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Hematoma usually associated with traumatic brain injury
If the bleeds are large enough to put pressure on the brain, signs of increased intracranial pressure or brain damage will be present. 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 ringing in the ears (tinnitus)
Blurred vision
Deviated gaze, or abnormal movement of the eyes. There are claims that they can occur in cases of shaken baby syndrome, although there is no scientific evidence for this. They are also commonly seen in the elderly and in people with an alcohol use disorder who have evidence of cerebral atrophy. It is also more common in patients on anticoagulants or antiplatelet medications, such as warfarin and aspirin, respectively.

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 cover a wider distance, making them more vulnerable to tears. The elderly also have more brittle veins, making chronic subdural bleeds more common. Other risk factors include taking blood thinners (anticoagulants), long term excessive alcohol consumption, dementia, and cerebrospinal fluid leaks.

Acute subdural hematoma is usually caused by external trauma that creates tension in the wall of a bridging vein as it passes between the arachnoid and dural layers of the brain's lining—i. e., the subdural space. The circumferential arrangement of collagen surrounding the vein makes it susceptible to such tearing. Intracerebral hemorrhage and ruptured cortical vessels (blood vessels on the surface of the brain) can also cause subdural hematoma. In these cases, blood usually accumulates between the two layers of the dura mater. This can cause ischemic brain damage by two mechanisms: one, pressure on the cortical blood vessels, and two, vasoconstriction due to the substances released from the hematoma, which causes further ischemia by restricting blood flow to the brain. When the brain is denied adequate blood flow, a biochemical cascade known as the ischemic cascade is unleashed, and may ultimately lead to brain cell death. Subdural hematomas grow continually larger as a result of the pressure they place on the brain: As intracranial pressure rises, blood is squeezed into the dural venous sinuses, raising the dural venous pressure and resulting in more bleeding from the ruptured bridging veins. They stop growing only when the pressure of the hematoma equalizes with the intracranial pressure, as the space for expansion shrinks. Craniotomy for unruptured intracranial aneurysm is another risk factor for the development of chronic subdural hematoma. The incision in the arachnoid membrane during the operation causes cerebrospinal fluid to leak into the subdural space, leading to inflammation. This complication usually resolves on its own.

Subdural hematomas are classified as acute, subacute, or chronic, depending on the speed of their onset. Acute bleeds often develop after high speed acceleration or deceleration injuries. They are most severe if associated with cerebral contusions. The mortality rate is higher than that of epidural hematomas and diffuse brain injuries because the force required to cause subdural hematomas tends to cause other severe injuries as well. Chronic subdural bleeds develop over a period of days to weeks, often after minor head trauma, though 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 hematoma is slow and usually stops by itself. Because these hematomas progress slowly, they can more often be stopped before they cause significant damage, especially if they are less than a centimeter wide. In one study, only 22% of patients with chronic subdural bleeds had outcomes worse than "good" or "complete recovery". The injured vessels must be repaired. Postoperative complications can include increased intracranial pressure, brain edema, new or recurrent bleeding, infection, and seizures. In patients with a chronic subdural hematoma but no history of seizures, it is unclear whether anticonvulsants are harmful or beneficial. Those with chronic subudural haematoma (CSDH) with few or no symptoms or have high risk of complication during surgery may be treated conservatively with medications such as atorvastatin, dexamethasone, and mannitol, although supporting conservative treatment is still weak. HMG CoA reductase inhibitor such as Atorvastatin can reduce the haematoma volume and improving neurological function in eight weeks. HMG CoA reductase inhibitor may also reduce risk of recurrences in CSDH. Dexamethasone, when used together with surgical drainage, may reduce the recurrence rate of subdural haematoma. Even with surgical evacuation of chronic subdural haematoma, the recurrence rate is high, ranging from 7 to 20%. Higher Glasgow Coma Scale score, younger age and responsive pupils are associated with better outcomes in acute subdural hematomas, while the time between the injury and the surgical evacuation, or the type of surgery, do not have a statistically significant impact on the outcomes. Additionally, chronic subdural hematomas (CSDHs) have a relatively high mortality rate (up to 16.7% in patients over the age of 65); however, they have an even higher rate of recurrence (as mentioned in the previous section). For the aforementioned reasons, researchers have developed predictive grading scales to identify patients at high risk of CSDH recurrence, one of which is the Puerto Rico Recurrence Scale developed by Mignucci Jiménez et al.