"Enlarged parietal foramina" is a congenital malformation with autosomal dominant inheritance. The condition is usually self-limiting and doesn't require any treatment. However, it may also be associated with encephalocele, vascular anomalies or may be a part of syndrome. We present a case of enlarged parietal foramina in a child and discuss its imaging findings and the associated intracranial vascular malformations.
Thrombosis of the deep cerebral venous system in the absence of superficial sinus thrombosis is a very rare disease. The clinical and radiological findings can be diagnostically challenging due to the subtle appearances on computed tomography (CT) scan. Magnetic resonance imaging (MRI) examination is a preferred imaging modality to complement the CT findings for an accurate diagnosis of venous sinus thrombosis. We present a case of this unusual condition which present as unilateral thalamic lesion on CT scan and the role of contrast enhanced MRI with fast spoiled gradient echo (FSPGR) sequence and 3D reconstruction which led to the diagnosis of thrombosis in the deep cerebral venous system.
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.
The pathogenesis of fatal cerebral malaria (CM) is not well understood, in part because data from patients in whom a clinical diagnosis was established prior to death are rare. In a murine CM model, platelets accumulate in brain microvasculature, and antiplatelet therapy can improve outcome. We determined whether platelets are also found in cerebral vessels in human CM, and we performed immunohistopathology for platelet-specific glycoprotein, GPIIb-IIIa, on tissue from multiple brain sites in Malawian children whose fatal illness was severe malarial anemia, CM, or nonmalarial encephalopathy. Platelets were observed in 3 locations within microvessels: between malaria pigment and leukocytes, associated with malaria pigment, or alone. The mean surface area of platelet staining and the proportion of vessels showing platelet accumulation were significantly higher in patients with CM than in those without it. Platelet accumulation occurs in the microvasculature of patients with CM and may play a role in the pathogenesis of the disease.
Cerebral venous thrombosis (CVT) is a neurological condition occurring because of thrombosis involving the cerebral venous sinuses. This case report is an unusual clinical manifestation of cerebral venous thrombosis in a 76-year-old Chinese man who presented with restricted eye movement and double vision. Despite extensive investigation, there was no better explanation for his clinical symptom and sign apart from cerebral venous thrombosis which was confirmed by magnetic resonance venography (MRV) of the brain. Once cerebral venous thrombosis was diagnosed, he was initiated on anticoagulation and discharged with oral warfarin. This case emphasizes the need to consider cerebral venous thrombosis as one of the rare causes of complex ophthalmoplegia especially when typical cardiovascular risk factors are lacking in an individual.