Cavernous hemangiomas are the most common benign tumors of the liver. Usually one tumor exists, but multiple lesions can occur in the left or right lobe of the liver in 40% of patients. Their sizes can range from a few millimeters to 20 centimetres. Those over 5 cm are often referred to as "giant hemangiomas".

In the eye, it is known as orbital cavernous hemangioma and is found in women more frequently than men, most commonly between the ages of 20-40. This neoplasm is usually located within the muscle cone, which is lateral to the optic nerve. It is not usually treated unless the patient is symptomatic. Visual impairment happens when the optic nerve is compressed or the extraocular muscles are surrounded.

Clinical symptoms of CNS origin include recurrent headaches, focal neurological deficits, hemorrhagic stroke, and seizures, but CCM can also be asymptomatic. The nature and severity of the symptoms depend on the lesion's location.

Central nervous system cavernous hemangioma is a cavernous hemangioma that arises in the central nervous system (CNS). It can be considered to be a variant of hemangioma, and is characterized by grossly large dilated blood vessels and large vascular channels, less well circumscribed, and more involved with deep structures, with a single layer of endothelium and an absence of neuronal tissue within the lesions. These thinly walled vessels resemble sinusoidal cavities filled with stagnant blood. Blood vessels in patients with cerebral cavernous malformations (CCM) can range from a few millimeters to several centimeters in diameter. Most lesions occur in the brain, but any organ may be involved.

Patients with arachnoid cysts may never show symptoms, even in some cases where the cyst is large. Therefore, while the presence of symptoms may provoke further clinical investigation, symptoms independent of further data cannot—and should not—be interpreted as evidence of a cyst's existence, size, location, or potential functional impact on the patient.

Symptoms vary by the size and location of the cyst(s), though small cysts usually have no symptoms and are discovered only incidentally. On the other hand, a number of symptoms may result from large cysts:

- Cranial deformation or macrocephaly (enlargement of the head), particularly in children

- Cysts in the suprasellar region in children have presented as bobbing and nodding of the head called bobble-head doll syndrome.

- Cysts in the left middle cranial fossa have been associated with ADHD in a study on affected children.

- Headaches. A patient experiencing a headache does not necessarily have an arachnoid cyst.

- In a 2002 study involving 78 patients with a migraine or tension-type headache, CT scans showed abnormalities in over a third of the patients, though arachnoid cysts only accounted for 2.6% of patients in this study.

- A study found 18% of patients with intracranial arachnoid cysts had non-specific headaches. The cyst was in the temporal location in 75% of these cases.

- Seizures

- Hydrocephalus (excessive accumulation of cerebrospinal fluid)

- Increased intracranial pressure

- Developmental delay

- Behavioral changes

- Nausea

- Hemiparesis (weakness or paralysis on one side of the body)

- Ataxia (lack of muscle control)

- Musical hallucination

- Pre-senile dementia, a condition often associated with Alzheimer's disease

- In elderly patients (>80 years old) symptoms were similar to chronic subdural hematoma or normal pressure hydrocephalus:

- Dementia

- Urinary incontinence

- Hemiparesis

- Headache

- Seizures

Sinus pericranii typically present as soft palpable masses along midline skull, which may fluctuate in size depending on body positioning. Classically, these lesions are not associated with color change of the overlying skin, such as with other vascular lesions such as hemangioma.

A cerebral arteriovenous malformation (cerebral AVM, CAVM, cAVM) is an abnormal connection between the arteries and veins in the brain—specifically, an arteriovenous malformation in the cerebrum.

Arachnoid cysts can be found on the brain or on the spine. Intracranial arachnoid cysts usually occur adjacent to the arachnoidal cistern. Spinal arachnoid cysts may be extradural, intradural, or perineural and tend to present with signs and symptoms indicative of a radiculopathy.

Arachnoid cysts may also be classified as primary (congenital) or secondary (acquired) and have been reported in humans, cats, and dogs.

Arachnoid cysts can be relatively or present with symptoms; for this reason, diagnosis is often delayed.

The most frequently observed problems, related to an AVM, are headaches and seizures, backaches, neckaches and eventual nausea, as the coagulated blood makes its way down to be dissolved in the individual's spinal fluid. It is supposed that 15% of the population, at detection, have no symptoms at all. Other common symptoms are a pulsing noise in the head, progressive weakness and numbness and vision changes as well as debilitating, excruciating pain.

In serious cases, the blood vessels rupture and there is bleeding within the brain (intracranial hemorrhage). Nevertheless, in more than half of patients with AVM, hemorrhage is the first symptom. Symptoms due to bleeding include loss of consciousness, sudden and severe headache, nausea, vomiting, incontinence, and blurred vision, amongst others. Impairments caused by local brain tissue damage on the bleed site are also possible, including seizure, one-sided weakness (hemiparesis), a loss of touch sensation on one side of the body and deficits in language processing (aphasia). Ruptured AVMs are responsible for considerable mortality and morbidity.

AVMs in certain critical locations may stop the circulation of the cerebrospinal fluid, causing accumulation of the fluid within the skull and giving rise to a clinical condition called hydrocephalus. A stiff neck can occur as the result of increased pressure within the skull and irritation of the meninges.

Patients come to clinical attention early in life (usually at birth or within the first few months), with a firm subcutaneous nodule at bridge of nose, or as a polypoid mass within the nasal cavity, or somewhere along the upper border of the nasal bow. If the patient presents with an intranasal mass, there may be obstruction, chronic rhinosinusitis, or nasal drainage. If there is a concurrent cerebrospinal fluid (CSF) leak, then an encephalocele is much more likely.

This lesion is separated into two types based on the anatomic site of presentation:

1. Extranasal (60%): Subcutaneous bridge of nose

2. Intranasal (30%): Superior nasal cavity

3. Mixed (10%): Subcutaneous tissues and nasal cavity (larger lesions)

Sinus pericranii (SP) is a rare disorder characterized by a congenital (or occasionally, acquired) epicranial venous malformation of the scalp. Sinus pericranii is an abnormal communication between the intracranial and extracranial venous drainage pathways. Treatment of this condition has mainly been recommended for aesthetic reasons and prevention of hemorrhage.

Typically not diagnosed until late childhood or later, Bonnet–Dechaume–Blanc syndrome usually presents itself with a combination of central nervous system features (midbrain), ophthalmic features (retina), and facial features. The degree of expression of the syndrome's components varies both clinically and structurally. Common symptoms that lead to diagnosis are headaches, retro-orbital pain and hemianopia.

The ophthalmic features of the Bonnet–Dechaume–Blanc syndrome occur as retinal arteriovenous malformation (AVMs). There are three categories of AVMs that are categorized depending on the severity of the malformation. The first category consists of the patient having small lesions that usually are asymptomatic. The second category, more severe than the first, is when the patient’s malformation is missing a connecting capillary. The missing capillary is meant to serve as a link between an artery and a vein; without it, edemas, hemorrhages, and visual impairments can result. Category three, the most severe, occurs when the patient’s malformations are so severe that the dilated vessels cause no distinction between artery and vein. When the symptoms are this severe, the patient has a significantly increased risk of developing vision loss. Since the retinal lesions categorized vary from large vascular malformations that affect a majority of the retina to malformations that are barely visible, the lesions cause a wide range of symptoms including decrease in visual sharpness, proptosis, pupillary defects, optic degeneration and visual field defects. The most common type of visual field impairment due to AVMs is homonymous hemianopia. Homonymous hemianopia typically presents unilaterally, but bilateral cases have been reported as well.

The extent of the central nervous system (CNS) features/symptoms of Bonnet–Dechaume–Blanc syndrome is highly dependent of the location of the cerebral AVMs and the extent of the malformation. The most common symptom affecting the CNS is an intracranial hemangioma in the midbrain. Along with hemangiomas, the malformations result in severe headaches, cerebral hemorrhages, vomiting, meningism, seizures, acute strokes or progressive neurological deficits due to acute or chronic ischaemia caused by arteriovenous shunting.

The distinguishable facial features that result from Bonnet–Dechaume–Blanc syndrome vary from case to case. A person showing signs of the syndrome may display faint skin discoloration, nevi and angiomas of the skin. Some patients with this disorder also present with high flow arteriovenous malformations of the maxillofacial or mandibular (jaw) regions. Another facial indicator of this disease is malformations affecting the frontal and/or maxillary sinuses.

While nasal glial heterotopia (NGH) is the preferred term, synonyms have included nasal glioma. However, this term is to be discouraged, as it implies a neoplasm or tumor, which it is not. By definition, nasal glial heterotopia is a specific type of choristoma. It is not a teratoma, however, which is a neoplasm comprising all three germ cell layers (ectoderm, endoderm, mesoderm). As a congenital malformation or ectopia, it is distinctly different from the trauma or iatrogenic development of an encephalocele.

Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately but can be delayed as much as 2 weeks. If the bleeds are large enough to put pressure on the brain, signs of increased ICP (intracranial pressure) or damage to part of the brain will be present.

Other signs and symptoms of subdural hematoma can include any combination of the following:

- A history of recent head injury

- Loss of consciousness or fluctuating levels of consciousness

- Irritability

- Seizures

- Pain

- Numbness

- Headache (either constant or fluctuating)

- Dizziness

- Disorientation

- Amnesia

- Weakness or lethargy

- Nausea or vomiting

- Loss of appetite

- Personality changes

- Inability to speak or slurred speech

- Ataxia, or difficulty walking

- Loss of muscle control

- Altered breathing patterns

- Hearing loss or hearing ringing (tinnitus)

- Blurred Vision

- Deviated gaze, or abnormal movement of the eyes.

A developmental venous anomaly (DVA, formerly known as venous angioma) is a congenital variant of the cerebral venous drainage. On imaging it is seen as a number of small deep parenchymal veins converging toward a larger collecting vein.

Signs of the tumor resulting from increased intracranial pressure are present in 91% of patients, with vomiting, homonymous visual field defects and headache being the most common symptoms.

Other symptoms are ear ringing and dizziness.

It is not known what percentage of people with IIH will remit spontaneously, and what percentage will develop chronic disease.

IIH does not normally affect life expectancy. The major complications from IIH arise from untreated or treatment-resistant papilledema. In various case series, the long-term risk of ones vision being significantly affected by IIH is reported to lie anywhere between 10 and 25%.

Subdural hematomas are divided into acute, subacute, and chronic, depending on the speed of their onset. Acute subdural hematomas that are due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression.

Acute bleeds often develop after high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas. They are most severe if associated with cerebral contusions. Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the typically arterial bleeding of an epidural hemorrhage. Acute subdural bleeds have a high mortality rate, higher even than epidural hematomas and diffuse brain injuries, because the force (acceleration/deceleration) required to cause them causes other severe injuries as well. The mortality rate associated with acute subdural hematoma is around 60 to 80%.

Chronic subdural bleeds develop over a period of days to weeks, often after minor head trauma, though such a cause is not identifiable in 50% of patients. They may not be discovered until they present clinically months or years after a head injury. The bleeding from a chronic bleed is slow, probably from repeated minor bleeds, and usually stops by itself. Since these bleeds progress slowly, they present the chance of being stopped before they cause significant damage. Small chronic subdural hematomas, those less than a centimeter wide, have much better outcomes than acute subdural bleeds: in one study, only 22% of patients with chronic subdural bleeds had outcomes worse than "good" or "complete recovery". Chronic subdural hematomas are common in the elderly.

Subdural hematoma occurs when there is tearing of the bridging vein between the cerebral cortex and a draining venous sinus. At times they may be caused by arterial lacerations on the brain surface. Acute subdural hematomas are usually associated with cerebral cortex injury as well and hence the prognosis is not as good as extra dural hematomas. Clinical features depend on the site of injury and severity of injury. Patients may have a history of loss of consciousness but they recover and do not relapse. Clinical onset occurs over hours. A crescent shaped hemorrhage compressing the brain that does cross suture lines will be noted on CT of the head. Craniotomy and surgical evacuation is required if there is significant pressure effect on the brain.Complications include focal neurologic deficits depending on the site of hematoma and brain injury, increased intra cranial pressure leading to herniation of brain and ischemia due to reduced blood supply and seizures.

Patients with third ventricular colloid cysts become symptomatic when the tumor enlarges rapidly, causing CSF obstruction, ventriculomegaly, and increased intracranial pressure. Some cysts enlarge more gradually, however, allowing the patient to accommodate the enlarging mass without disruption of CSF flow, and the patient remains asymptomatic. In these cases, if the cyst stops growing, the patient can maintain a steady state between CSF production and absorption and may not require neurosurgical intervention.

Bonnet–Dechaume–Blanc syndrome, also known as Wyburn-Mason syndrome, is a rare congential arteriovenous malformation of the brain, retina or facial nevi. The syndrome has a number of possible symptoms and can affect the skin, bones, kidneys, muscles, and gastrointestinal tract. When the syndrome affects the brain, people can experience severe headaches, seizures, acute stroke, meningism and progressive neurological deficits due to acute or chronic ischaemia caused by arteriovenous shunting.

As for the retina, the syndrome causes retinocephalic vascular malformations that tend to be present with intracranial hemorrhage and lead to decreased visual acuity, proptosis, pupillary defects, optic atrophy, congestion of bulbar conjunctiva, and visual field defects. Retinal lesions can be unilateral and tortuous, and symptoms begin to appear in the second and third decades of life.

The syndrome can present cutaneous lesions, or skin with different texture, thickness, and color, usually on the face. The facial features caused by the syndrome vary from slight discoloration to extensive nevi and angiomas of the skin. In some cases, the frontal and maxillary sinus can present problems in the subject due to the syndrome.

There have only been 52 reported cases of patients with Bonnet–Dechaume–Blanc syndrome as of 2012. Symptoms are rarely noticed in children and the syndrome is often diagnosed in late childhood or early adulthood when visual impairment is noticed. Fluorescein angiography is commonly used to diagnose the syndrome.

There have been several methods in treating patients who display Bonnet–Dechaume–Blanc syndrome. However, which method seems to work the most is within argument. Patients with intracranial lesions have been treated with surgical intervention and in some cases, this procedure has been successful. Other treatments include embolization, radiation therapy, and continued observation.

With limited research on Bonnet–Dechaume–Blanc syndrome, researchers have focused on the clinical and radiological findings rather than how to manage this rare and non-heritable syndrome.

Brain herniation is a potentially deadly side effect of very high pressure within the skull that occurs when a part of the brain is squeezed across structures within the skull. The brain can shift across such structures as the falx cerebri, the tentorium cerebelli, and even through the foramen magnum (the hole in the base of the skull through which the spinal cord connects with the brain). Herniation can be caused by a number of factors that cause a mass effect and increase intracranial pressure (ICP): these include traumatic brain injury, intracranial hemorrhage, or brain tumor.

Herniation can also occur in the absence of high ICP when mass lesions such as hematomas occur at the borders of brain compartments. In such cases local pressure is increased at the place where the herniation occurs, but this pressure is not transmitted to the rest of the brain, and therefore does not register as an increase in ICP.

Because herniation puts extreme pressure on parts of the brain and thereby cuts off the blood supply to various parts of the brain, it is often fatal. Therefore, extreme measures are taken in hospital settings to prevent the condition by reducing intracranial pressure, or decompressing (draining) a hematoma which is putting local pressure on a part of the brain.

Epidural hematoma (EDH) is a rapidly accumulating hematoma between the dura mater and the cranium. These patients have a history of head trauma with loss of consciousness, then a lucid period, followed by loss of consciousness. Clinical onset occurs over minutes to hours. Many of these injuries are associated with lacerations of the middle meningeal artery. A "lenticular", or convex, lens-shaped extracerebral hemorrhage that does not cross suture lines will likely be visible on a CT scan of the head. Although death is a potential complication, the prognosis is good when this injury is recognized and treated.

Most people who develop SCSFLS feel the sudden onset of a severe and acute headache. It is a headache usually made worse by standing, typically becoming prominent throughout the day, with the pain becoming less severe when lying down. Orthostatic headaches can become chronic and disabling to the point of incapacitation. Some patients with SCSFLS will develop headaches that begin in the afternoon. This is known as "second-half-of-the-day headache". This may be an initial presentation of a spontaneous CSF leak or appear after treatment such as an epidural patch, and likely indicates a slow CSF leak.

Apart from headache, about 50% of patients experience neck pain or stiffness, nausea, and vomiting. Other symptoms include dizziness and vertigo, facial numbness or weakness, unusually blurry or double vision, neuralgia, fatigue, or a metallic taste in the mouth. Leaking CSF can sometimes be felt or observed as a discharge from the nose or ear.

Lack of CSF pressure and volume can allow the brain to sag and descend through the foramen magnum (large opening) of the occipital bone, at the base of the skull. The lower portion of the brain is believed to stretch or impact one or more cranial nerve complexes, thereby causing a variety of sensory symptoms. Nerves that can be affected and their related symptoms are detailed in the table at right.

A colloid cyst is a tumor containing gelatinous material in the brain. It is almost always found just posterior to the foramen of Monro in the anterior aspect of the third ventricle, originating from the roof of the ventricle. Because of its location, it can cause obstructive hydrocephalus and increased intracranial pressure. Colloid cysts represent 0.5–1% of intracranial tumors.

Symptoms can include headache, vertigo, memory deficits, diplopia, behavioral disturbances and in extreme cases, sudden death. Intermittency of symptoms is characteristic of this lesion. Untreated pressure caused by these cysts can result in brain herniation. Colloid cyst symptoms have been associated with 4 variables: cyst size, cyst imaging characteristics, ventricular size, and patient age. The developmental origin is unclear, though they may be of endodermal origin, which would explain the mucin-producing, ciliated cell type. These cysts can be surgically resected, and opinion is divided about the advisability of this.