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Familial parkinsonism, dementia, and Lewy body disease: study of family G.

https://arctichealth.org/en/permalink/ahliterature207512
Source
Ann Neurol. 1997 Oct;42(4):638-43
Publication Type
Article
Date
Oct-1997
Author
M A Denson
Z K Wszolek
R F Pfeiffer
E K Wszolek
T M Paschall
R D McComb
Author Affiliation
Department of Internal Medicine, University of Nebraska Medical Center, Omaha 68198-2045, USA.
Source
Ann Neurol. 1997 Oct;42(4):638-43
Date
Oct-1997
Language
English
Publication Type
Article
Keywords
Aged
Amygdala - pathology
Dementia - ethnology - genetics - pathology
Female
Genes, Dominant
Humans
Lewy Bodies - pathology
Locus Coeruleus - pathology
Male
Middle Aged
Nebraska
Neocortex - pathology
Organ Size
Parkinson Disease - ethnology - genetics - pathology
Pedigree
Phenotype
Russia - ethnology
Substantia Innominata - pathology
Substantia Nigra - pathology
Abstract
Genetic influences are thought by many to play an important role in the cause of Parkinson's disease. We studied two closely intermarried families (Family G) whose ancestors immigrated to the United States from Russia. We investigated this family clinically, genealogically, and pathologically. Our pedigree contained 102 members spanning six generations, with 10 affected individuals and 1 affected spouse. Detailed telephone interviews were conducted with affected individuals, with their spouses, and with their at-risk siblings. Medical records of deceased and living affected patients were collected. Physical examinations were performed on 7 at-risk and 5 affected persons. Typical levodopa-responsive parkinsonism with bradykinesia, rigidity, resting tremor, and impaired postural reflexes was seen in 4 members, dementia was present in 3, and 3 had both dementia and parkinsonism. An autopsy completed on 1 individual, our index case, demonstrated Lewy bodies in the brainstem and neocortex and ubiquitin-positive neuritic degeneration in the CA2-3 region of the hippocampus, consistent with the limbic (transitional) form of Lewy body disease. This family is distinct both clinically and pathologically from several previously reported parkinsonian kindreds.
PubMed ID
9382476 View in PubMed
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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
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Pre- and perinatal hypoxia associated with hippocampus/amygdala volume in bipolar disorder.

https://arctichealth.org/en/permalink/ahliterature261475
Source
Psychol Med. 2014 Apr;44(5):975-85
Publication Type
Article
Date
Apr-2014
Author
U K Haukvik
T. McNeil
E H Lange
I. Melle
A M Dale
O A Andreassen
I. Agartz
Source
Psychol Med. 2014 Apr;44(5):975-85
Date
Apr-2014
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Amygdala - pathology
Asphyxia Neonatorum - epidemiology - pathology
Bipolar Disorder - epidemiology - pathology
Comorbidity
Female
Fetal Hypoxia - epidemiology - pathology
Hippocampus - pathology
Humans
Magnetic Resonance Imaging
Male
Norway - epidemiology
Registries - statistics & numerical data
Young Adult
Abstract
Pre- and perinatal adversities may increase the risk for schizophrenia and bipolar disorder. Hypoxia-related obstetric complications (OCs) are associated with brain anatomical abnormalities in schizophrenia, but their association with brain anatomy variation in bipolar disorder is unknown.
Magnetic resonance imaging brain scans, clinical examinations and data from the Medical Birth Registry of Norway were obtained for 219 adults, including 79 patients with a DSM-IV diagnosis of bipolar disorder (age 29.4 years, s.d. = 11.8 years, 39% male) and 140 healthy controls (age 30.8 years, s.d. = 12.0 years, 53% male). Severe hypoxia-related OCs throughout pregnancy/birth and perinatal asphyxia were each studied in relation to a priori selected brain volumes (hippocampus, lateral ventricles and amygdala, obtained with FreeSurfer), using linear regression models covarying for age, sex, medication use and intracranial volume. Multiple comparison adjustment was applied.
Perinatal asphyxia was associated with smaller left amygdala volume (t = -2.59, p = 0.012) in bipolar disorder patients, but not in healthy controls. Patients with psychotic bipolar disorder showed distinct associations between perinatal asphyxia and smaller left amygdala volume (t = -2.69, p = 0.010), whereas patients with non-psychotic bipolar disorder showed smaller right hippocampal volumes related to both perinatal asphyxia (t = -2.60, p = 0.015) and severe OCs (t = -3.25, p = 0.003). No associations between asphyxia or severe OCs and the lateral ventricles were found.
Pre- and perinatal hypoxia-related OCs are related to brain morphometry in bipolar disorder in adulthood, with specific patterns in patients with psychotic versus non-psychotic illness.
Notes
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PubMed ID
23803260 View in PubMed
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Progression in temporal lobe epilepsy: differential atrophy in mesial temporal structures.

https://arctichealth.org/en/permalink/ahliterature173652
Source
Neurology. 2005 Jul 26;65(2):223-8
Publication Type
Article
Date
Jul-26-2005
Author
Neda Bernasconi
Jun Natsume
Andrea Bernasconi
Author Affiliation
Department of Neurology and Neurosurgery, McGill University, Montreal Neurological Institute and Hospital, Quebec, Canada.
Source
Neurology. 2005 Jul 26;65(2):223-8
Date
Jul-26-2005
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age of Onset
Aged
Amygdala - pathology - physiopathology
Atrophy - epidemiology - pathology - physiopathology
Comorbidity
Cross-Sectional Studies
Disease Progression
Electroencephalography - methods
Entorhinal Cortex - pathology - physiopathology
Epilepsy, Temporal Lobe - epidemiology - pathology - physiopathology
Female
Hippocampus - pathology - physiopathology
Humans
Magnetic Resonance Imaging
Male
Middle Aged
Quebec - epidemiology
Regression Analysis
Seizures, Febrile - epidemiology
Temporal Lobe - pathology - physiopathology
Abstract
To determine the relationship between hippocampal, amygdalar, and entorhinal cortex atrophy and duration of epilepsy, presence of secondary generalized seizures, and prolonged childhood febrile convulsions in patients with pharmacologically intractable temporal lobe epilepsy (TLE).
Volumetric MRI of the hippocampus, amygdala, and entorhinal cortex were performed in 86 consecutive patients with TLE and 44 age- and sex-matched healthy control subjects. Linear regression analysis was used to explore the relation between the volumetric measurements and the clinical parameters.
In simple regressions, duration of epilepsy but not age at seizure onset was related to hippocampal (r2 = 0.19, p
PubMed ID
16043790 View in PubMed
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