Methods.
2.1 Bio- and Radioisotope Assays.
2.2 Microdialysis and Electrochemical Detection.
2.3 Chromatography.
2.4 Autoradiography.
2.5 Immunohistochemical Methods.
2.6 In situ Hybridization.
2.7 Staining and Neuroanatomical Tract Tracing.
2.8 Electrophysiology.
2.9 Behavioral Testing.

3 Neurotransmitters.
3.1 Acetylcholine.
3.2 Dopamine.
3.3 Amino Butyric Acid.
3.4 Glutamate and Aspartate.
3.5 Glycine.
3.6 Histamine.
3.7 Norepinephrine.
3.8 Serotonin (5-Hydroxytryptamine).

4 Neuromodulators.
4.1 Adrenocorticotropic Hormone.
4.2 Anandamide (Endocannabinoids).
4.3 Angiotensin.
4.4 Atrial Natriuretic Factor.
4.5 Bombesin and Related Neuropeptides.
4.6 Calcitonin and Calcitonin Gene-related Protein.
4.7 Cholecystokinin.
4.8 Corticotropin-releasing Factor.
4.9 Dynorphin.
4.10 Eicosanoids and Arachidonic Acid.
4.11 Endorphin.
4.12 Enkephalin.
4.13 Fibroblast Growth Factors.
4.14 Galanin.
4.15 Ghrelin.
4.16 Gonadotropin-releasing Hormone.
4.17 Growth Hormone-releasing Hormone.
4.18 Hypocretin (Orexin).
4.19 Interleukin.
4.20 Melanin-concentrating Hormone.
4.21 Melanocyte-stimulating Hormone.
4.22 Neuropeptide Y.
4.23 Neurotensin.
4.24 Neurotrophins.
4.25 Nitric Oxide and Carbon Monoxide.
4.26 Nociceptin (Orphanin FQ).
4.27 Pituitary Adenylate Cyclase-activating Polypeptide.
4.28 Proopiomelanocortin.
4.29 Purines.
4.30 Somatostatin.
4.31 Substance P and Tachykinins.
4.32 Thyrotropin-releasing Hormone.
4.33 The Tyr-MIF-1 Family.
4.35 Vasopressin and Oxytocin.
4.36 Deorphanized Neuropeptides.

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NCQABack Pain Recognition Program

04-16-2009

FUNTIONAL NEUROLOGISTS MIGHT CONSIDER BEING LISTED AS BEING INCLUDED IN THE RECOGNIZED PHYSICIAN DIRECTORY OF NCQA

NCQA Recognizes physicians who take a patient-centered approach and deliver care in accordance with widely accepted, evidence-based guidelines.

Recognition Program Training for Physicians:    Back Pain Recognition Program (BPRP)

FREE Education Programs:  AVAILABLE APRIL-JUNE 2009

NCQA has developed a series of training programs on each of the Physician Recognition Programs to help you complete the application and the submission process.  Each type of program is offered multiple times to accommodate as many people as possible.  All training sessions are program-specific and have been scheduled as Eastern Time.

http://www.ncqa.org/tabid/109/Default.aspx

 

Treatment for uncomplicated low back pain varies widely.  While most physicians follow the recommended approach of pain management and gradual return to physical activity, some prematurely prescribe costly imaging, epidural steroid injections-or refer their patients to surgery.

NCQA’s new Back Pain Recognition Program (BPRP) seeks to recognize physicians and chiropractors who deliver superior care to millions of Americans who suffer from low back pain.  The BPRP program consists of 13 clinical measures and three structural standards such as the elements of the physical exam and advice for the return to normal activities.  These requirements address the broad spectrum of low back pain and focus on underuse, misuse and overuse of treatment modalities.

NCQA developed BPRP requirements from widely accepted medical evidence, with significant input from physician specialists and health plan and employer representatives.

Eligible physicians will abstract data from the charts of 35 low back pain patients and submit this information to NCQA for review along with documentation of patient education and evaluation of patient experience.

ACCREDITATION

Accreditation is a rigorous and comprehensive evaluation process through which NCQA assesses the quality of the key systems and processes that define health care organizations.   Accreditation includes an assessment of the care and service that plans deliver in important areas like childhood immunizations and ensuring that women receive mammograms as appropriate.  NCQA began accrediting MCOs in 1991, in response to the need for standardized, objective information about the quality of these health care organizations.

Employers, consumers, regulators and health plans turn to NCQA Accreditation as the gold standard in evaluating health care quality. NCQA regularly revises and improves standards in order to keep the Accreditation Program current and to address pressing health care issues. 

 

 

About NCQA
 

The National Committee for Quality Assurance is a private, 501(c)(3) not-for-profit organization dedicated to improving health care quality. Since its founding in 1990, NCQA has been a central figure in driving improvement throughout the health care system, helping to elevate the issue of health care quality to the top of the national agenda.

The NCQA seal is a widely recognized symbol of quality. Organizations incorporating the seal into advertising and marketing materials must first pass a rigorous, comprehensive review and must annually report on their performance. For consumers and employers, the seal is a reliable indicator that an organization is well-managed and delivers high quality care and service.

NCQA has helped to build consensus around important health care quality issues by working with large employers, policymakers, doctors, patients and health plans to decide what’s important, how to measure it, and how to promote improvement. That consensus is invaluable — transforming our health care system requires the collected will and resources of all these constituencies and more.

NCQA’s programs and services reflect a straightforward formula for improvement: Measure. Analyze. Improve. Repeat. NCQA makes this process possible in health care by developing quality standards and performance measures for a broad range of health care entities. These measures and standards are the tools that organizations and individuals can use to identify opportunities for improvement. The annual reporting of performance against such measures has become a focal point for the media, consumers, and health plans, which use these results to set their improvement agendas for the following year.

NCQA’s contribution to the health care system is regularly measured in the form of statistics that track the quality of care delivered by the nation’s health plans. Every year for the past five years, these numbers have improved; health care protocols have been refined, doctors have learned new ways to practice, and patients have become more engaged in their care. Those improvements in quality care translate into lives saved, illnesses avoided and costs reduced. For instance, for every additional person who receives beta blockers after a heart attack, chances of suffering a second, perhaps fatal, heart attack are reduced by up to 40%.

NCQA consistently raises the bar. Accredited health plans today face a rigorous set of more than 60 standards and must report on their performance in more than 40 areas in order to earn NCQA’s seal of approval. And even more stringent standards are being developed today. These standards will promote the adoption of strategies that we believe will improve care, enhance service and reduce costs, such as paying providers based on performance, leveraging the Web to give consumers more information, disease management and physician-level measurement.

You play a role in making NCQA successful. Whether you’re a consumer, a legislator or an employer, the most valuable thing you can do is simply to use NCQA’s information — and encourage others to use it too. Doing so sends a powerful message: quality matters.

If you’re a provider or a health plan, we invite you to participate in our voluntary programs — doing so will help you achieve your potential and demonstrate to the world that you care about quality.


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Lack of Sleep in Children Linked to ADHD Symptoms

05-07-2009

Inadequate sleep in children appears to be an independent risk factor for behavioral symptoms of attention-deficit/hyperactivity disorder (ADHD), new research suggests.

In a cross-sectional study of 7- to 8-year-old children, investigators at the University of Helsinki, Finland, found that short sleepers — those who got less than 7.7 hours of sleep per night — were significantly more likely to be hyperactive/inattentive compared with children who were moderate or longer sleepers.

"There is a large amount of literature linking sleeping difficulties to behavioral symptoms. However, this study shows short sleep duration itself is related to behavioral symptoms, independent of sleeping difficulties," principal investigator E. Juulia Paavonen, MD, PhD, 

Abstract

Pediatrics. 2009 May;123(5):e857-64

Short sleep duration and behavioral symptoms of attention-deficit/hyperactivity disorder in healthy 7- to 8-year-old children.

Departments of Psychology, University of Helsinki, Helsinki, Finland.

OBJECTIVE: It has been hypothesized that sleep deprivation may manifest in children as behavioral symptoms rather than as tiredness, but only a few studies have investigated this hypothesis. The objective of our study was to evaluate whether short sleep is associated with behavioral symptoms of attention-deficit/hyperactivity disorder in 7- to 8-year-old children. METHODS: We performed a cross-sectional study of children born in 1998 in Helsinki, Finland. The participants included 280 (146 girls, 134 boys) children with a mean age of 8.1 years (SD: 0.3; range: 7.4-8.8). Sleep quality was measured by using actigraphs. The Sleep Disturbance Scale for Children and the Attention-Deficit/Hyperactivity Disorder Rating Scale IV were administered to parents. RESULTS: Children whose average sleep duration as measured by actigraphs was short (<10th percentile, ie, <7.7 hours) and had a higher hyperactivity/impulsivity score (9.7 vs 7.8 or 7.5) and a higher attention-deficit/hyperactivity disorder total score (17.3 vs 14.5 or 13.1) but a similar inattention score (7.6 vs 6.7 or 5.6) compared with children sleeping 7.7 to 9.4 hours or >9.4 hours. In multivariate statistical models, short sleep duration remained a statistically significant predictor of hyperactivity/impulsivity, and sleeping difficulties were associated with hyperactivity/impulsivity, inattention, and the total score. There were no significant interactions between short sleep and sleeping difficulties. CONCLUSIONS: Children's short sleep duration and sleeping difficulties increase the risk for behavioral symptoms of attention-deficit/hyperactivity disorder.

 

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Comparative Vertebrate Neuroanatomy: Evolution and Adaptation, 2nd Edition

05-20-2009

This unique reference provides the only comprehensive survey of the field of comparative neuroanatomy, with an authoritative account of the evolution of vertebrate brains. The authors have achieved unparalleled breadth of coverage. This book sets forth a modern conceptual framework for understanding this topic and in doing so constitutes a landmark contribution to the field of evolutionary neurobiology.

It offers a revolutionary conceptual analysis of the evolution and development in the nervous system. This new edition will incorporate the vast amount of new research findings revealed since publication of the original work.

Comparative Vertebrate Neuroanatomy: Evolution and Adaptation, Second Edition Ann B. Butler and William Hodos The Second Edition of this landmark text presents a broad survey of comparative vertebrate neuroanatomy at the introductory level, representing a unique contribution to the field of evolutionary neurobiology. It has been extensively revised and updated, with substantially improved figures and diagrams that are used generously throughout the text.

Through analysis of the variation in brain structure and function between major groups of vertebrates, readers can gain insight into the evolutionary history of the nervous system. Comparative Vertebrate Neuroanatomy is geared to upper-level undergraduate and graduate students in neuroanatomy, but anyone interested in the anatomy of the nervous system and how it corresponds to the way that animals function in the world will find this text fascinating.

Here is an overview of the book sections:

PART ONE: EVOLUTION AND THE ORGANIZATION OF THE CENTRAL NERVOUS SYSTEM.
1. Evolution and Variation.
2. Neurons and Sensory Receptors.
3. The Vertebrate Central Nervous System.
4. Vertebrate Phylogeny and Diversity in Brain Organization.
5. Evolution and Adaptation of the Brain, Behavior, and Intelligence.
6. Theories of Brain Evolution.

PART TWO: THE SPNIAL CORD AND HINDBRAIN.
7. Overview of Spinal Cord and Hindbrain.
8. The Spinal Cord.
9. Segmental Organization of the Head, Brain, and Cranial Nerves.
10. Functional Organization of the Cranial Nerves.
11. Sensory Cranial Nerves of the Brainstem.
12. Motor Cranial Nerves.
13. The Reticular Formation.
14. The Cerebellum.

PART THREE: THE MIDBRAIN.
15. Overview of the Midbrain.
16. Isthmus.
17. Tegmentum and Tori.
18. Optic Tectum.

PART FOUR: THE FOREBRAIN: DIENCEPHALON.
19. Overview of the Forebrain.
20. Pretectum. Accessory Optic System, and Migrated Posterior Tuberculum.
21. Epithalamus.
22. Dorsal Thalamus.
23. The Visceral Brain: The Hypothalamus and the Autonomic Nervous System.

PART FIVE: THE FOREBRAIN: TELENCEPHALON.
24. Basal Telencephalon.
25. Nonlimbic Pallium.
26. Visual Forebrain in Amniotes.
27. Somatosensory and Motor Forebrain in Amniotes.
28. Auditory and Vocal Forebrain Amniotes.
29. Terminal Nerve and Olfactory Forebrain.
30. Limbic Telencephalon.

PART SIX: CONCLUSION.
31. Evolution of Brains: A Bilaterian View.
Appendix:
Terms Used in Neuroanatomy.
Glossary.
Index.

Interested clinicians might order the book directly from Amazon.com

http://www.amazon.com/s/ref=nb_ss_gw?url=search-alias%3Daps&field-keywords=Comparative+Vertebrate+Neuroanatomy%3A+Evolution+and+Adaptation%2C+2nd+Edition+&x=15&y=20

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No Significant Reduction of CV Events With Aspirin in Peripheral Artery Disease

05-20-2009

A new meta-analysis of randomized trials assessing the effects of aspirin with or without dipyridamole in patients with peripheral artery disease (PAD) finds only a statistically nonsignificant 12% reduction in cardiovascular events with treatment. There was a significant reduction in nonfatal stroke with aspirin therapy, but this was a secondary end point in their analysis.

Aspirin for the prevention of cardiovascular events in patients with peripheral artery disease: a meta-analysis of randomized trials. Berger JS, Krantz MJ, Kittelson JM, Hiatt WR. JAMA. 2009 May 13;301(18):1909-19.

 

Abstract:

CONTEXT: Randomized trials have shown that aspirin decreases the risk of cardiovascular events in patients with symptomatic coronary and cerebrovascular disease. Despite guideline recommendations for secondary prevention in peripheral artery disease (PAD), the effect of aspirin in this population is not well established. OBJECTIVE: To investigate the effect of aspirin on cardiovascular event rates in patients with PAD. DATA SOURCES AND STUDY SELECTION: MEDLINE, the Cochrane Central Register of Controlled Trials, EMBASE, Science Citation Index (1966 to December 2008), and unpublished studies from the supplemental index of the Antithrombotic Trialists' Collaboration. Eligible studies were prospective, randomized controlled trials of aspirin therapy, with or without dipyridamole that reported cardiovascular event rates. Eighteen trials involving 5269 individuals were identified. DATA EXTRACTION: Studies were reviewed to determine the number of participants, mean follow-up, and the primary end point of cardiovascular events (nonfatal myocardial infarction [MI], nonfatal stroke, and cardiovascular death). Data on the secondary end points of all-cause mortality, major bleeding, and the individual components of the primary outcome measure were also abstracted. For the primary end point, the analysis had 88% power to detect a 25% reduction and 70% power to detect a 20% reduction in cardiovascular events in the aspirin group compared with the control group. DATA SYNTHESIS: Among 5269 participants, cardiovascular events were experienced by 251 (8.9%) of 2823 patients taking aspirin (alone or with dipyridamole) and by 269 (11.0%) of 2446 in the control group (pooled relative risk [RR], 0.88; 95% confidence interval [CI], 0.76-1.04). Aspirin therapy was associated with a reduction in the secondary outcome of nonfatal stroke (52 of 2823 vs 76 of 2446; RR, 0.66; 95% CI, 0.47-0.94) but was not associated with significant reductions in all-cause or cardiovascular mortality, MI, or major bleeding. In the subset of 3019 participants taking aspirin alone vs control, aspirin was associated with a nonsignificant reduction in cardiovascular events (125 of 1516 vs 144 of 1503; RR, 0.75; 95% CI, 0.48-1.18), a significant reduction in nonfatal stroke (32 of 1516 vs 51 of 1503; RR, 0.64; 95% CI, 0.42-0.99), but no statistically significant reductions in all-cause or cardiovascular mortality, MI, or major bleeding. CONCLUSIONS: In patients with PAD, treatment with aspirin alone or with dipyridamole resulted in a statistically nonsignificant decrease in the primary end point of cardiovascular events and a significant reduction in nonfatal stroke. Results for the primary end point may reflect limited statistical power. Additional randomized controlled trials of aspirin therapy are needed to establish the net benefit and bleeding risks in PAD.

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Drinking Up to Half a Glass of Wine Daily May Increase Longevity in Men

05-20-2009

Drinking up to half a glass of wine daily may increase longevity by 5 years in men, but more studies are needed, according to the results of a study reported online first in the April 30 issue of the Journal of Epidemiology and Community Health.
 
Long-term wine consumption is related tocardiovascular mortality and life expectancyindependently of moderate alcohol intake: theZutphen Study.

Abstract:

BACKGROUND: Light to moderate alcohol intake lowers therisk of cardiovascular mortality, but whether thisprotective effect can be attributed to a specific type ofbeverage remains unclear. Moreover, little is known aboutthe effects of long-term alcohol intake on life expectancy. METHODS: The impact of long-term alcohol intake and typesof alcoholic beverages consumed on cardiovascular mortalityand life expectancy at age 50 was investigated in theZutphen Study, a cohort of 1373 men born between 1900and 1920 and examined repeatedly between 1960 and2000. Hazard ratios (HRs) for total alcohol intake and alcoholfrom wine, beer and spirits were obtained from timedependentCox regression models. Life expectancy at age 50was calculated from areas under survival curves. RESULTS: Long-term light alcohol intake, that is (20 gper day, compared with no alcohol, was strongly andinversely associated with cerebrovascular (HR 0.43, 95%CI 0.26 to 0.70), total cardiovascular (HR 0.70, 95% CI0.55 to 0.89) and all-cause mortality (HR 0.75, 95% CI0.63 to 0.91). Independent of total alcohol intake, longtermwine consumption of, on average, less than half aglass per day was strongly and inversely associated withcoronary heart disease (HR 0.61, 95% CI 0.41 to 0.89),total cardiovascular (HR 0.68, 95% CI 0.53 to 0.86) andall-cause mortality (HR 0.73, 95% CI 0.62 to 0.87). Theseresults could not be explained by differences in socioeconomicstatus. Life expectancy was about 5 yearslonger in men who consumed wine compared with thosewho did not use alcoholic beverages. CONCLUSION: Long-term light alcohol intake loweredcardiovascular and all-cause mortality risk and increasedlife expectancy. Light wine consumption was associatedwith 5 years longer life expectancy; however, morestudies are needed to verify this result.

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From Reuters Health Information Faster BMI Drop in Old Age May Indicate Underlying Dementia

05-20-2009

NEW YORK (Reuters Health) May 18 - A lower BMI at baseline or a faster decline in BMI in late life may suggest an underlying dementing illness, according to a report in the May 19th issue of Neurology.

"Dementia has been shown to develop in the brain decades before any symptoms develop. These findings likely reflect that process," lead author Dr. Tiffany F. Hughes, from the University of Pittsburgh School of Medicine, said in a statement.

She emphasized that older people should not take these findings as an endorsement of becoming overweight or obese. The results do not mean "that being obese or overweight is healthy for the mind or body, but losing weight may be a sign of emerging brain disease."

The findings come from an analysis of data for 1836 Japanese Americans who were living in King County, Washington and were enrolled in the Kame Project, a population-based prospective cohort study. The subjects were 71.8 years of age, on average, and were free from dementia when the study began from 1992 to 1994.

The authors found that subjects who were overweight or obese at baseline were 44% less likely to develop Alzheimer's disease than were normal or underweight individuals.

Overall, a slower drop in BMI (1.06 units less per year) reduced the risk of dementia by 63%. In subjects who were obese or overweight at baseline, the risk reduction was even more pronounced, 82%.

These findings "suggest that having a slow rate of a decline in weight if previously overweight or obese may reduce risk more than being overweight or obese alone in late life," the authors conclude.

Neurology 2009;72:1741-1746.

Abstract:

Neurology. 2009 May 19;72(20):1741-6. Association between late-life body mass index and dementia: The Kame Project.Hughes TF, Borenstein AR, Schofield E, Wu Y, Larson EB.

Department of Psychiatry, University of Pittsburgh School of Medicine

OBJECTIVE: To examine the association between body mass index (BMI), waist circumference (WC), and waist-to-hip ratio (WHR) and risk of dementia and its subtypes in late life. METHODS: Participants were members of the Kame Project, a population-based prospective cohort study of 1,836 Japanese Americans living in King County, WA, who had a mean age of 71.8 years and were dementia-free at baseline (1992-1994), and were followed for incident dementia through 2001. Cox proportional hazards models were used to estimate the risk of dementia, Alzheimer disease (AD), and vascular dementia (VaD) controlling for demographic and lifestyle characteristics and vascular comorbidities as a function of baseline BMI, WC, and WHR and change in BMI over time. RESULTS: Higher baseline BMI was significantly associated with a reduced risk of AD (hazard ratio [HR] = 0.56, 95% confidence interval [CI] = 0.33-0.97) in the fully adjusted model. Slower rate of decline in BMI was associated with a reduced risk of dementia (HR = 0.37, 95% CI = 0.14-0.98), with the association stronger for those who were overweight or obese (HR = 0.18, 95% CI = 0.05-0.58) compared to normal or underweight (HR = 1.00, 95% CI = 0.18-5.66) at baseline. CONCLUSION: Higher baseline body mass index (BMI) and slower declining BMI in late life are associated with a reduced risk of dementia, suggesting that low BMI or a faster decline in BMI in late life may be preclinical indicators of an underlying dementing illness, especially for those who were initially overweight or obese.

 

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Learning Abilities May Decrease During Menopause Transition, Then Rebound

05-28-2009

 

A new study suggests that learning abilities decrease during perimenopause and then rebound to premenopausal levels afterward.The data, from more than 2000 women in the Study of Women's Health Across the Nation (SWAN), a cohort study looking at menopausal transition (MT), also suggest that initiation of hormone therapy prior to a woman's last period appeared to provide a cognitive benefit, while initiation after the last period was detrimental."Consistent with transitioning women's perceived memory difficulties, perimenopause was associated with a decrement in cognitive performance, characterized by women not being able to learn as well as they had during premenopause," Gail A. Greendale, MD, from the David Geffen School of Medicine at the University of California, Los Angeles, and colleagues conclude."The good news is that the effect of perimenopause on learning seems to be temporary," Dr. Greendale said in a statement from the American Academy of Neurology (AAN). "Our study found that the amount of learning improved back to premenopausal levels during the postmenopausal stage." 

Abstract:

Effects of the menopause transition and hormone use on cognitive performance in midlife women.

Division of Geriatrics, David Geffen School of Medicine at UCLA, 10945 Le Conte Avenue, Suite 2339, Los Angeles, CA 90095-1687

BACKGROUND: There is almost no longitudinal information about measured cognitive performance during the menopause transition (MT). METHODS: We studied 2,362 participants from the Study of Women's Health Across the Nation for 4 years. Major exposures were time spent in MT stages, hormone use prior to the final menstrual period, and postmenopausal current hormone use. Outcomes were longitudinal performance in three domains: processing speed (Symbol Digit Modalities Test [SDMT]), verbal memory (East Boston Memory Test [EBMT]), and working memory (Digit Span Backward). RESULTS: Premenopausal, early perimenopausal, and postmenopausal women scored higher with repeated SDMT administration (p </= 0.0008), but scores of late perimenopausal women did not improve over time (p = 0.2). EBMT delayed recall scores climbed during premenopause and postmenopause (p </= 0.01), but did not increase during early or late perimenopause (p >/= 0.14). Initial SDMT, EBMT-immediate, and EBMT-delayed tests were 4%-6% higher among prior hormone users (p </= 0.001). On the SDMT and EBMT, compared to the premenopausal referent, postmenopausal current hormone users demonstrated poorer cognitive performance (p </= 0.05) but performance of postmenopausal nonhormone users was indistinguishable from that of premenopausal women. CONCLUSIONS: Consistent with transitioning women's perceived memory difficulties, perimenopause was associated with a decrement in cognitive performance, characterized by women not being able to learn as well as they had during premenopause. Improvement rebounded to premenopausal levels in postmenopause, suggesting that menopause transition-related cognitive difficulties may be time-limited. Hormone initiation prior to the final menstrual period had a beneficial effect whereas initiation after the final menstrual period had a detrimental effect on cognitive performance.

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Statin Therapy After First Stroke Reduces Recurrence and Improves Mortality

05-28-2009

Statin therapy after a first stroke reduces the 10-year risk of recurrent stroke, a new study has shown.   Statin use also reduced the risk of mortality, even after adjustment for potential confounders, such as blood-pressure control, report investigators.

Abstract:

Neurology. 2009 May 26;72(21):1816-22.

Statin therapy after first stroke reduces 10-year stroke recurrence and improves survival.

University of Ioannina School of Medicine, University Campus, 45110 Ioannina, Greece

OBJECTIVE: To determine whether statin therapy after hospital discharge affects ischemic stroke recurrence and long-term mortality in patients admitted for a first-ever occurrence of ischemic stroke. METHODS: This was a retrospective observational study involving linked hospitalization and death records. The cohort comprised a series of 794 consecutive, first-ever acute ischemic stroke patients from the Athenian Stroke Registry, admitted to the acute stroke unit and the general medicine and neurology ward of our institutions since January 1997 for whom there was available information covering a 10-year follow-up period. Cox proportional hazards model was used to identify risk factors for stroke recurrence and death. RESULTS: The recurrence rate was 16.3% among stroke patients not receiving a statin after hospital discharge compared with 7.5% among those who received statin therapy (p = 0.002). Cox regression analyses revealed only statin therapy postdischarge to be a significant independent predictor of stroke recurrence (adjusted hazard ratio [HR], 0.65, 95% confidence interval [CI] 0.39 to 0.97, p < 0.01). Similarly, patients receiving a statin had a significantly lower mortality during the 10-year period after the acute cerebrovascular event (adjusted HR, 0.43; 95% CI 0.29 to 0.61, p < 0.01). CONCLUSIONS: Prescribing statin therapy upon hospital discharge to patients with first-ever acute stroke lowers the risk of 10-year stroke recurrence and improves survival.

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7th International Conference on Frontotemporal Dementias

06-01-2009

October 6-8, 2010

Indianapolis at the Indiana University School of Medicine

Take part in the most comprehensive scientific event on the clinical and biological bases of FTD and related disroders.

http://www.ftd2010.org/

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