Subdural hematoma in adults: Etiology, clinical features, and diagnosis

INTRODUCTION — Subdural hematoma (SDH) is a form of intracranial hemorrhage characterized by bleeding into the space between the dural and arachnoid membranes surrounding the brain.

The pathophysiology, etiology, clinical features, and diagnostic evaluation of SDH will be discussed here. A rapid overview summarizes clinical features, evaluation, and management of SDH in adults (table 1).

Other aspects of SDH are reviewed separately.

●(See "Subdural hematoma in adults: Management and prognosis".)

●(See "Intracranial subdural hematoma in children: Epidemiology, anatomy, and pathophysiology".)

●(See "Intracranial subdural hematoma in children: Clinical features, evaluation, and management".)

Other forms of intracranial hemorrhage and intracerebral hemorrhage are discussed elsewhere.

●(See "Intracranial epidural hematoma in adults".)

●(See "Intracranial epidural hematoma in children".)

●(See "Aneurysmal subarachnoid hemorrhage: Epidemiology, risk factors, and pathogenesis" and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis" and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis".)

●(See "Nonaneurysmal subarachnoid hemorrhage".)

●(See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage".)

●(See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis" and "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".)

PATHOPHYSIOLOGY AND ETIOLOGY

Anatomy — SDH forms between the dural and the arachnoid membranes overlying the brain (image 1 and figure 1 and figure 2). Anatomic distinctions between the different forms of brain hemorrhage may be visible by imaging and may be used to help guide treatment and to identify underlying mechanisms.

●SDH is often crescent shaped because bleeding follows the contour of the overlying dura. SDH will typically span overlying epidural sutural margins but not the interhemispheric falx. Most SDH occur along the cerebral convexities. However, SDH may also occur in the subdural spaces between cerebral and cerebellar hemispheres or circumferentially around the brainstem [1]. Extracranial SDH along the spinal column is a rare site of bleeding [2,3].

Other forms of intracranial hemorrhage are defined by their distinct anatomic sites of bleeding:

●Subarachnoid hemorrhage (SAH) occurs between the arachnoid and pial membranes (image 2). Blood from SAH closely follows the contour of the overlying pial membrane and cortical gyri of the brain. Intraventricular blood may be seen in SAH because the subarachnoid space communicates with intraventricular foramen in the fourth ventricle. (See "Aneurysmal subarachnoid hemorrhage: Epidemiology, risk factors, and pathogenesis".)

●Epidural hematomas arise in the potential space between the dura and the inner table of the skull (image 3). Epidural hematomas often have a lens-shaped appearance because bleeding is typically restricted by calvarial sutures where the dura attaches to the skull. Epidural hematomas can span the underlying dural attachments including the interhemispheric falx. (See "Intracranial epidural hematoma in adults".)

●Intracerebral hemorrhage describes bleeding within the brain tissue (image 4). (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis".)

Pathophysiology — Acute SDH occurs due to bleeding within the subdural space and may resolve by resorption or become chronic by membranous encapsulation and hygroma formation.

Vascular injury in acute subdural hematoma — Acute SDH is usually caused by tearing of the veins located between the arachnoid membranes and the dura in most cases. These bridging veins drain from the surface of the brain into the dural sinuses [4]. Venous bleeding at this site is usually arrested by the rising intracranial pressure or compartmental tamponade by the clot itself.

Arterial rupture can also result in SDH in approximately 20 to 30 percent of SDH cases [5-7]. In an autopsy study of 46 patients with isolated SDH that included 23 caused by arterial injury, most were caused by injuries to small cortical arteries of <1 mm diameter [7]. Both arterial and venous SDHs had generally similar postmortem characteristics, although SDHs caused by arterial rupture were predominately located in the temporoparietal region, while those caused by bridging vein rupture were predominately frontoparietal.

Development of chronic subdural hematoma — Following the initial dural trauma and development of an acute SDH, the process of blood resorption begins with breakdown of erythrocytes and other cellular components. In addition, collagen synthesis is induced and fibroblasts spread over the inner surface of the dura to form a thick outer membrane [8,9]. Subsequently, a thinner inner membrane develops, resulting in complete encapsulation of the clot. This process typically occurs over a time course of approximately two weeks [9]. (See 'Imaging features' below.)

Some chronic SDH are subsequently resorbed completely. However, others may expand during this time. This may be due either to spontaneous or triggered recurrent bleeding ("acute-on-chronic" SDH) or to the formation of a subdural hygroma.

Development of subdural hygroma — Communication between the subdural and subarachnoid space may allow cerebrospinal fluid to accumulate and form a subdural hygroma. Membrane permeability during SDH resolution, an osmotic draw of water into the protein-rich SDH fluid, and injury to the arachnoid membrane may contribute to this process [9,10]. More than one-half of all subdural hygromas grow in size and may result in greater mass effect than the initial SDH [4]. Although the reason for this observation is unknown, a larger initial clot size appears to be related to a greater likelihood of subsequent expansion [11].

Most subdural hygromas will resolve slowly over several weeks with adequate reexpansion of the intracranial contents. However, some will persist [10]. The persistence of hygromas appears to be related to the formation of pseudomembranes that line the space created between the arachnoid and the dura during the acute phase. These subsequently become vascularized by abnormally permeable capillaries that allow for further accumulation of subdural fluid.

Specific etiologies — SDH may be spontaneous or triggered by an inciting event.

Trauma — Head trauma is the most common cause of SDH, with the majority of cases related to motor vehicle accidents, falls, and assaults [12]. The linear translation of acceleration along the diameter of the skull in the lateral direction can produce injury to veins, arteries, meninges, or brain parenchyma, resulting in multiple forms of intracranial hemorrhage, including SDH [13]. A retrospective cohort study of emergency department administrative claims data involving 27,502 patients with SDH identified a traumatic source in 71 percent [14]. (See "Traumatic brain injury: Epidemiology, classification, and pathophysiology".)

In addition, trivial or minor head trauma is frequently identified as an antecedent to acute or chronic SDH in susceptible patients with cerebral atrophy or other risk factors [15,16]. (See 'Cerebral atrophy' below.)

Intentional or inflicted head trauma is also a source for SDH, typically seen in infants and children. (See "Child abuse: Epidemiology, mechanisms, and types of abusive head trauma in infants and children", section on 'Intracranial bleeding' and "Intracranial subdural hematoma in children: Epidemiology, anatomy, and pathophysiology", section on 'Type of injury'.)

Intracranial hypotension — Low cerebrospinal fluid pressure (intracranial hypotension) is another mechanism that can result in SDH. Intracranial hypotension may be caused by a spontaneous or iatrogenic cerebrospinal fluid leak such as following lumbar puncture or ventriculostomy, lumboperitoneal shunt placement, or other neurosurgical procedures [17]. As the cerebrospinal fluid pressure decreases, reduction in the buoyancy (ie, sagging) of the brain causes traction on bridging veins and leads to tearing and rupture of these vessels. In addition, intracranial hypotension may lead to engorgement of cerebral veins and subsequent leakage of fluid into the subdural space (image 5). (See "Spontaneous intracranial hypotension: Pathophysiology, clinical features, and diagnosis" and "Normal pressure hydrocephalus", section on 'Shunt complications'.)

Less common causes

●Arterial sources – Arterial injury may coexist with venous injury in traumatic and other causes of SDH. In addition, arterial injuries occurring in the subdural space may be a cause of spontaneous SDH. Specific underlying arterial causes of SDH include:

•Intracerebral hemorrhage – Primary intracerebral hemorrhage may be accompanied by SDH when bleeding through the cortical surface extends into the subdural space. Intracerebral hemorrhages with SDH involving the cerebellum have been attributed to hypertension and those in lobar regions have been associated with cerebral amyloid angiopathy [18,19]. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis".)

•Ruptured cerebral aneurysm – A ruptured cerebral aneurysm causing SAH that extends into the subdural space occurs in approximately 0.5 up to 7.9 percent of cases [20-24]. Bleeding is typically visible on imaging at both sites. Very rarely, aneurysm rupture causes isolated SDH without visible SAH [24]. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis".)

•Cerebral vascular malformations – Rupture of an arteriovenous malformation, arteriovenous fistula, or cavernous malformation at the cortical surface may rarely present with isolated acute SDH [25-28]. (See "Brain arteriovenous malformations" and "Vascular malformations of the central nervous system".)

•Vasculopathy – Cocaine abuse with associated hypertension and vasospasm has been proposed as a rare cause of spontaneous SDH presumably via cortical vessel injury in the setting of vasospasm [29,30].

●Neoplasm – Neoplastic lesions may lead to SDH by vessel injury from mass effect or from neovascular rupture. SDH associated with dural (pachymeningeal) metastasis are commonly defined by clinical history and identification of dural nodules on magnetic resonance imaging or pathologic specimen [31-37]. The most common malignancies associated with dural metastases are breast, prostate, lung, and lymphoma [38]. (See "Brain metastases in breast cancer" and "Initial staging and evaluation of males with newly diagnosed prostate cancer", section on 'Metastasis (M)' and "Brain metastases in non-small cell lung cancer" and "Secondary central nervous system lymphoma: Clinical features and diagnosis".)

Rarely, primary brain tumors such as meningiomas may also be complicated by SDH [39,40]. (See "Epidemiology, pathology, clinical features, and diagnosis of meningioma".)

EPIDEMIOLOGY — While the exact incidence of SDH is unknown, acute SDH is found in approximately 11 percent of mild to moderate head injuries that require hospitalization [12,41,42] and approximately 20 percent of severe traumatic brain injuries [12,43-46]. The mean age of patients with SDH caused by head injuries is between approximately 30 and 50 years old, the majority of whom are males [12,41,42,47,48]. Motor vehicle accidents are the most common cause of traumatic SDH among younger adults, while falls are the most common cause among older adults [49]. SDH is a more common complication of trauma than epidural hematoma [50].

The incidence of chronic SDH ranges from 1.7 up to 20.6 per 100,000 persons/year [51]. This risk appears to be increasing over time, likely as a consequence of an aging population and the increased use of antiplatelet and anticoagulant medications [52]. Chronic SDH is more common in older than younger patients, who are likelier to have cerebral atrophy.

RISK FACTORS

Cerebral atrophy — Patients with significant cerebral atrophy are at an elevated risk for SDH. Cerebral atrophy results in a larger space between the dural membrane and cortical surface of the brain, which increases tension on bridging veins. Bleeding in the subdural space may occur when this tension leads to venous injury. Cerebral atrophy is common in older adults, those with a history of chronic alcohol abuse, and those with previous traumatic brain injury. In such patients, trivial head trauma or even pure whiplash injury in the absence of physical impact may produce an SDH [9,53].

Antithrombotic therapy — The use of antithrombotic agents increases the risk of SDH, as illustrated by a case-control study of 10,010 patients with a first-ever SDH [54]. An increased risk of SDH was associated with the use of the following antithrombotic medications:

●Aspirin (cases and controls 26.7 and 22.4 percent; adjusted odds ratio [OR] 1.24, 95% CI 1.15-1.33)

●Clopidogrel (cases and controls 5.0 and 2.2 percent; OR 1.87, 95% CI 1.57-2.24)

●Direct oral anticoagulant (cases and controls 1.0 and 0.6 percent; OR 1.73, 95% CI 1.31-2.28)

●Vitamin K antagonist (cases and controls 14.3 and 4.9 percent; OR 3.69, 95% CI 3.38-4.03)

The risk of SDH appears highest among patients taking warfarin and increases with the intensity of anticoagulation. A case-control analysis compared 121 consecutive adults who developed intracranial hemorrhage while taking warfarin (including 44 with SDH) with 363 matched controls managed by the outpatient anticoagulation clinic [55]. The risk of SDH was significantly associated with a prothrombin time ratio of >2, approximately equivalent to an international normalized ratio (INR) >4.

The increased risk of SDH with direct oral anticoagulants may be similar to aspirin. A clinical trial involving 27,395 patients randomized to rivaroxaban, aspirin, or low-dose rivaroxaban plus aspirin showed a similarly low incidence of SDH (0.04 to 0.06 per 100 patient-years) among the treatment arms [56]. A meta-analysis likewise showed that the risk of SDH for patients taking factor Xa inhibitors was similar to those taking aspirin (OR 0.97, 95% CI 0.52-1.81) [56].

Dual antiplatelet or combination antiplatelet plus anticoagulation therapy confers a higher risk of SDH than monotherapy [57,58]. In a meta-analysis of more than 23,000 patients from trials testing the addition of clopidogrel to aspirin, dual therapy was associated with an elevated risk (risk ratio 2.0, 95% CI 1.0-3.8) [57]. However, the absolute risk was low (1.1 per 1000 patient-years).

Other coagulopathies — The risk of traumatic and spontaneous SDH may be increased in patients with thrombocytopenia and those with liver disease [59-61]. (See "Approach to the adult with a suspected bleeding disorder".)

SDH is a reported complication of systemic thrombolysis, although the incidence is quite low. One trial reported that treatment with heparin, aspirin, and intravenous recombinant tissue-type plasminogen activator (rt-PA) at doses of either 150 or 100 mg was complicated by SDH in 0.2 and 0.1 percent of patients, respectively [62]. Another study found that SDH occurring in patients receiving rt-PA for acute myocardial infarction was associated with other risk factors such as a history of preexisting head trauma or older age [63].

CLINICAL MANIFESTATIONS — The initial presentation of SDH has a wide spectrum of manifestations. Patients with severe head trauma and SDH may present with symptoms related to coexisting epidural hematoma, subarachnoid hemorrhage, cerebral contusion, diffuse brain swelling, and fractures. Any of these injuries may coexist in a given patient following trauma, and their clinical manifestations can be difficult to distinguish [4,12,41,42]. Such patients may also present with coma due to the overall insult to the brain. The clinical features of patients with traumatic brain injury are discussed in greater detail separately. (See "Acute mild traumatic brain injury (concussion) in adults", section on 'Clinical features'.)

By contrast, patients with a mild or trivial trauma and those with spontaneous SDH are likelier to present with signs and symptoms due to the mass effect of the SDH alone.

SDH may also be asymptomatic, found incidentally on imaging obtained for unrelated symptoms.

Focal neurologic signs — Specific presenting symptoms may vary according to the location of the bleeding overlying the brain structures impacted.

●Frontal lobe – Hemiparesis, speech impairment (dominant hemisphere), executive dysfunction (nondominant hemisphere) [64]

●Parietal lobe – Speech impairment (dominant hemisphere), sensory impairment (nondominant hemisphere) [65]

●Posterior fossa – Headache, vomiting, anisocoria, dysphagia, cranial nerve palsies, nuchal rigidity, ataxia [66]

●Interhemispheric – Headache, paraparesis without facial weakness (falx syndrome) [67,68]

Focal deficits may be either ipsilateral or contralateral to the side of the SDH. Contralateral hemiparesis can occur due to direct compression of cortex underlying the hematoma, whereas ipsilateral hemiparesis can occur with lateral displacement of the midbrain caused by the mass effect of the hematoma. Such midbrain displacement results in compression of the contralateral cerebral peduncle against the free edge of the tentorium (image 6) [4,69].

Bilateral chronic SDH may present with intermittent paraparesis that is proximal and painless [70,71].

Headaches are commonly reported in alert patients with SDH, due to activation of nociceptors within the dura [72,73].

Seizures — Patients with acute or chronic SDH may also present with seizures or status epilepticus [74,75]. The incidence of early seizures (within seven days of onset) appears higher for patients with acute SDH than those with chronic SDH (28 versus 5 percent) [76]. Risk factors for seizures associated with acute SDH include lower Glasgow coma scale (GCS) score and the need for surgical evacuation with craniotomy [77]. For patients with chronic SDH, risks for seizures are related to premorbid conditions including prior alcohol use and prior stroke.

Acute large hematoma — Those with large SDH may present with more severe or progressive symptoms including stupor or herniation syndromes (table 2) due to shifting of midline brain structures [1]. Approximately 50 percent of patients may be comatose upon presentation. Up to one-third of these patients have an initial transient "lucid interval" after the acute injury that is followed by a progressive neurologic decline to coma [4,12].

In rare instances of SDH, cerebral hypoperfusion due to increased intracranial pressure or mass effect may culminate in cerebral infarction [78].

Chronic subdural hematoma — Patients who become symptomatic with chronic SDH are more likely to present with nonfocal symptoms than those with acute SDH. The onset of bleeding may be difficult to establish, and symptoms may not become evident until weeks after the injury or other inciting source. Vague or mild, nonfocal symptoms may become clinically apparent when persistent or progressive. Such symptoms may include new or unexplained, progressive symptoms such as:

●Headache [79,80]

●Light-headedness

●Cognitive impairment [4,81]

●Apathy or depression [82,83]

●Parkinsonism (eg, tremor, rigidity) [84,85]

●Gait ataxia [86]

●Somnolence [87]

●Seizures [4,12,78,79]

DIAGNOSIS AND EVALUATION — The diagnosis of SDH is made by neuroimaging, typically computed tomography (CT) of the head, as part of the evaluation of a patient with a head injury or work-up for other symptoms. (See 'Clinical manifestations' above.)

Other diagnostic imaging and laboratory testing may be indicated when the cause of the bleeding is not apparent.

Imaging features — Noncontrast head CT is the first-choice imaging study to rapidly diagnose SDH [88]. Brain magnetic resonance imaging (MRI) may also be used but typically takes longer to perform than CT and is less readily available in many facilities on an emergent basis. In addition, MRI may not be feasible for some patients with implanted metallic or electrical devices. (See "Patient evaluation for metallic or electrical implants, devices, or foreign bodies before magnetic resonance imaging".)

SDH may be categorized clinically by the time since onset of bleeding.

●Acute SDH presents 1 to 2 days after onset.

●Subacute SDH presents 3 to 14 days after onset.

●Chronic SDH presents 15 or more days after onset.

However, these categories of acute, subacute, and chronic SDH are defined somewhat arbitrarily as there is no consensus in the literature regarding time thresholds. When there is no history of trauma or other inciting event prior to the clinical presentation of SDH, the age of the bleeding may be approximated by imaging features, described immediately below.

Head CT — Computed tomography (CT) of the head is the most widely used imaging study for acute head trauma owing to its speed, relative simplicity, and widespread availability [88,89]. Specific imaging characteristics can also help identify acute and chronic SDH.

●Acute SDH is readily visualized on head CT as a uniformly high-density crescentic collection (image 7).

●Chronic SDH and hygromas appear as isodense to hypodense crescent-shaped lesions that may contain friable, vascularized pseudomembranes that enhance with intravenous contrast (image 8 and image 9).

●Mixed-density SDH (also called "hematohygroma") contain both hyperdense and hypodense components. They may be acute or chronic. Within days after onset of bleeding, an acute SDH may have a mixed density on CT due to sedimentation of erythrocytes in the hemorrhage. In addition, spontaneous or triggered rebleeding in a chronic SDH may appear as a mixed-density SDH.

Unilateral SDH with mass effect will typically distort brain anatomy on CT (image 10). However, careful evaluation may be needed to identify cases with subtle imaging features. Bilateral SDH may be missed, as the brain parenchyma can appear symmetric, while a resolving SDH may be isointense relative to brain (image 11) [4]. Head CT can also be used to help distinguish SDH from an epidural hematoma and other forms of intracranial hemorrhage by the pattern and shape of bleeding. (See 'Anatomy' above.)

In a study published in 1988, approximately 91 percent of SDHs ≥5 mm in thickness were identified on initial head CT [90]. By contrast, SDHs ≤3 mm in thickness were often missed initially but noted to be present retrospectively. With improvements in resolution, modern-generation CT scanners may provide even greater sensitivity for the detection of SDH. However, there have been no published data to confirm this impression.

Brain MRI — Brain magnetic resonance imaging (MRI) may be performed for the initial diagnosis of SDH. In a study of 40 patients with traumatic brain injury, MRI was as sensitive as CT for detecting acute hemorrhagic lesions including SDH [90]. Brain MRI may be the preferred imaging modality for the initial diagnosis or subsequent evaluation of SDH in specific circumstances:

●Identifying small bleeds – Small chronic SDH on head CT may be mistaken for brain tissue or cerebrospinal fluid (CSF) but may be more easily identified on MRI (image 11). For these patients, MRI may be preferred. Specific MRI sequences are sensitive for blood and may help identify small SDH:

•On fluid-attenuated inversion recovery (FLAIR) sequences, blood is typically hyperintense compared with CSF (image 12).

•On T2* (eg, gradient echo or susceptibility-weighted image) sequences, blood is typically hypointense.

●Determining the age of the bleed – Specific MRI sequences (eg, T1, T2, and T2* sequences) may help identify the age of a hemorrhagic lesion. The signal intensity of blood evolves as oxyhemoglobin in erythrocytes degrades to deoxyhemoglobin, methemoglobin, and finally hemosiderin. However, these imaging patterns used more commonly for intracerebral hemorrhage do not apply as well for SDH and other forms of extra-axial intracranial bleeding. The timing of MRI findings of an evolving SDH for an individual patient may vary by the size of the bleeding, presence of rebleeding, and extent of pseudomembrane formation [91].

●Evaluating for secondary causes – MRI can provide additional information regarding the presence and extent of associated intraparenchymal lesions such as intracerebral hemorrhage, arteriovenous malformations, or dural neoplasms [89,90]. (See 'Evaluation for underlying causes' below.)

●Confirming that the subdural lesion is hemorrhagic – MRI may be useful to identify the rare instances when a subdural lesion may be caused by a nonhemorrhagic source. Such patients typically lack a history of trauma or other risk factors for SDH or have atypical imaging findings on CT. In a review of 48 patients with SDH mimics, the most common causes of the subdural lesions were lymphoma, metastasis, sarcoma, and infection [92].

Follow-up imaging — Urgent repeat neuroimaging, typically with CT, is indicated for patients with clinical deterioration to assess for hematoma expansion or rebleeding and guide treatment options. Surveillance imaging is also performed for stable patients to confirm the SDH is stable by imaging. The role of imaging in the management of SDH is discussed in greater detail separately. (See "Subdural hematoma in adults: Management and prognosis", section on 'Follow-up imaging'.)

Evaluation for underlying causes — Patients with SDH attributed to trauma or in the setting of common risk factors (eg, older patient with baseline severe cerebral atrophy and chronic subdural hematoma) may not require additional imaging. Other patients without antecedent trauma or obvious risk factors for SDH should be evaluated for secondary causes.

●Brain and vascular imaging – We prefer brain MRI with contrast to evaluate for secondary causes such as intracranial hypotension, associated intracerebral hemorrhage, or neoplasm. Repeat head CT with contrast may be performed as an alternative. (See 'Brain MRI' above.)

Noninvasive angiography (eg, magnetic resonance angiography [MRA] or CT angiography [CTA]) may be indicated to evaluate for a vascular etiology when the history and initial imaging reveal no other obvious cause [24]. Digital subtraction angiography is performed when there is suspicion for an underlying vascular lesion that was not detected by noninvasive MRA or CTA. As an example, spontaneous SDH can rarely occur as a consequence of intracranial aneurysmal rupture, and angiography may be necessary to fully evaluate the possibility of an underlying vascular lesion [93]. (See 'Less common causes' above.)

●Laboratory testing – A complete blood count, liver function tests, and prothrombin time (PT)/international normalized ratio (INR) and partial thromboplastin time (PTT) testing may identify patients with SDH due to coagulopathy. Electrolytes are useful to identify hyponatremia or other derangements which may increase the risk of seizures.

Lumbar puncture is contraindicated due to the risk of herniation for patients with a space-occupying lesions such as an SDH.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".)

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Subdural hematoma and epidural hematoma (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Anatomy – Subdural hematoma (SDH) forms between the dural and the arachnoid membranes overlying the brain (figure 2 and image 1). SDH often has a crescent-shaped appearance because bleeding follows the contour of the overlying dura. Most SDHs occur along the cerebral convexities but may also occur in the subdural spaces between cerebral and cerebellar hemispheres or circumferentially around the brainstem (figure 1). (See 'Anatomy' above.)

●Pathophysiology – Acute SDH is usually caused by tearing of the veins located between the arachnoid membranes and the dura in most cases. An arterial source may be found in approximately 20 to 30 percent of SDH cases.

●Etiologies – SDH may be spontaneous or triggered by an inciting event. (See 'Specific etiologies' above.)

•Head trauma is the most common cause of SDH, with most cases related to motor vehicle accidents, falls, and assaults.

•Low cerebrospinal fluid pressure (intracranial hypotension) may cause SDH by a spontaneous or iatrogenic cerebrospinal fluid leak such as following lumbar puncture or ventriculostomy, lumboperitoneal shunt placement, or other neurosurgical procedures.

•Arterial causes of SDH include trauma, intracerebral hemorrhage, ruptured cerebral aneurysm, cerebral arteriovenous malformation, or vasculopathy.

•Neoplastic lesions may lead to SDH by mass effect or neovascular rupture. SDH associated with dural (pachymeningeal) metastasis are breast, prostate, lung, and lymphoma. Primary brain tumors are a rare source of SDH.

●Epidemiology – Acute SDH complicates approximately 11 percent of mild to moderate head injuries that require hospitalization and approximately 20 percent of severe traumatic brain injuries. The incidence of chronic SDH ranges from 1.7 up to 20.6 per 100,000 persons/year. (See 'Epidemiology' above.)

●Risk factors – Patients with significant cerebral atrophy, those who use antithrombotic medications, or who have other sources of coagulopathy are at an elevated risk for SDH. (See 'Risk factors' above.)

●Clinical manifestations – The initial presentation of SDH has a wide spectrum of manifestations. Patients with severe head trauma and SDH may present with coma due to the overall insult to the brain, while those with a mild or trivial trauma and those with spontaneous SDH are likelier to present with symptoms due to the SDH alone (table 1). (See 'Clinical manifestations' above.)

•Symptoms of acute SDH include weakness, numbness, visual impairment, and seizures.

•Patients who become symptomatic with chronic SDH are more likely to present with nonfocal symptoms than those with acute SDH.

•SDH may also be asymptomatic, found incidentally on imaging obtained for unrelated symptoms.

●Imaging features – Noncontrast head computed tomography (CT) is the first-choice imaging study to rapidly diagnose SDH. Brain magnetic resonance imaging (MRI) may also be used but typically takes longer to perform than CT and is less readily available in many facilities. However, MRI may be preferred for small chronic SDH and to identifying possible underlying causes (image 11). (See 'Imaging features' above.)

●Evaluation for underlying etiology – Patients without antecedent trauma or obvious risk factors for SDH should be evaluated for secondary causes. This may include brain MRI or other imaging, angiography in selected cases, and laboratory evaluation for coagulopathy. (See 'Evaluation for underlying causes' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges David Brock, MD, CIP, who contributed to an earlier version of this topic review.