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162 results on '"Langbehn, D."'

1. Mild cognitive impairment in prediagnosed Huntington disease(e–Pub ahead of print)

Author

Duff, K, Paulsen, J, Mills, J, Beglinger, LJ, Moser, DJ, Smith, MM, Langbehn, D, Stout, J, Queller, S, and Harrington, DL

Subjects
Rare Diseases, Aging, Alzheimer's Disease, Neurodegenerative, Acquired Cognitive Impairment, Clinical Research, Huntington's Disease, Brain Disorders, Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurosciences, Neurological, Adult, Cognition Disorders, Female, Humans, Huntington Disease, Male, Middle Aged, Predictive Value of Tests, Prospective Studies, Risk Factors, PREDICT-HD Investigators and Coordinators of the Huntington Study Group, Clinical Sciences, Cognitive Sciences, Neurology & Neurosurgery
Abstract

BackgroundCognitive decline has been reported in Huntington disease (HD), as well as in the period before diagnosis of motor symptoms (i.e., pre-HD). However, the severity, frequency, and characterization of cognitive difficulties have not been well-described. Applying similar cutoffs to those used in mild cognitive impairment (MCI) research, the current study examined the rates of subtle cognitive dysfunction (e.g., dysfunction that does not meet criteria for dementia) in pre-HD.MethodsUsing baseline data from 160 non-gene-expanded comparison participants, normative data were established for cognitive tests of episodic memory, processing speed, executive functioning, and visuospatial perception. Cutoff scores at 1.5 standard deviations below the mean of the comparison group were then applied to 575 gene-expanded pre-HD participants from the observational study, PREDICT-HD, who were stratified by motor signs and genetic risk for HD.ResultsNearly 40% of pre-HD individuals met criteria for MCI, and individuals closer to HD diagnosis had higher rates of MCI. Nonamnestic MCI was more common than amnestic MCI. Single-domain MCI was more common than multiple-domain MCI. Within the nonamnestic single-domain subtype, impairments in processing speed were most frequent.ConclusionsConsistent with the Alzheimer disease literature, MCI as a prodromal period is a valid concept in pre-HD, with nearly 40% of individuals showing this level of impairment before diagnosis. Future studies should examine the utility of MCI as a marker of cognitive decline in pre-HD.

Published
2010

2. Intellectual enrichment and genetic modifiers of cognition and brain volume in Huntington's disease.

Author

Papoutsi, M, Flower, M, Hensman Moss, DJ, Holmans, P, Estevez-Fraga, C, Johnson, EB, Scahill, RI, Rees, G, Langbehn, D, Tabrizi, SJ, Track-HD Investigators, Papoutsi, M, Flower, M, Hensman Moss, DJ, Holmans, P, Estevez-Fraga, C, Johnson, EB, Scahill, RI, Rees, G, Langbehn, D, Tabrizi, SJ, and Track-HD Investigators

Abstract

An important step towards the development of treatments for cognitive impairment in ageing and neurodegenerative diseases is to identify genetic and environmental modifiers of cognitive function and understand the mechanism by which they exert an effect. In Huntington's disease, the most common autosomal dominant dementia, a small number of studies have identified intellectual enrichment, i.e. a cognitively stimulating lifestyle and genetic polymorphisms as potential modifiers of cognitive function. The aim of our study was to further investigate the relationship and interaction between genetic factors and intellectual enrichment on cognitive function and brain atrophy in Huntington's disease. For this purpose, we analysed data from Track-HD, a multi-centre longitudinal study in Huntington's disease gene carriers and focused on the role of intellectual enrichment (estimated at baseline) and the genes FAN1, MSH3, BDNF, COMT and MAPT in predicting cognitive decline and brain atrophy. We found that carrying the 3a allele in the MSH3 gene had a positive effect on global cognitive function and brain atrophy in multiple cortical regions, such that 3a allele carriers had a slower rate of cognitive decline and atrophy compared with non-carriers, in agreement with its role in somatic instability. No other genetic predictor had a significant effect on cognitive function and the effect of MSH3 was independent of intellectual enrichment. Intellectual enrichment also had a positive effect on cognitive function; participants with higher intellectual enrichment, i.e. those who were better educated, had higher verbal intelligence and performed an occupation that was intellectually engaging, had better cognitive function overall, in agreement with previous studies in Huntington's disease and other dementias. We also found that intellectual enrichment interacted with the BDNF gene, such that the positive effect of intellectual enrichment was greater in Met66 allele carriers than non

Published
2022

3. Second Annual Huntington Disease Clinical Research Symposium: Organized by the Huntington Study Group

Author

Sabine, Charles, Trembath, K., Churchyard, A., Horton, Z., Tippett, L., Hogg, V., Roxburgh, R., Velakoulis, D., Collins, V., Delatycki, M., Aylward, E., Nopoulos, P., Johnson, H., Juhl, A., Magnotta, V., Pierson, R., Langbehn, D., Ross, C., Paulsen, J., Maltby, Lewis, Poston, K. L., Tang, C., Feigin, A., Ma, Y., Guttman, M., Paulsen, J. S., Dhawan, V., Eidelberg, D., Katz, Russell, Goodman, L. Veatch, Giuliano, J., Lovecky, D., Quaid, K., Dure, L., Goh, A., Yastrubetskaya, O., Chiu, E., Evans, K., Anderson, K., Borowsky, B., Duff, K., Ho, A., Sills, T., Vaccarino, A., Van Kammen, D., Block, R. C., Dorsey, E. R., Beck, C. A., Shoulson, I., Pirogovsky, E., Bartlett, B., Callazo, A., Goldstein, J., Peavy, G., Jacobson, M., Corey-Bloom, J., Gilbert, P., Lessig, S., Peavy, G. M., Weaver, K. E., Richards, T. L., Liang, O., Aylward, E. H., Beglinger, L. J., Adams, W. H., Paulson, H., Fiedorowicz, J. G., Langbehn, D. R., Leserman, A., Conley, K. E., Jubrias, S., Amara, C., Shankland, E., Marcinek, D. J., O’Rourke, J. F., Wang, C., Stout, J. C., Rowe, K., Kloos, A. D., Kegelmeyer, D. A., Kostyk, S. K., Chua, P., Desmond, P., Christensen, S., Steward, C., Judd, F., Lloyd, J., Tress, B., Pugliese, M., Phan, P., Sanchez-Ramos, J., Oster, E., Bausch, J., Shinaman, A., Kayson, E., Oakes, D., Oelke, L., Butterfield, L., Cimino, C., McCall, M., Ling, L., Stell, B., Annis, J., Cha, J., Como, P., PREDICT-HD Investigators of the Huntington Study Group, The Huntington Study Group, FuRST-pHD and PREDICT-HD Investigators and Coordinators of the Huntington Study Group, Huntington Study Group TREND-HD Investigators, PREDICT-HD Investigators of the Huntington Study Group, Huntington Study Group PHAROS Investigators, and Huntington Study Group COHORT Investigators

Published
2009
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4. Inaugural Huntington Disease Clinical Research Symposium Organized by the Huntington Study Group

Author

Moser, Katharine, Biglan, K. M., Ross, C. A., Langbehn, D. R., Aylward, E., Stout, J. C., Queller, S., Carlozzi, N., Duff, K., Beglinger, L. J., Paulsen, J. S., Tomusk, A., Lifer, S., Hastings, S., Dawson, J., Walker, B., Whitlock, K., Johnson, S., Pacifici, Robert, Hersch, S., Dorsey, E. R., Katz, Russell, Tempkin, T., Wheelock, V., Schwartz, G., Corey-Bloom, J., Mattis, P., Feigin, A., Young, P., McArthur, D. L., Perlman, S., Higginson, C., Carr, L., Sigvardt, K., Chirieac, M. C., Shinaman, A., Shoulson, I., Kane, A. E., Peavy, G. M., Goldstein, J. L., Jacobson, M. W., Lessig, S., Wasserman, L., Kayson, E. P., Tang, C., Zgaljardic, D., Ma, Y., Dhawan, V., Guttman, M., Eidelberg, D., Peng, S., Kingsley, P., Rosas, H. D., Gevorkian, S., Oakes, D., Matson, W., Massood, T., Latourelle, J., Mysore, J. Srinidhi, Fossale, E., Gillis, T., Gusella, J. F., MacDonald, M. E., Myers, R. H., Yastrubetskaya, O., Preston, J., Chiu, E., Goh, A., Oster, E., Bausch, J., Kayson, E., Quaid, K., Sims, S., Swenson, M., Harrison, J., Moskowitz, C., Stepanov, N., Suter, G., Westphal, B., Johnson, S. A., Langbehn, D., Paulsen, J., Nopoulos, P., Beglinger, L., Johnson, H., Magnotta, V., Pierson, R., Lipe, H., Bird, T. D., McCusker, E. A., Lownie, A., Lechich, A. J., Montas, S., Duckett, A., Klager, J., Sandler, S., Pae, A., Apostol, B. L., Simmons, D. A., Zuccato, C., Illes, K., Pallos, J., Casale, M., Kathuria, S., Cattaneo, E., Marsh, J. L., Thompson, L. Michels, Patzke, H., Chesworth, R., Li, Z., Rahil, G., Wang, J., Smith, J., Huet, F. L., Shapiro, G., Leit, S., Beaulieu, P., Raeppel, F., Fournel, M., Sainte-Croix, H., Nolan, S. J., Albayya, F. P., Barbier, A., Besterman, J., Ahlijanian, M. K., Deziel, R., Aubeeluck, A., Buchanan, H., Ross, C., Biglan, K., Landwehrmeyer, B., Whitlock, K. B., Carlozzi, N. E., Mickes, L., Lee, J., Kim, R. Y., Di Toro, B., Fine, E., Cahill, T., Johnson, D., Goldstein, J., Peavy, G., Jacobson, M., Goodman, L. Veatch, Como, P. G., Cha, J. H., Beck, C., Adams, M., Chadwick, G., de Blieck, E. A., McCallum, C., Deuel, L., Clarke, A., Stewart, R., Adams, W. H., Paulson, H., Fiedorowicz, J. G., Hanson, J. M., Ramza, N., Priller, J., Ecker, D., PREDICT-HD Investigators of the Huntington Study Group, Huntington Study Group CoHort Investigators, Huntington Study Group PHAROS Investigators, PREDICT-HD Investigators and Coordinators of the Huntington Study Group, Huntington Study Group TREND-HD Investigators, and EHDN Working Group ‘Symptomatic Treatment.’

Published
2008
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5. Third Annual Huntington Disease Clinical Research Symposium: Organized by the Huntington Study Group

Author

Dubinsky, Richard, Roberson, Judy, Battaglia, G., Cannella, M., Riozzi, B., Orobello, S., Maat-Schieman, M. L., Aronica, E., Busceti, C. Letizia, Ciarmiello, A., Alberti, S., Sassone, J., Sipione, S., Bruno, V., Frati, L., Nicoletti, F., Squitieri, F., Rao, A., Gordon, A., Marder, K., Nolta, Jan, Anderson, K., Gruber-Baldini, A., Medalie, J., Reich, S., Fishman, P., Robottom, B., Weiner, W., Shulman, L., Langbehn, D., Paulsen, J., Witten, Celia, Cox, M., Feigin, A., Napolitano, B., Goh, A., Yastrubetskaya, O., Chiu, E., Cloud, L., Helmers, S., Jones, R., Factor, S., Emory, C. Testa, Kegelmeyer, D., Kostyk, S., Fritz, N., Kloos, A., Lessig, S., Goldstein, J., Corey-Bloom, J., Simonelli, M., Martino, T., Colonnese, C., Callaghan, J., Arran, N., Boisse, M. F., Coleman, A., Dar Santos, R., Dumas, E., Hart, E. ’t, Justo, D., Read, J., Say, M., Van Den Bogaard, S., Durr, A., Leavitt, B., Roos, R., Tabrizi, S., Bourdet, C., van Duijn, E., Craufurd, D., Evans, K., Vaccarino, A., Aylward, E., Nopoulos, P., Ross, C., Pierson, R., Mills, J., Magnotta, V., Johnson, H., Mitchell, A., Cortes, J. C., Dahmubed, A., Krakauer, J., Mazzoni, P., Russell, D., Jennings, D., Tamagnan, G., Seibyl, J., Koren, A., Zubal, G., Marek, K., Goodman, L., Carnes, R., Giuliano, J., Vetter, L., MacDonald, M., Lee, J. Min, Seong, I. Sik, Fossale, E., Anderson, M. A., Wheeler, V., Gusella, J., Johnson, J., Yu, T., Jones, D., Chan, A., Richardson, K., McCusker, E., Loy, C., Griffith, J., Paulsen, J. S., Waters, S., Tedroff, J., Kieburtz, K., Krogh, P. Lindskov, Buusman, A., Rembratt, Å., Dorey, J., Lamure, M., Toumi, M., von der Schulenburg, J. -M. Graf, Pettersson, F., Dyhring, T., Sonesson, C., Waters, N., Pontén, H., Erwin, C., Williams, J., Juhl, A., Adams, W., Byars, J., O’Rourke, J., Flynn, A., Fiedorowicz, J., Duff, K., Leserman, A., Beglinger, L., Smith, M., Stout, J., Queller, S., Rao, S., Zimbelman, J., Groves, M., Guttman, M., Wexler, E., Perlman, S., Burgunder, J. -M., Rosenblatt, A., van Kammen, D., PREDICT-HD Investigators of the Huntington Study Group, TRACK-FID Investigators, TRACK-HD Investigators, PREDICT-HD Investigators and Coordinators of the Huntington Study Group, PREDICT-HD Investigators of the Huntington Study Group, Investigators of the Huntington Study Group, Huntington Study Group PHAROS Investigators, and PREDICT-HD Investigators of the Huntington Study Group

Published
2010
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30. Apathy associated with impaired recognition of happy facial expressions in Huntington's disease

Author

Osborne-Crowley, K., Andrews, S.C., Labuschagne, I., Nair, A., Scahill, R., Craufurd, D., Tabrizi, S.J., Stout, J.C., Campbell, C., Campbell, M., Frajman, E., Milchman, C., O'Regan, A., Coleman, A., Santos, R.D., Decolongon, J., Sturrock, A., Bardinet, E., Jauffret, C., Justo, D., Lehericy, S., Marelli, C., Nigaud, K., Pourchot, P., Valabregue, R., Bechtel, N., Bohlen, S., Reilmann, R., Hoffman, A., Kraus, P., Landwehrmeyer, B., Bogaard, S.J.A. van den, Dumas, E.M., Grond, J. van der, t'Hart, E.P., Jurgens, C., Witjes-Ane, M.N., Arran, N., Callaghan, J., Stopford, C., Frost, C., Jones, R., Berna, C., Crawford, H., Fox, N., Gibbard, C., Hobbs, N., Lahiri, N., Malone, I., Ordidge, R., Owen, G., Patel, A., Pepple, T., Read, J., Say, M., Whitehead, D., Wild, E., Keenan, S., Cash, D.M., Hicks, S., Kennard, C., Acharya, T., Axelson, E., Johnson, H., Langbehn, D., Wang, C., Lee, S., Monaco, W., Rosas, H., Queller, S., Whitlock, K., Borowsky, B., Tobin, A., and TRACK-HD Investigators

Subjects
Adult, Male, cognition, Emotions, emotion, apathy, Neuropathology, Article, social behavior, Huntington's disease, Rating scale, cognition disorders, medicine, Humans, Psychological testing, Apathy, Cognitive skill, Facial expression, General Neuroscience, Cognition, Middle Aged, medicine.disease, Facial Expression, Psychiatry and Mental health, Clinical Psychology, Huntington Disease, Social Perception, Female, Neurology (clinical), medicine.symptom, Psychology, Facial Recognition, Clinical psychology, Huntington’s disease
Abstract

Objectives: Previous research has demonstrated an association between emotion recognition and apathy in several neurological conditions involving fronto-striatal pathology, including Parkinson’s disease and brain injury. In line with these findings, we aimed to determine whether apathetic participants with early Huntington’s disease (HD) were more impaired on an emotion recognition task compared to non-apathetic participants and healthy controls. Methods: We included 43 participants from the TRACK-HD study who reported apathy on the Problem Behaviours Assessment – short version (PBA-S), 67 participants who reported no apathy, and 107 controls matched for age, sex, and level of education. During their baseline TRACK-HD visit, participants completed a battery of cognitive and psychological tests including an emotion recognition task, the Hospital Depression and Anxiety Scale (HADS) and were assessed on the PBA-S. Results: Compared to the non-apathetic group and the control group, the apathetic group were impaired on the recognition of happy facial expressions, after controlling for depression symptomology on the HADS and general disease progression (Unified Huntington’s Disease Rating Scale total motor score). This was despite no difference between the apathetic and non-apathetic group on overall cognitive functioning assessed by a cognitive composite score. Conclusions: Impairment of the recognition of happy expressions may be part of the clinical picture of apathy in HD. While shared reliance on frontostriatal pathways may broadly explain associations between emotion recognition and apathy found across several patient groups, further work is needed to determine what relationships exist between recognition of specific emotions, distinct subtypes of apathy and underlying neuropathology. (JINS, 2019, 25, 453–461)

Published
2019

31. Apathy predicts rate of cognitive decline over 24 months in premanifest Huntington's disease.

Author

Andrews, S. C., Langbehn, D. R., Craufurd, D., Durr, A., Leavitt, B. R., Roos, R. A., Tabrizi, S. J., and Stout, J. C.

Subjects
*APATHY, *COGNITION disorders, *RESEARCH, *CONFIDENCE intervals, *AGE distribution, *MEDICAL cooperation, *COGNITION, *GENETIC carriers, *MENTAL depression, *DESCRIPTIVE statistics, *HUNTINGTON disease, *ODDS ratio, *LONGITUDINAL method
Abstract

Background: Cognitive impairment is a core feature of Huntington's disease (HD), however, the onset and rate of cognitive decline is highly variable. Apathy is the most common neuropsychiatric symptom of HD, and is associated with cognitive impairment. The aim of this study was to investigate apathy as a predictor of subsequent cognitive decline over 2 years in premanifest and early HD, using a prospective, longitudinal design. Methods: A total of 118 premanifest HD gene carriers, 111 early HD and 118 healthy control participants from the multi-centre TRACK-HD study were included. Apathy symptoms were assessed at baseline using the apathy severity rating from the Short Problem Behaviours Assessment. A composite of 12 outcome measures from nine cognitive tasks was used to assess cognitive function at baseline and after 24 months. Results: In the premanifest group, after controlling for age, depression and motor signs, more apathy symptoms predicted faster cognitive decline over 2 years. In contrast, in the early HD group, more motor signs, but not apathy, predicted faster subsequent cognitive decline. In the control group, only older age predicted cognitive decline. Conclusions: Our findings indicate that in premanifest HD, apathy is a harbinger for cognitive decline. In contrast, after motor onset, in early diagnosed HD, motor symptom severity more strongly predicts the rate of cognitive decline. [ABSTRACT FROM AUTHOR]

Published
2021
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32. MSH3 modifies somatic instability and disease severity in Huntington's and myotonic dystrophy type 1

Author

Flower, M, Lomeikaite, V, Ciosi, M, Cumming, S, Morales, F, Lo, K, Hensman Moss, D, Jones, L, Holmans, P, Monckton, DG, Tabrizi, SJ, Kraus, P, Hoffman, R, Tobin, A, Borowsky, B, Keenan, S, Whitlock, KB, Queller, S, Campbell, C, Wang, C, Langbehn, D, Axelson, E, Johnson, H, Acharya, T, Cash, DM, Frost, C, Jones, R, Jurgens, C, Hart, EPT, Van Der Grond, J, Witjes- Ane, MNN, Roos, RAC, Dumas, EM, Van Den Bogaard, SJA, Stopford, C, Craufurd, D, Callaghan, J, Arran, N, Rosas, DD, Lee, S, Monaco, W, O'Regan, A, Milchman, C, Frajman, E, Labuschagne, I, Stout, J, Campbell, M, Andrews, SC, Bechtel, N, Reilmann, R, Bohlen, S, Kennard, C, Berna, C, Hicks, S, Durr, A, Pourchot, C, Bardinet, E, Nigaud, K, Valabrègue, R, Lehericy, S, Marelli, C, Jauffret, C, Justo, D, Leavitt, B, Decolongon, J, Sturrock, A, Coleman, A, Dar Santos, R, Patel, A, Gibbard, C, Whitehead, D, Wild, E, Owen, G, Crawford, H, Malone, I, Lahiri, N, Fox, NC, Hobbs, NZ, Scahill, RI, Ordidge, R, Pepple, T, Read, J, Say, MJ, Landwehrmeyer, B, Daidj, F, Bassez, G, Lignier, B, Couppey, F, Delmas, S, Deux, JF, Hankiewicz, K, Dogan, C, Minier, L, Chevalier, P, Hamadouche, A, Catt, M, Van Hees, V, Catt, S, Schwalber, A, Dittrich, J, Flower, M, Lomeikaite, V, Ciosi, M, Cumming, S, Morales, F, Lo, K, Hensman Moss, D, Jones, L, Holmans, P, Monckton, DG, Tabrizi, SJ, Kraus, P, Hoffman, R, Tobin, A, Borowsky, B, Keenan, S, Whitlock, KB, Queller, S, Campbell, C, Wang, C, Langbehn, D, Axelson, E, Johnson, H, Acharya, T, Cash, DM, Frost, C, Jones, R, Jurgens, C, Hart, EPT, Van Der Grond, J, Witjes- Ane, MNN, Roos, RAC, Dumas, EM, Van Den Bogaard, SJA, Stopford, C, Craufurd, D, Callaghan, J, Arran, N, Rosas, DD, Lee, S, Monaco, W, O'Regan, A, Milchman, C, Frajman, E, Labuschagne, I, Stout, J, Campbell, M, Andrews, SC, Bechtel, N, Reilmann, R, Bohlen, S, Kennard, C, Berna, C, Hicks, S, Durr, A, Pourchot, C, Bardinet, E, Nigaud, K, Valabrègue, R, Lehericy, S, Marelli, C, Jauffret, C, Justo, D, Leavitt, B, Decolongon, J, Sturrock, A, Coleman, A, Dar Santos, R, Patel, A, Gibbard, C, Whitehead, D, Wild, E, Owen, G, Crawford, H, Malone, I, Lahiri, N, Fox, NC, Hobbs, NZ, Scahill, RI, Ordidge, R, Pepple, T, Read, J, Say, MJ, Landwehrmeyer, B, Daidj, F, Bassez, G, Lignier, B, Couppey, F, Delmas, S, Deux, JF, Hankiewicz, K, Dogan, C, Minier, L, Chevalier, P, Hamadouche, A, Catt, M, Van Hees, V, Catt, S, Schwalber, A, and Dittrich, J

Abstract

The mismatch repair gene MSH3 has been implicated as a genetic modifier of the CAG·CTG repeat expansion disorders Huntington's disease and myotonic dystrophy type 1. A recent Huntington's disease genome-wide association study found rs557874766, an imputed single nucleotide polymorphism located within a polymorphic 9 bp tandem repeat in MSH3/DHFR, as the variant most significantly associated with progression in Huntington's disease. Using Illumina sequencing in Huntington's disease and myotonic dystrophy type 1 subjects, we show that rs557874766 is an alignment artefact, the minor allele for which corresponds to a three-repeat allele in MSH3 exon 1 that is associated with a reduced rate of somatic CAG·CTG expansion (P = 0.004) and delayed disease onset (P = 0.003) in both Huntington's disease and myotonic dystrophy type 1, and slower progression (P = 3.86 × 10-7) in Huntington's disease. RNA-Seq of whole blood in the Huntington's disease subjects found that repeat variants are associated with MSH3 and DHFR expression. A transcriptome-wide association study in the Huntington's disease cohort found increased MSH3 and DHFR expression are associated with disease progression. These results suggest that variation in the MSH3 exon 1 repeat region influences somatic expansion and disease phenotype in Huntington's disease and myotonic dystrophy type 1, and suggests a common DNA repair mechanism operates in both repeat expansion diseases.

Published
2019

34. Natural variation in sensory-motor white matter organization influences manifestations of Huntington's disease

Author

Orth, M., Gregory, S., Scahill, R.I., Mayer, I.S.M., Minkova, L., Kloppel, S., Seunarine, K.K., Boyd, L., Borowsky, B., Reilmann, R., Landwehrmeyer, G.B., Leavitt, B.R., Roos, R.A.C., Durr, A., Rees, G., Rothwell, J.C., Langbehn, D., Tabrizi, S.J., and TRACK-On Investigators

Subjects
biological variation, effective connectivity, principal component analysis, grip force, somatosensory evoked potentials, cortical thickness, biological trait
Published
2016

35. Association of HOPA polymorphisms with Major Depression and Phobia

Author

Philibert, R.A., Kaspers, K., Langbehn, D., Troughton, E.P., Yucuis, R., Sandhu, H.K., and Cadoret, R.J.

Subjects
Human genetics -- Research, Genetic disorders -- Research, Central nervous system -- Physiological aspects, Depression, Mental -- Genetic aspects, Psychoses -- Genetic aspects, Hypothyroidism -- Genetic aspects, Biological sciences
Published
2001

36. The Iowa Personality Disorder Screen: A validation study in a psychiatric population that receives long‐term group psychotherapy for personality related problems.

Author

Selvik, S. G., Hummelen, B., Romild, U., Langbehn, D. R., and Pedersen, G.

Subjects
PERSONALITY disorder diagnosis, PERSONALITY disorder treatment, CLASSIFICATION, GROUP psychotherapy, LONG-term health care, RESEARCH methodology, PATIENTS, PERSONALITY tests, PSYCHODYNAMIC psychotherapy, PSYCHOTHERAPY, PSYCHOTHERAPY patients, PREDICTIVE tests, RESEARCH methodology evaluation
Abstract

Abstract: Personality disorder (PD) is common among psychiatric patients, and diagnosing such disorders is of great importance for the choice of treatment. Diagnosing PD is a demanding and time‐consuming process. The utilities of several PD screening instruments have been studied in different populations, but not in a population who receives long‐term group psychotherapy. In the current study, we investigate the predictive properties of the Iowa Personality Disorder Screen (IPDS) in a sample of 694 psychiatric outpatients with and without PD who were admitted for psychodynamic long‐term group therapy from 2012 to 2014. The definitive, reference diagnoses were defined according to the SCID‐II, by which 484 patients (68%) warranted a PD diagnosis. The IPDS correctly classified 67.4 percent of all participants. Sensitivity (0.75) and specificity (0.51) were lower than in previous validation studies of IPDS. We discuss possible explanations related to the general concept of PD and, more specifically, to our study sample. Because of the weaker predictive properties of IPDS, we advise caution in use of the IPDS in similar clinical settings. Copyright © 2018 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Published
2018
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39. Mild cognitive impairment in prediagnosed Huntington disease.

Author

Duff, K, Duff, K, Paulsen, J, Mills, J, Beglinger, LJ, Moser, DJ, Smith, MM, Langbehn, D, Stout, J, Queller, S, Harrington, DL, PREDICT-HD Investigators and Coordinators of the Huntington Study Group, Duff, K, Duff, K, Paulsen, J, Mills, J, Beglinger, LJ, Moser, DJ, Smith, MM, Langbehn, D, Stout, J, Queller, S, Harrington, DL, and PREDICT-HD Investigators and Coordinators of the Huntington Study Group

Abstract

BackgroundCognitive decline has been reported in Huntington disease (HD), as well as in the period before diagnosis of motor symptoms (i.e., pre-HD). However, the severity, frequency, and characterization of cognitive difficulties have not been well-described. Applying similar cutoffs to those used in mild cognitive impairment (MCI) research, the current study examined the rates of subtle cognitive dysfunction (e.g., dysfunction that does not meet criteria for dementia) in pre-HD.MethodsUsing baseline data from 160 non-gene-expanded comparison participants, normative data were established for cognitive tests of episodic memory, processing speed, executive functioning, and visuospatial perception. Cutoff scores at 1.5 standard deviations below the mean of the comparison group were then applied to 575 gene-expanded pre-HD participants from the observational study, PREDICT-HD, who were stratified by motor signs and genetic risk for HD.ResultsNearly 40% of pre-HD individuals met criteria for MCI, and individuals closer to HD diagnosis had higher rates of MCI. Nonamnestic MCI was more common than amnestic MCI. Single-domain MCI was more common than multiple-domain MCI. Within the nonamnestic single-domain subtype, impairments in processing speed were most frequent.ConclusionsConsistent with the Alzheimer disease literature, MCI as a prodromal period is a valid concept in pre-HD, with nearly 40% of individuals showing this level of impairment before diagnosis. Future studies should examine the utility of MCI as a marker of cognitive decline in pre-HD.

Published
2010

41. Tapping linked to function and structure in premanifest and symptomatic Huntington disease

Author

Bechtel, N., primary, Scahill, R. I., additional, Rosas, H. D., additional, Acharya, T., additional, van den Bogaard, S. J. A., additional, Jauffret, C., additional, Say, M. J., additional, Sturrock, A., additional, Johnson, H., additional, Onorato, C. E., additional, Salat, D. H., additional, Durr, A., additional, Leavitt, B. R., additional, Roos, R. A. C., additional, Landwehrmeyer, G. B., additional, Langbehn, D. R., additional, Stout, J. C., additional, Tabrizi, S. J., additional, and Reilmann, R., additional

Published
2010
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42. F14 Speeded tapping assesses progression of huntington's disease within one year—results from the track-HD study

Author

Bechtel, N, primary, Acharya, T, additional, Sturrock, A, additional, Jauffret, C, additional, Say, M J, additional, Patel, A, additional, Read, J E, additional, t'Hart, E, additional, van den Bogaard, S J A, additional, Dürr, A, additional, Leavitt, B R, additional, Roos, R A C, additional, Langbehn, D R, additional, Tabrizi, S J, additional, and Reilmann, R, additional

Published
2010
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46. Acid-Sensing Ion Channel-1a in the Amygdala, a Novel Therapeutic Target in Depression-Related Behavior

Author

Coryell, M. W., primary, Wunsch, A. M., additional, Haenfler, J. M., additional, Allen, J. E., additional, Schnizler, M., additional, Ziemann, A. E., additional, Cook, M. N., additional, Dunning, J. P., additional, Price, M. P., additional, Rainier, J. D., additional, Liu, Z., additional, Light, A. R., additional, Langbehn, D. R., additional, and Wemmie, J. A., additional

Published
2009
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