Benign vascular lesions such as developmental venous anomalies (DVAs ) or capillary telangiectasias, are commonly encountered incidental findings on neuroimaging. DVAs (Fig. 18.1) are one of the most commonly encountered vascular lesions with an overall prevalence of 2–9 % [3, 4]. They are thought to be anatomic variants of normal venous drainage and are not considered pathologic. They are believed to form during embryogenesis as a result of adaptations to accidents during development. They form as compensatory pathways and are almost always asymptomatic, incidentally noted lesions with no clinical significance. There are only very rare reports of thrombosis and/or ischemia from these lesions. If they are associated with hemorrhage, it is usually because there is an associated cavernous malformation, which is another type of benign congenital vascular lesion with a significantly higher risk for hemorrhage.

Capillary telangiectasias (Fig. 18.2) account for 16–20 % of intracranial vascular malformations [5] and are similarly asymptomatic. These appear as vascular channels interspersed in normal brain parenchyma on imaging. They occur most often in the brainstem or spinal cord. Multiple capillary telangiectasias are associated with syndromes such as Osler–Weber–Rendu, ataxia telangiectasia, or Sturge–Weber syndrome.

Pineal cysts are incidentally found on a large number of MR studies in pediatric patients with reported prevalence ranging from 1.9 to 57 % [6]. The primary function of the pineal gland is to produce melatonin for circadian rhythm regulation. Pineal cysts are benign nonneoplastic glial-lined cysts within the pineal gland. They are asymptomatic and require no imaging follow-up because they have no potential for malignant transformation. There are certain imaging features that may indicate malignancy, but if a cyst has these features, they will not be described as simple pineal cyst by the radiologist interpreting the examination. Rarely, if the cysts are large enough (>1 cm) they can cause headaches or other neurologic issues such as compression of the cerebral aqueduct with secondary hydrocephalus. Some recommend following cysts if they are greater than 1 cm, although there is no reported increased incidence of malignant transformation in larger cysts [6].

Another common incidental finding seen on pediatric neuroimaging is an arachnoid cyst. Arachnoid cysts are CSF-filled sacs within the arachnoid space that do not communicate with the ventricular system. They are generally well demarcated and are characteristically CSF-density on all MR pulse sequences (Fig. 18.3). They are most commonly seen in the middle cranial fossa, but can also be seen in the posterior fossa or in other intracranial locations. Patients with large arachnoid cysts are slightly more likely to develop subdural hematomas, with a cited 5 % risk in patients with middle cranial fossa arachnoid cysts [7, 8] (Fig. 18.4). Most commonly, they are incidental findings requiring no further treatment. Very large arachnoid cysts or those causing hydrocephalus can be intervened upon, either with resection or fenestration. Usually children with large arachnoid cysts are evaluated by a pediatric neurosurgeon.

Sinus disease is also a fairly commonly encountered incidental finding on neurologic imaging. While sinusitis is a clinical diagnosis, certain imaging findings suggest more acute sinus disease while others suggest chronicity. Bony remodeling and expansion of the sinus cavities as well as mucous retention cysts are seen in chronic sinus disease. Air-fluid levels or aerosolized secretions suggest acute infection, but are nonspecific findings so clinical judgment is required to make the diagnosis. Since sinusitis is a clinical diagnosis, imaging is not usually necessary, but when surgical intervention is indicated or extra-sinus extension of infection is suspected (e.g., into the anterior cranial fossa or orbit), a maxillofacial CT is the preferred diagnostic study.

Other incidental findings are fetal arterial anastomoses, such as a persistent trigeminal artery. Other less common fetal arterial anastomoses include persistent hypoglossal artery, persistent otic artery, persistent stapedial artery, fenestration of the basilar or other arteries, and fetal origin of the posterior cerebral artery. The persistent trigeminal artery is the most common persistent carotid–vertebrobasilar anastomosis with prevalence reported to be 0.1–0.6 % [9]. A persistent trigeminal artery originates from the internal carotid artery and anastomoses with the basilar artery (Fig. 18.5). This incidental finding is important in patients from a neurosurgical perspective because in transsphenoidal surgery, accidental transection may lead to significant hemorrhage. There is an estimated 25 % association between persistent trigeminal arteries and other vascular anomalies [9].

Arachnoid granulations, also known as Pacchonian granulations, are arachnoid villi that project into the lumen of dural venous sinuses and can be mistaken for dural venous thrombosis (Fig. 18.6). Arachnoid granulations are asymptomatic with rare exception; it is theoretically possible, although very unlikely, to develop a headache secondary to a pressure gradient leading to venous hypertension. If a patient has an aberrant arachnoid granulation, they can be followed and surgical dural repair may be necessary if there is a persistent CSF leak. However, for the majority of patients, arachnoid granulations are incidental findings requiring no further imaging follow-up. They are commonly only described on imaging examinations simply so the finding is not confused with a dural sinus thrombosis.

Benign enlargement of the subarachnoid space in infancy (BESSI ) is often discovered incidentally or in the workup of infants with macrocephaly. It is considered to be a variant of normal development of the brain in which transient accumulation of CSF is seen around the frontal lobes, probably secondary to immature CSF drainage pathways leading to a buildup of CSF (Fig. 18.7). It is most commonly seen in children ages 3–8 months and resolves without therapy between 12 and 24 months [10]. Children with BESSI have a slightly increased chance of developing subdural hemorrhage either spontaneously or after minor trauma [11].

Arterial dissections in the head and neck are not uncommon in the pediatric population. They most commonly occur secondary to trauma but can also be seen in the setting of craniocervical fusion abnormalities or connective tissue diseases. Symptoms for arterial dissection resemble stroke and vary depending on where in the cerebral circulation the dissection occurs. A dissection in the anterior circulation, may present with hemiparesis or aphasia. A dissection in the posterior circulation (i.e., vertebral artery) may cause vague symptoms including dizziness or vertigo. If a dissection is suspected in a pediatric patient, MR angiography (MRA) and MR imaging, preferably with intravenous contrast, are considered first line imaging to avoid excessive radiation while identifying the arterial dissection, subintimal thrombus, and possible brain infarction with very high accuracy (Fig. 18.8). However, CTA may be performed when MR is unavailable, when the patient is too unstable for MR imaging, or as a problem-solving tool when MR is not definitive. CTA provides excellent anatomic imaging of arterial stenoses and dissection flaps but is less sensitive than MRI to acute brain infarctions. Interventional neuroradiology (INR) may also perform a catheter digital subtraction angiogram (DSA ) to further evaluate the area of dissection. Catheter-directed DSA is still considered the gold standard for diagnosis of dissection, but is not always necessary prior to initiating treatment. Patients with dissection are generally treated with anticoagulation alone. While more invasive treatment is possible, it is not often utilized in pediatric patients.

Bacterial meningitis and its associated complications is a relatively common and potentially devastating pediatric neurologic issue. Although CSF sampling via lumbar puncture is the mainstay for diagnosis of meningitis, imaging can be used to supplement the diagnosis, determine the extent of disease, and to evaluate for other complications such as empyema, ventriculitis, abscess, or hydrocephalus (Fig. 18.9). When meningitis is a diagnostic possibility, a contrast-enhanced MRI is the exam of choice. NCCT of the head is less helpful but in some cases, hydrocephalus, subdural effusions, or increased attenuation in the basilar cisterns or Sylvian fissures may be seen. Contrast-enhanced MRI is far more sensitive, with findings of failure of intra-sulcal and intra-cisternal fluid suppression on T2W FLAIR and/or diffusion restriction on DWI representing exudative material within the subarachnoid spaces. Enhancement of the leptomeninges and subarachnoid spaces can also be seen, suggesting meningitis. Importantly, it is possible for neuroimaging to be negative in a patient with meningitis so lumbar puncture and CSF sampling is crucial to making the diagnosis and imaging should be used as a supplement to evaluate for secondary complications. Complications such as subdural empyema or abscess (Fig. 18.10) generally require neurosurgical intervention. In the setting of an aseptic viral meningitis, imaging is usually normal and not routinely indicated, although diffuse brain edema, sulcal effacement and/or mild communicating hydrocephalus may be clues as to an underlying viral infection.