The clinical onset of intracranial neoplasia is typically subacute and progressive, or characterized by episodes of epilepsy; however, it is not infrequent for a tumour to present with an acute clinical syndrome, requiring emergency diagnostic imaging. This need arises in cases associated with an abrupt onset of intracranial hypertension, seizure or focal neurological deficit. This acute onset can be caused by alterations that result in a progressive mass effect of the neoplasia upon the adjacent nervous tissue and subarachnoid spaces, including the changes of perilesional oedema, haemorrhage and hydrocephalus. The volume of the tumour can vary suddenly in response to involutional intrinsic tumoral phenomena such as necrosis or haemorrhage. These effects usually take place secondary to the inadequacy of the neoplastic vascular architecture, but can also be a result of the effects of radio- or chemotherapy. In addition, in certain tumours such as astrocytomas, primitive neuroectodermal tumours (PNET) and craniopharyngiomas, the formation and/or distension of an internal cyst may take place very quickly. Perilesional vasogenic oedema, a result of the primitive nature of the neovasculature of the tumour, the intratumoral degenerative effects described above and the effects of these phenomena upon the surrounding neural tissue, increases the overall volume of the area involved and therefore causes an increase in the so-called tumoral mass effect. The most severe consequence of neoplastic mass effect is internal cerebral herniation. Perilesional vasogenic oedema is variably proportionate to the size of the tumour, its speed of growth, its internal constitution including its vascular supply, and the effects of the lesion upon the surrounding tissue. Therefore, small intraparenchymal metastatic lesions are typically accompanied by substantial vasogenic oedema, whereas benign tumours such as meningiomas, which are slow-growing and extraaxial, often have no perilesional oedema unless they have grown through the overlying pia mater of the underlying brain or have internal complication (e.g., intrinsic necrosis). Hydrocephalus, which can also be limited to one or more ventricular cavities (i.e., caused by entrapment), is usually a result of the mass effect of the neoplasm; a typical example is monoventricular hydrocephalus secondary to the distortional parenchymal effect that causes effacement and ultimate obstruction of the foramen of Monro. Certain intraventricular tumours, or those adjacent to critical points of CSF outflow (aqueduct of Sylvius), can be the direct cause of subarachnoid space obstruction. However, in such cases the hydrocephalic condition usually sets in slowly and symptoms have a subacute although progressive pattern. In this summarized introduction dedicated to neoplastic emergencies, we will briefly consider examination technique, the key points of imaging findings and certain particular posttraumatic clinical and diagnostic situations.
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