A case of frontotemporal lobar degeneration with ubiquitin-positive intraneuronal inclusions.

The case of a 57-year-old man is reported who has been treated several times because of his relatively expedite mental decline which has begun four years before his death. His first complaints were forgetfulness, mild changes in his behaviour, confusion and difficulty in speech. The neuropsychiatric examinations displayed a mild difficulty in naming and sometimes comprehension of words, although his speech was grammatically correct.

A case of schizencephaly with polymicrogyria.

A case of extensive bilateral frontotemporal schizencephaly is alleged - more extensively in the left hemisphere - which associated with polymicrogyria. The cortical anomaly was discovered only incidentally by MR examination in a 22 year-old man who suffered from headache due to a mild head trauma. Neurological examination proved to be negative.

[Neuropathologic investigation in autopsies with special emphasis on findings in Alzheimer's disease].

Out of an average total of 1400 autopsies per year, neuropathological examinations were performed in 477 cases between 1997 and 1999 to investigate the incidence of dementias. The majority of the studied subjects were over 50 years old. Bielschowsky's and/or Gallyas's silver methods and, in some cases, protein tau (MAP) immunocytochemistry and amyloid staining were performed beside routine examination.

Tissue preconditioning may explain concentric lesions in Baló's type of multiple sclerosis.

Lesions of Baló's concentric sclerosis are characterized by alternating layers of myelinated and demyelinated tissue. The reason for concentric demyelination in this variant of multiple sclerosis is unclear. In the present study we investigated the immunopathology in autopsy tissue of 14 patients with acute multiple sclerosis or fulminant exacerbations of chronic multiple sclerosis with Baló-type lesions in the CNS, focusing on the patterns of tissue injury in actively demyelinating lesions.

[Intracranial cholesterol granulomas].

In the development of a cholesterol granuloma both cellular and vascular permeability factors have to be taken into consideration. It may arise as a special degradation product in a chronic cerebral infarct because of the partial insufficient activity of the macrophages. Consequently, the degradation of brain sphingolipids and other compounds does not follow the usual route of degradation and transportation by granular cells to the stage of neutral fat but the necrotic mass transforms into cholesterol esters.