Fifty-four per cent of 41 chronically institutionalized adult patients with epilepsy had ataxia of gait (wide mean stride width). None of the following correlated with stride width: serum phenytoin, previous phenytoin toxicity, seizure frequency, or status epilepticus. Seventeen of the 41 patients had computed tomographic head scans. Patients with radiological evidence of cerebellar atrophy had a wider mean stride width, later age of onset of seizures, greater peak serum concentrations of phenytoin than did those without cerebellar atrophy. Ataxia of gait was inconsistently associated with cerebellar atrophy. Elevated serum/plasma concentrations of phenytoin may be a risk factor for cerebellar atrophy, but seizure frequency or status epilepticus are not independently related to this complication.
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http://dx.doi.org/10.1017/s0317167100041238 | DOI Listing |
Alzheimers Dement
December 2024
CYRIC, Tohoku University, Sendai, Japan
Background: Reactive astrogliosis refers to functional and morphological changes in astrocytes that occur with neuronal damage in numerous neurological conditions. PET tracers targeting monoamine oxidase B (MAO‐B) are used to visualize reactive astrogliosis in the living brain. [F]SMBT‐1, a MAO‐B selective PET tracer, was developed by modifying the chemical structure of [F]THK5351.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Division of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
Background: Patterns of regional atrophy and hypometabolism have been observed in dementia with Lewy bodies (DLB). However, determinants of regional vulnerability to structural and functional neurodegeneration remain largely unexplored. First, we investigated the association between regional gene expression and grey matter volumes in probable DLB patients.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Mayo Clinic, Rochester, MN, USA
Background: Progressive supranuclear palsy (PSP) can present with different clinical variants which show distinct, but partially overlapping, patterns of neurodegeneration and tau deposition in a PSP network of regions, including cerebellar dentate, superior cerebellar peduncle, midbrain, thalamus, basal ganglia, and frontal lobe. We sought to determine whether disruptions in functional connectivity within this PSP network measured using resting‐state functional MRI (rs‐fMRI) differed between PSP‐Richardson’s syndrome and the cortical and subcortical variants of PSP.
Method: Structural MRI and rs‐fMRI scans were collected for 40 PSP‐RS, 24 PSP‐cortical (12 speech and language; 10 corticobasal syndrome; 2 frontal) and 36 PSP‐subcortical (18 parkinsonism; 11 progressive gait freezing; 6 postural instability; 1 oculomotor) participants who met the Movement Disorder Society PSP clinical criteria (Table 1).
Alzheimers Dement
December 2024
Combinostics Ltd, Tampere, Finland
Background: Accurate differential diagnosis of neurodegenerative diseases is challenging, but crucial for the management and treatment, particularly given the development of disease‐modifying drug therapies for Alzheimer’s disease (AD). In this work, we investigate imaging biomarkers derived from T1‐weighted magnetic resonance imaging (MRI) with a focus on differentiating Parkinson‐plus syndromes from other relevant diagnostic groups in dementia and Parkinson’s disease (PD).
Method: MR scans from 1206 subjects and three cohorts were used: Parkinson’s Disease Biomarkers Program (PDBP), Amsterdam Dementia Cohort (ADC) and PredictND cohort (PND) (Table 1).
Background: Most evidence about early structural brain change in dementia derives from highly selected disease cohorts. However, at population level, dementia is typically due to mixed pathologies. We aimed to characterise distinct patterns of brain volume change in early all‐cause dementia in a population cohort.
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