10-15% of intracranial AV malformations are DAVFs. There is a higher preponderance in females (61-66%), and typically patients are in their fourth or fifth generation of life. DAVFs are rarer in children.

Manual carotid self compression is a controversial treatment for DAVF. Patients using this method are told to compress the carotid with the opposite hand for approximately 10 minutes daily, and gradually increasing the frequency and duration of compression. Currently, it is unclear whether this method is an effective therapy.

Vein of Galen malformations are devastating complications. Studies have shown that 77% of untreated cases result in mortality. Even after surgical treatment, the mortality rate remains as high as 39.4%. Most cases occur during infancy when the mortality rates are at their highest. Vein of Galen malformations are a relatively unknown affliction, attributed to the rareness of the malformations. Therefore, when a child is diagnosed with a faulty Great Cerebral Vein of Galen, most parents know little to nothing about what they are dealing with. To counteract this, support sites have been created which offer information, advice, and a community of support to the afflicted (, ).

The complications that are usually associated with vein of Galen malformations are usually intracranial hemorrhages. Over half the patients with VGAM have a malformation that cannot be corrected. Patients frequently die in the neonatal period or in early infancy.

Various classifications have been proposed for CCF. They may be divided into low-flow or high-flow, traumatic or spontaneous and direct or indirect. The traumatic CCF typically occurs after a basal skull fracture. The spontaneous dural cavernous fistula which is more common usually results from a degenerative process in older patients with systemic hypertension

and atherosclerosis. Direct fistulas occur when the Internal Carotid artery (ICA) itself fistulizes into the Cavernous sinus whereas indirect is when a branch of the ICA or External Carotid artery (ECA) communicates with the cavernous sinus.

A popular classification divides CCF into four varieties depending on the type of arterial supply.

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.

Carotid cavernous fistulae may form following closed or penetrating head trauma, surgical damage, rupture of an intracavernous aneurysm, or in association with connective tissue disorders, vascular diseases and dural fistulas.

The nature of this malformation remains unclear. Congenital, spontaneous, and acquired origins are accepted. The hypothesis of a spontaneous origin in the current case of SP is supported by no evidence of associated anomalies, such as cerebral aneurysmal venous malformations, systemic angiomas, venous angioma dural malformation, internal cerebral vein aneurysm, and cavernous hemangiomas.

The prevalence of congenital Chiari I malformation, defined as tonsilar herniations of 3 to 5 mm or greater, was previously believed to be in the range of one per 1000 births, but is likely much higher. Women are three times more likely than men to have a congenital Chiari malformation. Type II malformations are more prevalent in people of Celtic descent. A study using upright MRI found cerebellar tonsillar ectopia in 23% of adults with headache from motor-vehicle-accident head trauma. Upright MRI was more than twice as sensitive as standard MRI, likely because gravity affects cerebellar position.

Cases of congenital Chiari malformation may be explained by evolutionary and genetic factors. Typically, an infant's brain weighs around 400g at birth and triples to 1100-1400g by age 11. At the same time the cranium triples in volume from 500 cm to 1500 cm to accommodate the growing brain. During human evolution, the skull underwent numerous changes to accommodate the growing brain. The evolutionary changes included increased size and shape of the skull, decreased basal angle and basicranial length. These modifications resulted in significant reduction of the size of the posterior fossa in modern humans. In normal adults, the posterior fossa comprises 27% of the total intracranial space, while in adults with Chiari Type I, it is only 21%. If a modern brain is paired with a less modern skull, the posterior fossa may be too small, so that the only place where the cerebellum can expand is the foramen magnum, leading to development of Chiari Type I. H. neanderthalensis had platycephalic (flattened) skull. Some cases of Chiari are associated with platybasia (flattening of the skull base).

Factors increasing the risk of a subdural hematoma include very young or very old age. As the brain shrinks with age, the subdural space enlarges and the veins that traverse the space must travel over a wider distance, making them more vulnerable to tears. This and the fact that the elderly have more brittle veins make chronic subdural bleeds more common in older patients. Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults. For this reason, subdural hematoma is a common finding in shaken baby syndrome. In juveniles, an arachnoid cyst is a risk factor for a subdural hematoma.

Other risk factors for subdural bleeds include taking blood thinners (anticoagulants), long-term alcohol abuse, dementia, and the presence of a cerebrospinal fluid leak.

The radiocephalic arteriovenous fistula (RC-AVF) is a shortcut between cephalic vein and radial artery at the wrist. It is the recommended first choice for hemodialysis access. Possible underlying causes for failure are stenosis and thrombosis especially in diabetics and those with low blood flow such as due to narrow vessels, arteriosclerosis and advanced age. Reported patency of fistulae after 1 year is about 62.5%.

A 1994 community-based study indicated that two out of every 100,000 people suffered from SCSFLS, while a 2004 emergency room-based study indicated five per 100,000. SCSFLS generally affects the young and middle aged; the average age for onset is 42.3 years, but onset can range from ages 22 to 61. In an 11-year study women were found to be twice as likely to be affected as men.

Studies have shown that SCSFLS runs in families and it is suspected that genetic similarity in families includes weakness in the dura mater, which leads to SCSFLS. Large scale population-based studies have not yet been conducted. While a majority of SCSFLS cases continue to be undiagnosed or misdiagnosed, an actual increase in occurrence is unlikely.

The most widely accepted pathophysiological mechanism by which Chiari type I malformations occur is by a reduction or lack of development of the posterior fossa as a result of congenital or acquired disorders. Congenital causes include hydrocephalus, craniosynostosis (especially of the lambdoid suture), hyperostosis (such as craniometaphyseal dysplasia, osteopetrosis, erythroid hyperplasia), X-linked vitamin D-resistant rickets, and neurofibromatosis type I. Acquired disorders include space occupying lesions due to one of several potential causes ranging from brain tumors to hematomas.

Head trauma may cause cerebellar tonsillar ectopia, possibly because of dural strain. Additionally, ectopia may be present but asymptomatic until whiplash causes it to become symptomatic. Posterior fossa hypoplasia causes reduced cerebral and spinal compliance.

Subdural hematomas are most often caused by head injury, when rapidly changing velocities within the skull may stretch and tear small bridging veins. Subdural hematomas due to head injury are described as traumatic. Much more common than epidural hemorrhages, subdural hemorrhages generally result from shearing injuries due to various rotational or linear forces. Subdural hemorrhage is a classic finding in shaken baby syndrome, in which similar shearing forces classically cause intra- and pre-retinal hemorrhages. Subdural hematoma is also commonly seen in the elderly and in alcoholics, who have evidence of cerebral atrophy. Cerebral atrophy increases the length the bridging veins have to traverse between the two meningeal layers, hence increasing the likelihood of shearing forces causing a tear. It is also more common in patients on anticoagulants or antiplatelet drugs, such as warfarin and aspirin. Patients on these medications can have a subdural hematoma after a relatively minor traumatic event.

A further cause can be a reduction in cerebral spinal fluid pressure which can create a low pressure in the subarachnoid space, pulling the arachnoid away from the dura mater and leading to a rupture of the blood vessels.

Vascular malformation is a blood vessel abnormality. There are many types, but the most common is arteriovenous malformation.

It may cause aesthetic problems as it has a growth cycle and can continue to grow throughout life. This is also known as Vascular giantism or lymphangiomas.

Intracranial hemorrhage is a serious medical emergency because the buildup of blood within the skull can lead to increases in intracranial pressure, which can crush delicate brain tissue or limit its blood supply. Severe increases in intracranial pressure (ICP) can cause brain herniation, in which parts of the brain are squeezed past structures in the skull.

A spontaneous CSF leak is idiopathic, meaning the cause in unknown. Various scientists and physicians have suggested that this condition may be the result of an underlying connective tissue disorder affecting the spinal dura. It may also run in families and be associated with aortic aneurysms and joint hypermobility. Up to two thirds of those afflicted demonstrate some type of generalized connective tissue disorder. Marfan syndrome, Ehlers-Danlos syndrome and autosomal dominant polycystic kidney disease are the three most common connective tissue disorders associated with SCSFLS.

Roughly 20% of patients with SCSFLS exhibit features of Marfan syndrome, including tall stature, hollowed chest (pectus excavatum), joint hypermobility and arched palate. However these patients do not exhibit any other Marfan syndrome presentations.

When Tarlov cysts are ruptured or drained they cause leakage of cerebrospinal fluid (CSF). Ruptures of Tarlov cysts have been reported associated with communicating aneurysms and from fracture in the proximity of the cysts. An undetected rupture can cause intracranial hypotension, including orthostatic neurological symptoms along with headache, nausea, and vomiting that improve when supine. The ruptured cysts can be patched either with a biosynthetic dural patch or using a blood patch to stem the flow of CSF.

The birth defect affects men and women equally, and is not limited to any racial group. It is not certain if it is genetic in nature, although testing is ongoing. There is some evidence that it may be associated with a translocation at t(8;14)(q22.3;q13). Some researchers have suggested AGGF1 has an association.

Intracranial hemorrhage (ICH), also known as intracranial bleed, is bleeding within the skull. It includes intracerebral bleeds (intraventricular bleeds and intraparenchymal bleeds), subarachnoid bleeds, epidural bleeds, and subdural bleeds.

Intracerebral bleeding affects 2.5 per 10,000 people each year.

Just like berry aneurysm, an intracerebral arteriovenous fistula can rupture causing subarachnoid hemorrhage.

All fast-flow malformations are malformations involving arteries. They constitute about 14% of all vascular malformations.

- Arterial malformation

- Arteriovenous fistula (AVF) : a lesion with a direct communication via fistulae between an artery and a vein.

- Arteriovenous malformation : a lesion with a direct connection between an artery and a vein, without an intervening capillary bed, but with an interposed nidus of dysplastic vascular channels in between.

Tarlov cysts are known to have the tendency to enlarge over time. The prominent theory that explains this phenomenon reasons the enlargement of the cysts is due to the cerebrospinal fluid being pushed into the cyst during systole pulsation, but unable to get out during the diastole phase, resulting in enlargement observed in clinical settings over time. Increased ICP from trauma or other injury, childbirth, and overextertion are thought to trigger enlargement along with inflammation and hemorrhagic infiltration. With the cysts often containing a valve like mechanism fluid becomes trapped, and the meningeal sac or nerve sheath grows in size. Some patients have been diagnosed for up to 20 years with little change in size, and those with small stable cysts may avoid much progression of symptoms. Those with generally larger sacral cysts pressed along the sacrum cause the sacrum to become eroded and thin.

When an arteriovenous fistula is formed involving a major artery like the abdominal aorta, it can lead to a large decrease in peripheral resistance. This lowered peripheral resistance causes the heart to increase cardiac output to maintain proper blood flow to all tissues. The physical manifestations of this would be a relatively normal systolic blood pressure with a decreased diastolic blood pressure resulting in a wide pulse pressure.

Normal blood flow in the brachial artery is 85 to 110 milliliters per minute (mL/min). After the creation of a fistula, the blood flow increases to 400–500 mL/min immediately, and 700–1,000 mL/min within 1 month. A bracheocephalic fistula above the elbow has a greater flow rate than a radiocephalic fistula at the wrist. Both the artery and the vein dilate and elongate in response to the greater blood flow and shear stress, but the vein dilates more and becomes "arterialized". In one study, the cephalic vein increased from 2.3 mm to 6.3 mm diameter after 2 months. When the vein is large enough to allow cannulation, the fistula is defined as "mature".

An arteriovenous fistula can increase preload. AV shunts also decrease the afterload of the heart. This is because the blood bypasses the arterioles which results in a decrease in the total peripheral resistance (TPR). AV shunts increase both the rate and volume of blood returning to the heart.

a combination of various vascular malformations. They are 'complex' because they involve a combination of two different types of vessels.

- CVM: capillary venous malformation

- CLM: capillary lymphatic malformation

- LVM: lymphatic venous malformation

- CLVM: capillary lymphatic venous malformation. CLVM is associated with Klippel-Trenaunay syndrome

- AVM-LM: Arteriovenous malformation- lymphatic malformation

- CM-AVM: capillary malformation- arteriovenous malformation