PubMed · 1530221
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C Geny, S Amselem, C Danan, J D Degos. 1992. [Mitochondrial dysfunction in human pathology].. https://pubmed.ncbi.nlm.nih.gov/1530221/
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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.
Celiac disease is an enteropathy occurring in genetically predisposed individuals due to a dietary intolerance to gluten. Patients with celiac disease may develop a neurological disorder of unknown cause, although autoimmune mechanisms are suspected. We report on a 56-year-old man with celiac disease, who became refractory to a gluten-free diet and died of a rapidly progressive encephalopathy. Magnetic resonance imaging indicated focal lesions of the cerebellum and brainstem, and electrodiagnostic studies suggested an axonal neuropathy. Autopsy revealed a flattened small-bowel mucosa with intraepithelial lymphocytosis, a spectrum of degenerative changes of the intra-abdominal and mediastinal lymph nodes, including cavitary degeneration, and splenomegaly. Histologically, the lymph nodes showed pseudocyst formation and lymphocytic vasculitis with fibrinoid necrosis, and sections of the brain exhibited fibrinoid degeneration of small blood vessels, sparse perivascular lymphocytic infiltrates, and perivascular ischemic lesions. Identical T-cell clones were identified in the duodenum, stomach, lymph nodes, and spleen. This patient had an unusual neurological disorder related to a vasculopathy, probably mediated by a circulating neoplastic clone of activated T cells.