It has been long known that affective disorders as a result of organic brain diseases are not uncommon. Neurological disorders seem to be significant as risk factors for newly diagnosed mania in the elderly. It has been theorized that lesions in the right cerebral hemisphere and limbic structures may produce symptoms suggestive of mania. Even though specific areas of involvement had not been determined, this case discussed below clearly reports a right sided lesion. One of the reasons why not much is known yet about this clinical entity is the rarity of this occurrence. In fact, in one large scale study, only 2 patients out of 700 were identified with mania.
A 20 year old male presented to the emergency department with generalized tonic clonic convulsions and up rolling of eye balls. He had history of seizure disorder for three years and on regular medical treatment and is compliant to medication. A non-contrast CT scan of the head was only done on 14th day of admission which showed hypodense areas in the right and left cerebellar hemisphere. MR imaging was performed four days later revealed high signal intensity in the both cerebellar hemispheres, both external capsules, both occipital and right parietal regions on fluid-attenuated inversion recovery (FLAIR). The post contrast MR imaging revealed diffuse cerebral and cerebellar hypervascularity in the similar region. This change of diffuse hypervascularity of both cerebral and cerebellar associated with seizure activity on post-contrast magnetic resonance imaging (MRI) has not been reported in any literature.
This is an unusual case report of an infant, who initially presented with a facial haemangioma and was later diagnosed to have a dural sinus malformation (DSM) involving the torcula. The DSM increased in size lateralising to the right transverse sinus at three months of age. Postnatal enlargement of the dural sinus has not been described before suggesting a delay in the maturation of the dural sinus which normally would occur antenatally. There was a further association with a complex developmental venous anomaly (DVA) draining the right cerebral hemisphere into the deep cerebral vein and multiple cavernous malformations. The DVA was not clearly demonstrated at age one month but was more obvious at age three months. This would be the first reported case of DSM associated with a DVA. Increasing venous hypertension probably contributed to the poor opacification of the DVA on follow-up angiography at age six months and to the haemorrhagic changes within the cavernomas on magnetic resonance imaging (MRI). The therapeutic goal was to correct venous hypertension by partially embolising the dural shunts to remodel the cerebral vasculature and preserve the patent sinus. The treatment strategy and possible link between the complex disease entities presented in this infant are discussed. Despite these attemps, the lesion continued to grow compressing the posterior fossa structures. The infant died at nine months of age.