Wyburn-Mason syndrome (WMS), also known as the Bonnet-Dechaume-Blancsyndrome, is a rare non hereditary phakomatosis characterized by congenital retinal, orbital, and brainstem (usually midbrain) arteriovenous malformations (AVMs), and, less frequently, facial AVMs. With the increased availability of noninvasive brain imaging, intracranial AVMs are detected. Recognition of the association between the retinal and intracranial lesions is important because it allows early identification of the associated intracranial and facial AVMs. This chapter discusses the historical features, pathophysiology, and treatment options for WMS. Retinal AVMs usually do not grow or bleed, and are usually not responsible for significant visual loss. Due to their size and location, WMS AVMs are usually not amenable to surgical removal or radiosurgery. Embolization carries an increased risk because the lesions share a blood supply with vital brainstem structures. Therefore, patients are usually left untreated until the AVMs bleed, at which time heroic measures may be necessary.

Patients with mild traumatic brain injury (TBI) can have normal neurological and physical examinations. Mild traumatic brain injury is not always clinically apparent. The findings include: any period of loss of consciousness, amnesia of the event, and change in mental status such as feeling dizzy or disoriented. Focal motor findings in the unconscious patient with TBI can localize intracranial lesions or spinal cord injuries. Noncontrast computerized tomography (CT) provides useful anatomical and pathological information regarding the location, extent, and nature of the TBI within minutes. Although available evidence does not show that prevention of early posttraumatic seizures improves outcomes following TBI, anticonvulsants are an option in patients at high risk for seizures following head injury (Glasgow Coma Scale less than 9). TBI is the cause of death in approximately 40% of childhood injuries, and occurs more frequently in males and infants or adolescents.