ABSTRACT
BACKGROUND: Septo-optic dysplasia, a variable combination of abnormalities of cerebral midline structures, is a clinically heterogeneous syndrome in which the midline defects may be implicated in psychiatric disturbances. OBJECTIVE: To describe a case of septo-optic dysplasia associated with depression and psychosis and to discuss the role of these developmental abnormalities in psychiatric disturbances. METHODS: The patient's clinico-anamnestic, neuroradiologic, neuropsychiatric, endocrinologic, ophthalmologic, and genetic profile was evaluated. CONCLUSIONS: Developmental abnormalities due to disruption of the complex neural network linking the septum pellucidum with other limbic structures may have been involved in the affective and psychotic disturbances observed in our patient.
Subject(s)
Depressive Disorder/psychology , Psychotic Disorders/psychology , Septo-Optic Dysplasia/psychology , Antimanic Agents/therapeutic use , Antipsychotic Agents/therapeutic use , Benzodiazepines/therapeutic use , Depressive Disorder/complications , Depressive Disorder/drug therapy , Female , Humans , Magnetic Resonance Imaging , Middle Aged , Neuropsychological Tests , Olanzapine , Psychotic Disorders/complications , Psychotic Disorders/drug therapy , Septo-Optic Dysplasia/complications , Septo-Optic Dysplasia/drug therapy , Tomography, X-Ray Computed , Valproic Acid/therapeutic use , Visual Fields , Wechsler ScalesABSTRACT
In 31 patients with probable Alzheimer's disease (AD), 19 with probable vascular dementia (VaD) and 20 with Possible AD and Possible VaD, cerebrospinal fluid (CSF) tau levels hyperphosphorylated at threonine 181 (Ptau) were measured by ELISA. Thirty-six age-matched subjects were used as controls. The severity of the cognitive decline was assessed at the time of CSF analysis and after a 12-month follow-up. The groups had comparable age, degree of cognitive impairment and disease duration; these parameters were not related to P-tau levels. P-tau discriminated between demented patients and controls, but no significant difference emerged between AD and the other groups. By contrast, higher P-tau values were found to predict, independently of the clinical diagnosis, a more rapid evolution of cognitive decline. Whether these findings are due to a lack of CSF P-tau specificity or to the low reliability of clinical and radiological criteria remains unclear. P-tau may be useful in the evaluation of disease evolution, by predicting the rate of cognitive decline.
