PubMed · 14829959
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P COSSA, P MARTIN. 1951. [On temporal hallucinations].. https://pubmed.ncbi.nlm.nih.gov/14829959/
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Glioneuronal lesions are frequently observed in biopsy specimens obtained from patients with pharmacoresistant epilepsies, comprising focal cortical dysplasias (FCD) and gangliogliomas. Recent findings point to the phosphoinositide 3-kinase (PI3K) pathway and tuberin/hamartin signaling cascade as being compromised in these lesions. Ezrin, radixin and moesin (ERM-/band-4.1 proteins) genes represent downstream effectors of the PI3K pathway, are involved in cytoskeleton-membrane interference, cell growth, migration and differentiation, and harbor tumor suppressor motifs. Accumulation of band-4.1 proteins has been identified in cortical tubers of tuberous sclerosis patients, which share neuropathological similarities with FCD and gangliogliomas. Here, we have studied the immunohistochemical distribution pattern of ERMs, as well as allelic variants, occurring in gangliogliomas (n=20) and FCDs (FCD(IIa), n=7; FCD(IIb), n=37). Aberrant accumulation of ERMs was observed in dysplastic neurons of FCDs and gangliogliomas as well as in balloon cells. Adjacent brain tissue without structural abnormalities was used as control and showed only faint neuropil staining. Mutational screening revealed silent polymorphisms in the ezrin gene in two individuals suffering from FCD(IIb). A transition from G to A in radixin exon 2 resulted in an exchange of valine by isoleucine at codon 50 in an additional FCD(IIb) specimen. Such sequence alterations were not found in controls. The present data suggest accumulation of ERM expression in dysplastic cellular components but do not favor mutational events of ERM in the pathogenesis of FCDs or gangliogliomas. Aberrant expression of ERMs is, however, compatible with compromised PI3K-pathway signaling in glioneuronal lesions characterized by abnormal cellular differentiation and aberrant network formation.
The production of novel, motivated or useful material defines creativity, which appears to be one of the higher, specific, human brain functions. While creativity can express itself in virtually any domain, art might particularly well illustrate how creativity may be modulated by the normal or pathological brain. Evidence emphasizes global brain functioning in artistic creativity and output, but critical steps which link perception processing to execution of a work, such as extraction-abstraction, as well as major developments of non-esthetic values attached to art also underline complex activation and inhibition processes mainly localized in the frontal lobe. Neurological diseases in artists provide a unique opportunity to study brain-creativity relationships, in particular through the stylistic changes which may develop after brain lesion.
STUDY OBJECTIVE: Intracranial causes of sudden and unexpected death in children are uncommon and are usually due to trauma, epilepsy or to catastrophic haemorrhage associated with neoplasms or vascular malformations. We sought to review the presenting symptoms and signs of intracranial mass lesions that led to sudden death to guide clinicians in early identification of these potentially treatable conditions. METHODS: All cases of sudden unexpected death attributed to intracranial mass lesion that occurred from 1996 to 2002 at the Oxford Radcliffe Hospitals, NHS Trust, were reviewed. RESULTS: During the study period, six children, aged between 10 weeks and 12 years, died suddenly with intracranial mass lesions other than haematomas. All of them were unsuspected of having a neurological disease prior to death. All patients were found to have an intracranial mass lesion. There were colloid cyst (n=2), glioblastoma multiform (n=1), primitive neuro-ectodermal tumour (n=1), pyogenic abscess (n=1) and histologically unverified tumour (n=1). Presenting features included headache and vomiting in four cases, vomiting longer than 1 week in three and lethargy in four cases. Three patients were misdiagnosed with viral illness. CONCLUSION: The case series highlights a life-threatening but misleading presentation of intracranial mass lesions. The diagnosis of viral illness should be made cautiously when headache and vomiting occur in the absence of focal complaints. A history of vomiting exceeding a few days duration warrants further investigation. Persistent lethargy should be considered a neurological rather than a non-specific clinical sign.