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.

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.

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 subdural hygromas are small and clinically insignificant. Larger hygromas may cause secondary localized mass effects on the adjacent brain parenchyma, enough to cause a neurologic deficit or other symptoms. Acute subdural hygromas can be a potential neurosurgical emergency, requiring decompression. Acute hygromas are typically a result of head trauma—they are a relatively common posttraumatic lesion—but can also develop following neurosurgical procedures, and have also been associated with a variety of conditions, including dehydration in the elderly, lymphoma and connective tissue diseases.

In the majority of cases, if there has not been any acute trauma or severe neurologic symptoms, a small subdural hygroma on the head CT scan will be an incidental finding. If there is an associated localized mass effect that may explain the clinical symptoms, or concern for a potential chronic SDH that could rebleed, then an MRI, with or without neurologic consultation, may be useful.

It is not uncommon for chronic subdural hematomas (SDHs) on CT reports for scans of the head to be misinterpreted as subdural hygromas, and vice versa. Magnetic resonance imaging (MRI) should be done to differentiate a chronic SDH from a subdural hygroma, when clinically warranted. Elderly patients with marked cerebral atrophy, and secondary widened subarachnoid CSF spaces, can also cause confusion on CT. To distinguish chronic subdural hygromas from simple brain atrophy and CSF space expansion, a gadolinium-enhanced MRI can be performed. Visualization of cortical veins traversing the collection favors a widened subarachnoid space as seen in brain atrophy, whereas subdural hygromas will displace the cortex and cortical veins.

The clinical presentation of CST can be varied. Both acute, fulminant disease and indolent, subacute presentations have been reported in the literature.

The most common signs of CST are related to anatomical structures affected within the cavernous sinus, notably cranial nerves III-VI, as well as symptoms resulting from impaired venous drainage from the orbit and eye.

Classic presentations are abrupt onset of unilateral periorbital edema, headache, photophobia, and bulging of the eye (proptosis).

Other common signs and symptoms include:

Ptosis, chemosis, cranial nerve palsies (III, IV, V, VI). Sixth nerve palsy is the most common. Sensory deficits of the ophthalmic and maxillary branch of the fifth nerve are common. Periorbital sensory loss and impaired corneal reflex may be noted. Papilledema, retinal hemorrhages, and decreased visual acuity and blindness may occur from venous congestion within the retina. Fever, tachycardia and sepsis may be present. Headache with nuchal rigidity may occur. Pupil may be dilated and sluggishly reactive. Infection can spread to contralateral cavernous sinus within 24–48 hours of initial presentation.

Epidural, subdural, and subarachnoid hemorrhages are extra-axial bleeds, occurring outside of the brain tissue, while intra-axial hemorrhages, including intraparenchymal and intraventricular hemorrhages, occur within it.

Epidural hematomas may present with a lucid period immediately following the trauma and a delay before symptoms become evident. After the epidural hematoma begins collecting, it starts to compress intracranial structures which may impinge on the CN III. This can be seen in the physical exam as a fixed and dilated pupil on the side of the injury. The eye will be positioned down and out, due to unopposed CN IV and CN VI innervation.

Other manifestations will include weakness of the extremities on the opposite side as the lesion (except in rare cases), due to compression of the crossed pyramid pathways, and a loss of visual field opposite to the side of the lesion, due to compression of the posterior cerebral artery on the side of the lesion.

The most feared event that takes place is tonsillar herniation which could result in respiratory arrest since the medullary structures are compromised. The trigeminal nerve (CN V) may be involved late in the process as the pons becomes compressed, but this is not a significant clinical presentation, since by that time the patient may already be dead. In the case of epidural hematoma in the posterior cranial fossa, the herniation is tonsillar and causes the Cushing's triad: hypertension, bradycardia, and irregular respiration.

Epidural bleeding is rapid because it is usually from arteries, which are high pressure. Epidural bleeds from arteries can grow until they reach their peak size at six to eight hours post injury, spilling from 25 to 75 cubic centimeters of blood into the intracranial space. As the hematoma expands, it strips the dura from the inside of the skull, causing an intense headache. Epidural bleeds can become large and raise intracranial pressure, causing the brain to shift, lose blood supply, or be crushed against the skull. Larger hematomas cause more damage. Epidural bleeds can quickly expand and compress the brain stem, causing unconsciousness, abnormal posturing, and abnormal pupil responses to light.

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.

The symptoms of a cerebral contusion (bruising on the brain) depend on the severity of the injury, ranging from minor to severe. Individuals may experience a headache; confusion; sleepiness; dizziness; loss of consciousness; nausea and vomiting; seizures; and difficulty with coordination and movement. They may also have difficulty with memory, vision, speech, hearing, managing emotions, and thinking. Signs depend on the contusion's location in the brain.

Epidural hematoma is when bleeding occurs between the tough outer membrane covering the brain and the skull. Often there is loss of consciousness following a head injury, a brief regaining of consciousness, and then loss of consciousness again. Other symptoms may include headache, confusion, vomiting, and an inability to move parts of the body. Complications may include seizures.

The cause is typically head injury that results in a break of the temporal bone and bleeding from the middle meningeal artery. Occasionally it can occur as a result of a bleeding disorder or blood vessel malformation. Diagnosis is typically by a CT scan or MRI. When this condition occurs in the spine it is known as a spinal epidural hematoma.

Treatment in generally by urgent surgery in the form of a craniotomy or burr hole. Without treatment death typically results. The condition occurs in one to four percent of head injuries. Typically it occurs in young adults. Males are more often affected than females.

SCSFLS is classified into two main types, cranial leaks and spinal leaks. The vast majority of leaks are spinal. Cranial leaks occur in the head. In some of these cases, CSF can be seen dripping out of the nose, or ear. Spinal leaks occur when one or more holes form in the dura along the spinal cord. Both cranial and spinal spontaneous CSF leaks cause neurological symptoms as well as spontaneous intracranial hypotension, diminished volume and pressure of the cranium. While referred to as "intracranial hypotension", the intracranial pressure may be normal, with the underlying issue instead being low-volume CSF. For this reason SCSFLS is referred to as "CSF hypovolemia" as opposed to "CSF hypotension".

Cavernous sinus thrombosis (CST) is the formation of a blood clot within the cavernous sinus, a cavity at the base of the brain which drains deoxygenated blood from the brain back to the heart. The cause is usually from a spreading infection in the nose, sinuses, ears, or teeth. "Staphylococcus aureus" and "Streptococcus" are often the associated bacteria. Cavernous sinus thrombosis symptoms include: decrease or loss of vision, chemosis, exophthalmos (bulging eyes), headaches, and paralysis of the cranial nerves which course through the cavernous sinus. This infection is life-threatening and requires immediate treatment, which usually includes antibiotics and sometimes surgical drainage.

Numerous small contusions from broken capillaries that occur in grey matter under the cortex are called multiple petechial hemorrhages or multifocal hemorrhagic contusion. Caused by shearing injuries at the time of impact, these contusions occur especially at the junction between grey and white matter and in the upper brain stem, basal ganglia, thalamus and areas near the third ventricle. The hemorrhages can occur as the result of brain herniation, which can cause arteries to tear and bleed. A type of diffuse brain injury, multiple petechial hemorrhages are not always visible using current imaging techniques like CT and MRI scans. This may be the case even if the injury is quite severe, though these may show up days after the injury. Hemorrhages may be larger than in normal contusions if the injury is quite severe. This type of injury has a poor prognosis if the patient is comatose, even with no apparent causes for the coma.

Fever, headache, and neurological problems, while classic, only occur in 20% of people with brain abscess.

The famous triad of fever, headache and focal neurologic findings are highly suggestive of brain abscess. These symptoms are caused by a combination of increased intracranial pressure due to a space-occupying lesion (headache, vomiting, confusion, coma), infection (fever, fatigue etc.) and focal neurologic brain tissue damage (hemiparesis, aphasia etc.).

The most frequent presenting symptoms are headache, drowsiness, confusion, seizures, hemiparesis or speech difficulties together with fever with a rapidly progressive course. Headache is characteristically worse at night and in the morning, as the intracranial pressure naturally increases when in the supine position. This elevation similarly stimulates the medullary vomiting center and area postrema, leading to morning vomiting.

Other symptoms and findings depend largely on the specific location of the abscess in the brain. An abscess in the cerebellum, for instance, may cause additional complaints as a result of brain stem compression and hydrocephalus. Neurological examination may reveal a stiff neck in occasional cases (erroneously suggesting meningitis).

A hematoma (US spelling) or haematoma (UK spelling) is a localized collection of blood outside the blood vessels, due to either disease or trauma including injury or surgery and may involve blood continuing to seep from broken capillaries. A hematoma is initially in liquid form spread among the tissues including in sacs between tissues where it may coagulate and solidify before blood is reabsorbed into blood vessels. An ecchymosis is a hematoma of the skin larger than 10mm.

They may occur among/within many areas such as skin and other organs, connective tissues, bone, joints and muscle.

A collection of blood (or even a hemorrhage) may be aggravated by anticoagulant medication (blood thinner). Blood seepage and collection of blood may occur if heparin is given via an intramuscular route; to avoid this, heparin must be given intravenously or subcutaneously.

It is not to be confused with hemangioma, which is an abnormal buildup/growth of blood vessels in the skin or internal organs.

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

Symptoms often include:

- Seizures, especially in newborns

- Keeping one hand in a fist position, especially in infants

- Worsening or sudden headaches

- Sudden difficulty speaking, slurring of words or trouble understanding speech

- Hemiparesis, or a weakness on one side of the body

- Sudden loss of vision or abnormal eye movements

- Sudden loss of balance or trouble walking

Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g., headache, previous head injury).

Subdural empyaema is a form of empyema in the subdural space.

Bacterial or occasionally fungal infection of the skull bones or air sinuses can spread to the subdural space, producing a subdural empyema. The underlying arachnoid and subarachnoid spaces are usually unaffected, but a large subdural empyema may produce a mass effect. Further, a thrombophlebitis may develop in the bridging veins that cross the subdural space, resulting in venous occlusion and infarction of the brain. With treatment, including surgical drainage, resolution of the empyema occurs from the dural side, and, if it is complete, a thickened dura may be the only residual finding. Symptoms include those referable to the source of the infection. In addition, most patients are febrile, with headache and neck stiffness, and, if untreated, may develop focal neurologic signs, lethargy, and coma. The CSF profile is similar to that seen in brain abscesses, because both are parameningeal infectious processes. If diagnosis and treatment are prompt, complete recovery is usual.

It usually occurs in infancy. It can be associated with sinusitis.

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 diagnosis is established by a computed tomography (CT) (with contrast) examination. At the initial phase of the inflammation (which is referred to as cerebritis), the immature lesion does not have a capsule and it may be difficult to distinguish it from other space-occupying lesions or infarcts of the brain. Within 4–5 days the inflammation and the concomitant dead brain tissue are surrounded with a capsule, which gives the lesion the famous ring-enhancing lesion appearance on CT examination with contrast (since intravenously applied contrast material can not pass through the capsule, it is collected around the lesion and looks as a ring surrounding the relatively dark lesion). Lumbar puncture procedure, which is performed in many infectious disorders of the central nervous system is contraindicated in this condition (as it is in all space-occupying lesions of the brain) because removing a certain portion of the cerebrospinal fluid may alter the concrete intracranial pressure balances and causes the brain tissue to move across structures within the skull (brain herniation).

Ring enhancement may also be observed in cerebral hemorrhages (bleeding) and some brain tumors. However, in the presence of the rapidly progressive course with fever, focal neurologic findings (hemiparesis, aphasia etc.) and signs of increased intracranial pressure, the most likely diagnosis should be the brain abscess.

Some hematomas are visible under the surface of the skin (commonly called bruises) or possibly felt as masses/lumps. Lumps may be caused by the limitation of the blood to a sac, subcutaneous or intramuscular tissue space isolated by fascial planes. This is a key anatomical feature that helps prevent injuries from causing massive blood loss. In most cases the hematoma such as a sac of blood eventually dissolves; however, in some cases they may continue to grow such as due to blood seepage or show no change. If the sac of blood does not disappear, then it may need to be surgically cleaned out/repaired.

The slow process of reabsorption of hematomas can allow the broken down blood cells and hemoglobin pigment to move in the connective tissue. For example, a patient who injures the base of his thumb might cause a hematoma, which will slowly move all through the finger within a week. Gravity is the main determinant of this process.

Hematomas on articulations can reduce mobility of a member and present roughly the same symptoms as a fracture.

In most cases, movement and exercise of the affected muscle is the best way to introduce the collection back into the blood stream.

A mis-diagnosis of a hematoma in the vertebra can sometimes occur; this is correctly called a hemangioma (buildup of cells) or a benign tumor.

Transient ischemic attacks (TIAs) rarely affect the spinal cord and usually affect the brain; however, cases have been documented in these areas. Spinal ateriovenous malformations are the main cause and are represented later in this article. However, TIAs can result from emboli in calcific aortic disease and aortic coarctation.

Posterior spinal artery syndrome is much rarer than its anterior counterpart as the white matter structures that are present are much less vulnerable to ischemia since they have a better blood supply. When posterior spinal artery syndrome does occur, dorsal columns are damaged and ischemia may spread into the posterior horns. Clinically the syndrome presents as a loss of tendon reflexes and loss of joint position sense