Biomedical subjects

C Pennanen

Publications and source records attributed to C Pennanen.

4 recordsLinked to original sources

PubMed2006

Subarachnoid hemorrhage is followed by temporomesial volume loss: MRI volumetric study.

OBJECTIVE: To assess whether subarachnoid hemorrhage (SAH) and its treatment is followed by volume loss in temporomesial structures. METHODS: One hundred fifty-five consecutive patients with aneurysmal SAH were randomly assigned to surgical or endovascular treatment. Volumetric MRI was performed in 77 SAH patients with good or moderate clinical outcome 1 year after hemorrhage. A comprehensive neuropsychological test battery was used to evaluate the cognitive performance of the subjects. Thirty healthy individuals were imaged as MRI controls. RESULTS: The normalized hippocampal (HC) volumes were 24.7/23.7 (right/left), and the amygdaloid (AM) volumes were 21.0/20.5 in the matched control population. In SAH patients, the corresponding volumes were smaller, HC 23.2/21.3 (p = 0.072/0.002) and AM 18.4/18.7 (p = 0.012/0.045). In addition, the AM ipsilateral to the ruptured aneurysm was smaller in patients who had undergone surgical treatment (15.7) vs endovascular treatment (20.3; p < 0.001). Treatment modality did not significantly affect the measured HC volumes. The hippocampal but not amygdaloid volumes correlated with the scores of several neuropsychological tests. CONCLUSION: Subarachnoid hemorrhage and its treatment may be followed by atrophy in temporomesial structures. A clear correlation was demonstrated between neuropsychological performance and reduced temporomesial volumes.

Atrophy↗

PubMed2005

A voxel based morphometry study on mild cognitive impairment.

BACKGROUND: Mild cognitive impairment (MCI) is the most widely used concept in classifying cognitive impairment in the elderly who do not fulfil the criteria for dementia. MCI is considered to confer an increased risk of progressing to dementia and most often Alzheimer's disease (AD). Various approaches such as imaging of the brain have been applied to predict the conversion of MCI to dementia. A number of volumetric magnetic resonance imaging (MRI) studies have detected atrophy of the medial temporal lobe in subjects with MCI, but for the other cerebral regions the results have been inconsistent. OBJECTIVE: To study the pattern of brain atrophy in MCI. METHODS: Thirty two controls and 51 individuals with MCI deriving from population based cohorts were studied by MRI using voxel based morphometry. The threshold of t maps was set at p < 0.001. RESULTS: Individuals with MCI had significant unilateral atrophy in the medial temporal lobe on the right side. Less extensive atrophy was found elsewhere-for example, in the temporal lobe, left superior parietal lobule, left anterior cingulate gyrus, and bilaterally in the thalami. CONCLUSIONS: The MRI findings in MCI resemble those seen in early AD.

Aged↗

PubMed2004

Serum testosterone levels in males with Alzheimer's disease.

This study aimed to investigate whether there are differences in serum testosterone levels between male patients with Alzheimer's disease (AD) and cognitively normal male controls. Testosterone and sex hormone binding globulin (SHBG) levels were measured from 14 patients with mild to moderate AD and 16 age-matched control males. The AD patients had higher levels of serum total (P = 0.02) and free testosterone (P < 0.001), and higher free androgen index (FAI) (P = 0.02) compared to controls. No differences were found for the SHBG levels. These data provide no support for hypotheses of (disproportionally) decreased levels of serum testosterone in AD. These data also show that all cognitively normal controls had an FAI below the normal range.

Aged↗

PubMed2002

Amygdaloid atrophy in frontotemporal dementia and Alzheimer's disease.

Crude and corrected amygdaloid volumes were computed from magnetic resonance scans in ten patients with frontotemporal dementia (FTD), 25 patients with Alzheimer's disease (AD) and 27 controls. Amygdaloid atrophy was present in FTD (P<0.005) compared to controls, and a trend for increasing atrophy from controls, through FTD to AD (P for trend <0.00005) showed that FTD amygdaloid volumes were intermediate between controls and AD. Behavioral and Klüver-Bucy-like symptoms, characteristic of FTD, cannot be explained by amygdaloid atrophy alone.

Aged↗