Skip header and navigation

Refine By

18 records – page 1 of 2.

[Alzheimer's and related diseases: toward earlier and more accurate diagnosis].

https://arctichealth.org/en/permalink/ahliterature140023
Source
Rev Med Interne. 2010 Dec;31(12):846-53
Publication Type
Article
Date
Dec-2010
Author
M-P Fortin
P. Krolak-Salmon
Author Affiliation
Centre hospitalier affilié universitaire, hôpital de l'Enfant-Jésus, 1401, 18(e) rue, Québec, G1J 1Z4, Canada. mariefortin41@hotmail.com
Source
Rev Med Interne. 2010 Dec;31(12):846-53
Date
Dec-2010
Language
French
Publication Type
Article
Keywords
Alzheimer Disease - cerebrospinal fluid - diagnosis - epidemiology - radionuclide imaging
Amyloid beta-Protein Precursor - cerebrospinal fluid
Biological Markers - cerebrospinal fluid
Canada - epidemiology
Dementia - diagnosis
Diagnosis, Differential
Early Diagnosis
Hippocampus - pathology - radionuclide imaging
Humans
Positron-Emission Tomography
Predictive value of tests
Sensitivity and specificity
Tomography, Emission-Computed, Single-Photon
tau Proteins - cerebrospinal fluid
Abstract
Because of population ageing, the prevalence of Alzheimer's disease (AD), the most common cause of dementia, increases progressively. This condition is now considered as a public health priority. New disease modifying therapeutic strategies could be available in the next few years that would necessitate an accurate and early diagnosis of the disease. Recently developed diagnostic tools are being assessed. Development of structural brain imaging allows to measure the hippocampus volume. Metabolic imaging can assess a broad range of functional parameters such as cerebral blood flow and dopaminergic activity with single photon emission computed tomography, cerebral glucose metabolism and cerebral amyloid burden with positron emission tomography. Those imaging methods are under evaluation to appreciate cerebral abnormalities that may occur earlier than structural ones. Cerebrospinal fluid biomarkers, in particular amyloid and tau peptides, allow us to look at in vivo biochemical cerebral changes related to AD, before possible serum biomarkers. Studies are under way to confirm the relevance of these new diagnostic tools. It will help us to improve evaluation of patients with AD or related diseases.
PubMed ID
20952104 View in PubMed
Less detail

Association between duration of untreated psychosis and brain morphology in schizophrenia within the Northern Finland 1966 Birth Cohort.

https://arctichealth.org/en/permalink/ahliterature140885
Source
Schizophr Res. 2010 Nov;123(2-3):145-52
Publication Type
Article
Date
Nov-2010
Author
Matti Penttilä
Erika Jääskeläinen
Marianne Haapea
Päivikki Tanskanen
Juha Veijola
Khanum Ridler
Graham K Murray
Anna Barnes
Peter B Jones
Matti Isohanni
Hannu Koponen
Jouko Miettunen
Author Affiliation
University of Oulu, Institute of Clinical Medicine, Department of Psychiatry, P.O. Box 5000, FIN-90014 Oulu, Finland. mattipen@mail.student.oulu.fi
Source
Schizophr Res. 2010 Nov;123(2-3):145-52
Date
Nov-2010
Language
English
Publication Type
Article
Keywords
Adult
Brain - pathology
Diagnostic and Statistical Manual of Mental Disorders
Female
Finland - epidemiology
Follow-Up Studies
Functional Laterality
Hippocampus - pathology
Humans
Limbic System - pathology
Magnetic Resonance Imaging
Male
Medical Records Systems, Computerized
Psychotic Disorders - etiology - pathology
Regression Analysis
Schizophrenia - diagnosis - pathology
Schizophrenic Psychology
Time Factors
Abstract
Duration of untreated psychosis (DUP) has been linked with poor prognosis and changes in the brain structure in schizophrenia at least at the beginning of the disease, but it is still unknown whether DUP relates to brain morphometry in the longer term. Our aim was to analyze the relation between DUP and the brain structure in schizophrenia in the general population, after several years of illness.
Brains of subjects with psychosis from the Northern Finland 1966 Birth Cohort (NFBC 1966) were scanned with MRI during 1999-2001 after an 11-year follow-up. DUP was assessed from medical records and regressed against global and local tissue density measurements. The brain morphometric and the DUP information were available for 46 subjects with DSM-III-R schizophrenia.
The DUP did not correlate with volumes of the total gray or white matter or the cerebrospinal fluid. The length of DUP associated positively with reduced densities of the right limbic area and the right hippocampus.
Long DUP was slightly associated with reductions of gray matter densities in the limbic area and especially the hippocampus after several years follow-up, supporting the hypothesis that, compared to short DUP, long DUP might be a marker of different disease trajectories including subtle morphometric changes.
PubMed ID
20832996 View in PubMed
Less detail

Cardiovascular regulation and hippocampal sclerosis.

https://arctichealth.org/en/permalink/ahliterature53303
Source
Epilepsia. 2004 Aug;45(8):933-9
Publication Type
Article
Date
Aug-2004
Author
Hanna Ansakorpi
Juha T Korpelainen
Päivikki Tanskanen
Heikki V Huikuri
Antero Koivula
Uolevi Tolonen
Juhani Pyhtinen
Vilho V Myllylä
Jouko I T Isojärvi
Author Affiliation
Department of Neurology, University of Oulu, Finland. Hanna.Ansakorpi@oulu.fi
Source
Epilepsia. 2004 Aug;45(8):933-9
Date
Aug-2004
Language
English
Publication Type
Article
Keywords
Adult
Arrhythmia - diagnosis - physiopathology
Autonomic Nervous System - physiopathology
Cardiovascular System - physiopathology
Circadian Rhythm - physiology
Comparative Study
Electroencephalography - statistics & numerical data
Epilepsy, Temporal Lobe - pathology - physiopathology
Female
Heart Function Tests
Heart Rate - physiology
Hippocampus - pathology
Humans
Laterality
Magnetic Resonance Imaging
Male
Monitoring, Physiologic - statistics & numerical data
Sclerosis
Abstract
PURPOSE: Cardiovascular dysregulation has been detected in patients with temporal lobe epilepsy (TLE) by using cardiovascular reflex tests and analysis of heart rate variability (HRV). The two methods have not previously been used in the same study to compare them in the assessment of cardioregulatory function. Magnetic resonance imaging (MRI) is considered the best method to reveal structural changes such as hippocampal sclerosis associated with TLE. It is not known whether these structural changes modify cardioregulatory function in patients with TLE. METHODS: Standard cardiovascular reflex tests and analysis of spectral and dynamic measures from 24-h electrocardiogram (ECG) recordings were performed for eight patients with and 31 patients without hippocampal sclerosis and for 72 control subjects. MRI also was performed in each patient to reveal hippocampal sclerosis. RESULTS: Various measures of cardiovascular reflexes and HRV were diminished in patients with TLE compared with the control subjects. No significant differences were found in the measures obtained from the cardiovascular reflex tests or analysis of HRV between those with and without hippocampal sclerosis, although a nonsignificant trend toward reduced values was seen among those with hippocampal sclerosis. The values of cardiovascular reflexes and spectral analysis of HRV correlated with each other. CONCLUSIONS: These results suggest that functional rather than structural changes related to TLE are involved mainly as a mechanism of altered cardioregulatory function. The cardiovascular reflex test and analysis of HRV both appear to be useful in studying cardioregulation in patients with TLE.
PubMed ID
15270759 View in PubMed
Less detail

Comparison between visual assessment of MTA and hippocampal volumes in an elderly, non-demented population.

https://arctichealth.org/en/permalink/ahliterature124309
Source
Acta Radiol. 2012 Jun 1;53(5):573-9
Publication Type
Article
Date
Jun-1-2012
Author
Lena Cavallin
Lena Bronge
Yi Zhang
Anne-Rita Oksengård
Lars-Olof Wahlund
Laura Fratiglioni
Rimma Axelsson
Author Affiliation
CLINTEC, Division of Medical Imaging and Technology, Karolinska Institute, Karolinska University Hospital, Huddinge, Stockholm, Sweden. lena.cavallin@karolinska.se
Source
Acta Radiol. 2012 Jun 1;53(5):573-9
Date
Jun-1-2012
Language
English
Publication Type
Article
Keywords
Aged
Aging - physiology
Analysis of Variance
Atrophy - pathology
Female
Hippocampus - pathology
Humans
Image Interpretation, Computer-Assisted
Magnetic Resonance Imaging - methods
Male
Middle Aged
Reference Values
Reproducibility of Results
Sweden
Temporal Lobe - pathology
Abstract
It is important to have a replicable easy method for monitoring atrophy progression in Alzheimer's disease. Volumetric methods for calculating hippocampal volume are time-consuming and commonly used in research. Visual assessments of medial temporal lobe atrophy (vaMTA) is a rapid method for clinical use. This method has not been tested in a large non-demented population in comparison with volumetry measurements. Since hippocampal volume decreases with time even in normal aging there is also a need to study the normal age differences of medial temporal lobe atrophy.
To compare visual assessment of medial temporal lobe atrophy (vaMTA) with hippocampal volume in a healthy, non-demented elderly population. To describe normal ageing using vaMTA.
Non-demented individuals aged 60, 66, 72, 78, 81, 84, and =87 years old were recruited from the Swedish National study on Ageing and Care in Kungsholmen (SNAC-K), Sweden. Standard magnetic resonance imaging (MRI) scans, vaMTA, and calculations of hippocampal volumes were performed in 544 subjects.
Significant correlation (r(s) = -0.32, P 80-year-old individuals.
PubMed ID
22593123 View in PubMed
Less detail

Comparison of imaging biomarkers in the Alzheimer Disease Neuroimaging Initiative and the Mayo Clinic Study of Aging.

https://arctichealth.org/en/permalink/ahliterature122721
Source
Arch Neurol. 2012 May;69(5):614-22
Publication Type
Article
Date
May-2012
Author
Jennifer L Whitwell
Heather J Wiste
Stephen D Weigand
Walter A Rocca
David S Knopman
Rosebud O Roberts
Bradley F Boeve
Ronald C Petersen
Clifford R Jack
Author Affiliation
Department of Radiology, College of Medicine, Mayo Clinic, Rochester, MN 55905, USA. whitwell.jennifer@mayo.edu
Source
Arch Neurol. 2012 May;69(5):614-22
Date
May-2012
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Aging
Alzheimer Disease - complications - epidemiology - pathology
Biological Markers
Canada
Case-Control Studies
Cognition Disorders - etiology - pathology
Cohort Studies
Community Health Planning
Cross-Sectional Studies
Female
Hippocampus - pathology
Humans
Imaging, Three-Dimensional
Magnetic Resonance Imaging
Male
Mental Status Schedule
Questionnaires
United States
Abstract
To determine whether magnetic resonance imaging measurements observed in the Alzheimer Disease Neuroimaging Initiative (ADNI) convenience sample differ from those observed in the Mayo Clinic Study of Aging (MCSA) population-based sample.
Comparison of 2 samples.
Fifty-nine recruiting sites for the ADNI in the United States and Canada and the MCSA, a population-based cohort in Olmsted County, Minnesota.
Cognitively normal subjects and amnestic subjects with mild cognitive impairment were selected from the ADNI convenience cohort and MCSA population-based cohort. A simple random sample of subjects from both cohorts in the same age range was selected, and a second sample applied matching for age, sex, educational level, apolipoprotein E genotype, and Mini-Mental State Examination score.
Baseline hippocampal volumes and annual percentage of decline in hippocampal volume.
In the population-based sample, MCSA subjects were older, had less education, performed worse on the Mini-Mental State Examination, and had a family history of Alzheimer disease less often than did ADNI subjects. Baseline hippocampal volumes were larger in ADNI compared with MCSA cognitively normal subjects in the random sample, although no differences were observed after matching. Rates of decline in hippocampal volume were greater in the ADNI compared with the MCSA for cognitively normal subjects and those with amnestic mild cognitive impairment, even after matching.
Rates of decline in hippocampal volume suggest that ADNI subjects have a more aggressive brain pathologic process than MCSA subjects and hence may not be representative of the general population. These findings have implications for treatment trials that use ADNI-like recruitment mechanisms and for studies validating new diagnostic criteria for Alzheimer disease in its various stages.
Notes
Cites: Ann Neurol. 2009 Aug;66(2):200-819743450
Cites: Neurology. 2008 May 6;70(19 Pt 2):1778-8518184916
Cites: Neuroimage. 2009 Apr 15;45(3):855-6619162198
Cites: Neurology. 2009 Oct 13;73(15):1193-919822868
Cites: Acta Neuropathol. 2010 Apr;119(4):421-3320204386
Cites: J Alzheimers Dis. 2009;18(3):691-70119749406
Cites: Brain. 2010 Apr;133(Pt 4):1163-7220375138
Cites: Neurology. 2010 Sep 7;75(10):889-9720820000
Cites: J Am Geriatr Soc. 2010 Oct;58(10):1903-1020840461
Cites: Neurology. 2010 Nov 23;75(21):1879-8721098403
Cites: Alzheimers Dement. 2011 Jan;7(1):53-6021255743
Cites: Alzheimer Dis Assoc Disord. 2011 Jan-Mar;25(1):4-1020921881
Cites: Am J Epidemiol. 2011 May 1;173(9):1059-6821430193
Cites: Neurobiol Aging. 2011 Oct;32(10):1733-4120005012
Cites: J Geriatr Psychiatry Neurol. 1995 Oct;8(4):203-88561832
Cites: Neurology. 2002 Mar 12;58(5):750-711889239
Cites: Neuroreport. 2002 Oct 28;13(15):1939-4312395096
Cites: Neurology. 2003 Jan 28;60(2):253-6012552040
Cites: J Intern Med. 2004 Sep;256(3):183-9415324362
Cites: J Psychiatr Res. 1975 Nov;12(3):189-981202204
Cites: Neurology. 1993 Nov;43(11):2412-48232972
Cites: Mayo Clin Proc. 1996 Mar;71(3):266-748594285
Cites: J Clin Epidemiol. 1996 Jan;49(1):79-838598515
Cites: J Am Geriatr Soc. 1996 Jun;44(6):704-78642164
Cites: Brain. 1996 Dec;119 ( Pt 6):2001-79010004
Cites: IEEE Trans Med Imaging. 1998 Feb;17(1):87-979617910
Cites: AJNR Am J Neuroradiol. 1999 Feb;20(2):207-1110094339
Cites: Neurology. 1999 Apr 22;52(7):1397-40310227624
Cites: Stat Med. 2006 Feb 28;25(4):591-60216143965
Cites: Neuroimaging Clin N Am. 2005 Nov;15(4):869-77, xi-xii16443497
Cites: Neuroimage. 2006 Apr 1;30(2):436-4316300968
Cites: Arch Neurol. 2006 May;63(5):674-8116682537
Cites: J Neurol. 2006 Sep;253(9):1147-5316998650
Cites: Brain. 2007 Jul;130(Pt 7):1777-8617533169
Cites: Ann Hum Biol. 2007 Nov-Dec;34(6):593-60618092205
Cites: Neurology. 2008 Feb 12;70(7):512-2017898323
Cites: Brain. 2008 Mar;131(Pt 3):665-8018263627
Cites: Neuroepidemiology. 2008;30(1):58-6918259084
Cites: J Magn Reson Imaging. 2008 Apr;27(4):685-9118302232
Cites: Neuron. 2002 Jan 31;33(3):341-5511832223
Cites: Epilepsia. 2001 Aug;42(8):1021-411554888
Cites: Neurology. 2008 May 6;70(19 Pt 2):1740-5218032747
PubMed ID
22782510 View in PubMed
Less detail

Do cardiovascular risk factors explain the link between white matter hyperintensities and brain volumes in old age? A population-based study.

https://arctichealth.org/en/permalink/ahliterature267460
Source
Eur J Neurol. 2014 Aug;21(8):1076-82
Publication Type
Article
Date
Aug-2014
Author
R. Wang
L. Fratiglioni
A. Laveskog
G. Kalpouzos
C-H Ehrenkrona
Y. Zhang
L. Bronge
L-O Wahlund
L. Bäckman
C. Qiu
Source
Eur J Neurol. 2014 Aug;21(8):1076-82
Date
Aug-2014
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Aging - pathology
Apolipoproteins E - genetics
Atrophy - pathology
Cardiovascular Diseases - epidemiology
Cerebral Ventricles - pathology
Female
Genotype
Gray Matter - pathology
Hippocampus - pathology
Humans
Leukoencephalopathies - epidemiology - pathology
Magnetic Resonance Imaging
Male
Middle Aged
Risk factors
Sweden - epidemiology
White Matter - pathology
Abstract
White matter hyperintensities (WMHs) and brain atrophy frequently coexist in older people. However, it is unclear whether the association between these two brain lesions is dependent on the aging process, a vascular mechanism or genetic susceptibility. It was therefore investigated whether the association between load of WMHs and brain atrophy measures is related to age, vascular risk factors (VRFs) or the APOE-e4 allele.
This population-based study included 492 participants (age =60 years, 59.6% women) free of dementia and stroke. Data on demographics, VRFs and APOE genotypes were collected through interviews, clinical examination and laboratory tests. WMHs on magnetic resonance images were assessed using manual visual rating and automatic volumetric segmentation. Hippocampal and ventricular volumes were manually delineated, whereas total gray matter (GM) volume was measured by automatic segmentation. Data were analyzed with multivariate linear regression models.
More global WMHs, assessed using either a visual rating scale or a volumetric approach, were significantly associated with lower GM volume and higher ventricular volume; the associations remained significant after adjusting for age, VRFs and the APOE-e4 allele. In contrast, the association between global WMHs and hippocampal volume was no longer significant after adjusting for age, whereas adjustment for VRFs and APOE-e4 had no influential effect.
The association of global WMHs with lower GM volume and higher ventricular volume is independent of age, VRFs and APOE-e4 allele, suggesting that the process of cerebral microvascular disease and neurodegeneration are associated independently of the normal aging process, vascular mechanisms or genetic susceptibility.
PubMed ID
24313901 View in PubMed
Less detail

Febrile seizures and mesial temporal sclerosis: No association in a long-term follow-up study.

https://arctichealth.org/en/permalink/ahliterature31156
Source
Neurology. 2003 Jan 28;60(2):215-8
Publication Type
Article
Date
Jan-28-2003
Author
R. Tarkka
E. Pääkkö
J. Pyhtinen
M. Uhari
H. Rantala
Author Affiliation
Department of Pediatrics, University of Oulu, Finland.
Source
Neurology. 2003 Jan 28;60(2):215-8
Date
Jan-28-2003
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age of Onset
Amygdala - pathology
Brain Diseases - diagnosis - epidemiology
Causality
Child
Comorbidity
Comparative Study
Female
Finland - epidemiology
Follow-Up Studies
Hippocampus - pathology
Humans
Magnetic Resonance Imaging
Male
Recurrence
Research Support, Non-U.S. Gov't
Sclerosis
Seizures, Febrile - epidemiology
Temporal Lobe - pathology
Time
Abstract
OBJECTIVE: To determine whether febrile seizures cause mesial temporal sclerosis (MTS), the occurrence of MTS was evaluated in an unselected series of patients with febrile seizures. METHODS: Twenty-four patients with a prolonged first febrile seizure, 8 with an unprovoked seizure after the first febrile seizure, and 32 age-, sex-, and handedness-matched control subjects with a single simple febrile seizure without later unprovoked seizures were selected from 329 febrile seizure patients followed up prospectively. The occurrence of MTS was evaluated after a mean follow-up time of 12.3 years by MR volumetry of amygdala and hippocampal formation and qualitative analysis of mesial temporal structures. RESULTS: None of the patients had MTS. The mean total volumes of the right and left hippocampal formations and amygdala did not differ significantly between any of the three groups. The qualitative analysis revealed no sclerotic changes in the mesial temporal area. The patients with a prolonged initial febrile seizure had a lower mean right-left volume difference in hippocampal formations than the control subjects, but this had no effect on the outcome. CONCLUSION: The occurrence of MTS following even prolonged febrile seizures is an uncommon event, confirming the good clinical outcome of febrile seizures.
Notes
Comment In: Neurology. 2003 Aug 26;61(4):588; author reply 588-912939457
Comment In: Neurology. 2003 Jan 28;60(2):E1-212552071
PubMed ID
12552033 View in PubMed
Less detail

From lateral to mesial: the quest for a surgical cure for temporal lobe epilepsy.

https://arctichealth.org/en/permalink/ahliterature161167
Source
Epilepsia. 2008 Jan;49(1):98-107
Publication Type
Article
Date
Jan-2008
Author
Antonio Nogueira de Almeida
Manoel Jacoben Teixeira
William Howard Feindel
Author Affiliation
Departamento de Neurologia do Hospital das Clinicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil. almeidaan@globo.com
Source
Epilepsia. 2008 Jan;49(1):98-107
Date
Jan-2008
Language
English
Publication Type
Article
Keywords
Academies and Institutes - history
Amygdala - physiopathology
Anterior Temporal Lobectomy - history
Canada
Cooperative Behavior
Electroencephalography - history
Epilepsy, Complex Partial - pathology - surgery
Epilepsy, Temporal Lobe - history - pathology - surgery
Hippocampus - pathology - physiopathology - surgery
History, 20th Century
Humans
Neurology - history
Neurophysiology - history
Neurosurgical Procedures - history
Sclerosis
Temporal Lobe - pathology - surgery
Abstract
A gap of more than a hundred years occurred between the first accounts of mesial temporal sclerosis and recognition of its role in the pathogenesis of psychomotor seizures. This paper reviews how the understanding and surgical treatment of temporal lobe epilepsy developed, particularly from the work of Penfield, Jasper, and their associates at the Montreal Neurological Institute (MNI).
Publications on EEG and surgery for temporal lobe seizures from 1935 to 1953 were reviewed and charts of selected patients operated on at the MNI in the same period were examined. Attention was focused on the evolution of surgical techniques for temporal lobe epilepsy.
In the late 1930s, some EEG findings suggested deep-lying disturbances originating in the temporal lobe. However, it took another two decades before the correlation of clinical, neurophysiological, and anatomical findings provided evidence for the involvement of the mesial structures in psychomotor or temporal lobe seizures. From 1949 and onward, Penfield and his associates applied this evidence to extend the surgical resections to include the uncus and the hippocampus.
The collaborative work of a team led by Penfield and Jasper at the MNI helped to define the role of neurophysiological studies in epilepsy surgery. As a result, the importance of removing the mesial structures in order to obtain better seizure control in patients with temporal lobe epilepsy became firmly established.
Notes
Comment In: Epilepsia. 2008 Mar;49(3):543-418302632
PubMed ID
17888076 View in PubMed
Less detail

Hippocampal and ventricular changes in Parkinson's disease mild cognitive impairment.

https://arctichealth.org/en/permalink/ahliterature132469
Source
Neurobiol Aging. 2012 Sep;33(9):2113-24
Publication Type
Article
Date
Sep-2012
Author
Liana Apostolova
Guido Alves
Kristy S Hwang
Sona Babakchanian
Kolbjorn S Bronnick
Jan Petter Larsen
Paul M Thompson
Yi-Yu Chou
Ole B Tysnes
Hege K Vefring
Mona K Beyer
Author Affiliation
Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. lapostolova@mednet.ucla.edu
Source
Neurobiol Aging. 2012 Sep;33(9):2113-24
Date
Sep-2012
Language
English
Publication Type
Article
Keywords
Aged
Atrophy - pathology
Brain Mapping
Female
Hippocampus - pathology - physiopathology
Humans
Image Processing, Computer-Assisted
Lateral Ventricles - pathology - physiopathology
Magnetic Resonance Imaging
Male
Middle Aged
Mild Cognitive Impairment - pathology
Neuropsychological Tests
Norway
Parkinson Disease - pathology
Retrospective Studies
Statistics, nonparametric
Abstract
We analyzed T1-weighted brain magnetic resonance imaging data of 100 cognitively normal elderly controls (NC), 127 cognitively normal Parkinson's disease (PD; PDCN) and 31 PD-associated mild cognitive impairment (PDMCI) subjects from the Norwegian ParkWest study. Using automated segmentation methods, followed by the radial distance technique and multiple linear regression we studied the effect of clinical diagnosis on hippocampal and ventricular radial distance while adjusting for age, education, and scanning site. PDCN subjects had significantly smaller bilateral hippocampal radial distance relative to NC. Nonamnestic PDMCI subjects showed smaller right hippocampal radial distance relative to NC. PDMCI subjects showed significant enlargement of all portions of the lateral ventricles relative to NC and significantly larger bilateral temporal and occipital and left frontal lateral ventricular expansion relative to PDCN subjects. Nonamnestic PDMCI subjects showed significant ventricular enlargement spanning all parts of the lateral ventricle while those with amnestic PDMCI showed changes localized to the left occipital horn. Hippocampal atrophy and lateral ventricular enlargement show promise as structural biomarkers for PD.
Notes
Cites: Neurobiol Aging. 2008 Jul;29(7):1027-3917368653
Cites: Neuroimage. 2008 Apr 15;40(3):1003-1518280181
Cites: Neuroimage. 2009 Mar;45(1 Suppl):S3-1519041724
Cites: Neurology. 2009 Mar 31;72(13):1121-619020293
Cites: Eur J Neurol. 2009 Apr;16(4):475-8119187264
Cites: Parkinsonism Relat Disord. 2009 May;15(4):315-718793864
Cites: IEEE Trans Med Imaging. 2010 Jan;29(1):30-4319457748
Cites: Brain. 2009 Nov;132(Pt 11):2958-6919812213
Cites: J Neurol Neurosurg Psychiatry. 2009 Aug;80(8):851-719246476
Cites: Neuroimage. 2010 May 15;51(1):488-9920083211
Cites: Hum Brain Mapp. 2010 May;31(5):786-9720143386
Cites: Mov Disord. 2010 Apr 30;25(6):687-9520437538
Cites: Neurobiol Aging. 2010 Aug;31(8):1386-40020620663
Cites: Mov Disord. 2011 Feb 1;26(2):297-30121412836
Cites: Mov Disord. 2011 Jul;26(8):1443-5021442661
Cites: Neuroimage. 2001 May;13(5):856-7611304082
Cites: Neurosci Lett. 2002 Apr 19;323(1):29-3211911983
Cites: J Neurosci. 2003 Feb 1;23(3):994-100512574429
Cites: Mov Disord. 2003 Jul;18(7):784-9012815657
Cites: Neurosci Lett. 2004 Jan 16;354(3):177-8014700725
Cites: Brain. 2004 Apr;127(Pt 4):791-80014749292
Cites: Dement Geriatr Cogn Disord. 2004;17(4):311-515178943
Cites: Neuroimage. 2004 Aug;22(4):1754-6615275931
Cites: J Neurol Neurosurg Psychiatry. 2004 Oct;75(10):1467-915377698
Cites: Neurology. 1967 May;17(5):427-426067254
Cites: J Psychiatr Res. 1975 Nov;12(3):189-981202204
Cites: J Neurol Neurosurg Psychiatry. 1989 Nov;52(11):1221-72592966
Cites: J Comput Assist Tomogr. 1994 Mar-Apr;18(2):192-2058126267
Cites: Am J Epidemiol. 1995 Dec 15;142(12):1300-57503050
Cites: Neurology. 1996 Jul;47(1):1-98710059
Cites: Neurology. 1997 Sep;49(3):786-949305341
Cites: Mov Disord. 1998;13 Suppl 3:2-239827589
Cites: J Auton Nerv Syst. 1998 Dec 11;74(2-3):189-929915636
Cites: Arch Neurol. 1999 Jan;56(1):33-99923759
Cites: Folia Neuropathol. 2004;42(3):141-5015535032
Cites: Neurology. 2005 Jan 25;64(2):224-915668417
Cites: Neurology. 2005 Mar 8;64(5):861-515753423
Cites: Mov Disord. 2005 May;20(5):540-415645532
Cites: Neurology. 2005 Oct 25;65(8):1239-4516247051
Cites: Mov Disord. 2005 Dec;20(12):1571-616116613
Cites: J Neurol. 2005 Nov;252(11):1345-5215995795
Cites: Neurology. 2005 Dec 27;65(12):1863-7216237129
Cites: Arch Neurol. 2006 May;63(5):693-916682538
Cites: Mov Disord. 2006 Sep;21(9):1343-916721732
Cites: Brain. 2006 Nov;129(Pt 11):2867-7317018552
Cites: Mov Disord. 2007 Jan;22(1):141-517089386
Cites: Neurobiol Aging. 2007 Mar;28(3):389-9716504345
Cites: J Neurol Neurosurg Psychiatry. 2007 Mar;78(3):254-917028119
Cites: Alzheimer Dis Assoc Disord. 2007 Jan-Mar;21(1):14-2417334268
Cites: J Neurol Sci. 2007 Jun 15;257(1-2):97-10417316690
Cites: Neurotherapeutics. 2007 Jul;4(3):387-40017599704
Cites: Arch Neurol. 2007 Oct;64(10):1489-9517923632
Cites: Neuroimage. 2008 Apr 1;40(2):615-3018222096
Cites: Neuroimage. 2008 Oct 15;43(1):59-6818675918
PubMed ID
21813212 View in PubMed
Less detail

Long-term epilepsy surgery outcomes in patients with MRI-negative temporal lobe epilepsy.

https://arctichealth.org/en/permalink/ahliterature138453
Source
Epilepsia. 2010 Nov;51(11):2260-9
Publication Type
Article
Date
Nov-2010
Author
Arto Immonen
Leena Jutila
Anu Muraja-Murro
Esa Mervaala
Marja Äikiä
Salla Lamusuo
Jyrki Kuikka
Esko Vanninen
Irina Alafuzoff
Aki Ikonen
Ritva Vanninen
Matti Vapalahti
Reetta Kälviäinen
Author Affiliation
Department of Neurosurgery, Kuopio University Hospital, Kuopio, Finland. Arto.Immonen@kuh.fi
Source
Epilepsia. 2010 Nov;51(11):2260-9
Date
Nov-2010
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Anterior Temporal Lobectomy
Cognition Disorders - diagnosis - physiopathology
Dominance, Cerebral - physiology
Electrodes, Implanted
Electroencephalography
Epilepsy, Temporal Lobe - diagnosis - physiopathology - surgery
Female
Finland
Fluorodeoxyglucose F18 - diagnostic use
Follow-Up Studies
Hippocampus - pathology
Humans
Magnetic Resonance Imaging
Male
Middle Aged
Neuropsychological Tests
Positron-Emission Tomography
Signal Processing, Computer-Assisted
Temporal Lobe - physiopathology
Tomography, Emission-Computed, Single-Photon
Treatment Outcome
Wechsler Scales
Young Adult
Abstract
The outcome of surgery in patients with temporal lobe epilepsy (TLE) and normal high-resolution magnetic resonance imaging (MRI) has been significantly worse than in patients with unilateral hippocampal damage upon MRI. The purpose of this study was to determine the long-term outcomes of consecutive true MRI-negative TLE patients who all underwent standardized preoperative evaluation with intracranial electroencephalography (EEG) electrodes.
In this study we present all adult MRI-negative TLE surgery candidates evaluated between January 1990 and December 2006 at Kuopio Epilepsy Center in Kuopio University Hospital, which provides a national center for epilepsy surgery in Finland. During this period altogether 146 TLE surgery candidates were evaluated with intracranial electrodes, of whom 64 patients with normal high-resolution MRI were included in this study.
Among the 38 patients who finally underwent surgery, at the latest follow-up (mean 5.8 years), 15 (40%) were free of disabling seizures (Engel class I) and 6 (16%) were seizure-free (Engel class IA). Twenty-one (55%) of 38 patients had poor outcomes (Engel class III-IV). Outcomes did not change compared to 12-month follow-up. Histopathologic examination failed to reveal any focal pathology in 68% of our MR-negative cases. Only patients with noncongruent positron emission tomography (PET) results had worse outcomes (p = 0.044).
Our results suggest that epilepsy surgery outcomes in MRI-negative TLE patients are comparable with extratemporal epilepsy surgery in general. Seizure outcomes in the long-term also remain stable. Modern imaging techniques could further improve the postsurgical seizure-free rate. However, these patients usually require chronic intracranial EEG evaluation to define epileptogenic areas.
PubMed ID
21175607 View in PubMed
Less detail

18 records – page 1 of 2.