Primary Effects of CNS Trauma

Main Text

Preamble

Primary head injuries are defined as those that occur at the time of initial trauma, even though they may not be immediately apparent on initial evaluation.

Head injury can be caused by direct or indirect trauma. Direct trauma involves a blow to the head and is usually caused by automobile collisions, falls, or injury inflicted by an object, such as a hammer or baseball bat. Scalp lacerations, hematomas, and skull fractures are common. Associated intracranial damage ranges from none to severe.

Significant forces of acceleration/deceleration, linear translation, and rotational loading can be applied to the brain without direct head blows. Such indirect trauma is caused by angular kinematics and typically occurs in high-speed motor vehicle collisions (MVCs). Here, the brain undergoes rapid deformation and distortion. Depending on the site and direction of the force applied, significant injury to the cortex, axons, penetrating blood vessels, and deep gray nuclei may occur. Severe brain injury can occur in the absence of skull fractures or visible scalp lesions.

We begin our discussion with a consideration of scalp and skull lesions as we work our way from the outside to the inside of the skull. We then delineate the spectrum of intracranial trauma, starting with extraaxial hemorrhages. We conclude this chapter with a detailed discussion of injuries to the brain parenchyma [e.g., cortical contusion, diffuse axonal injury (DAI), and the serious deep subcortical injuries (SCIs)].

Scalp and Skull Injuries

Preamble

Scalp and skull injuries are common manifestations of cranial trauma. Although brain injury is usually the most immediate concern in managing traumatized patients, superficial lesions, such as scalp swelling and focal hematoma, can be helpful in identifying the location of direct head trauma. On occasion, these initially innocent-appearing “lumps and bumps” can become life threatening. Before turning our attention to intracranial traumatic lesions, we therefore briefly review scalp and skull injuries, delineating their typical imaging findings and clinical significance.

Scalp Injuries

Scalp injuries include lacerations and hematomas. Scalp lacerations can occur in both penetrating and closed head (CHIs) injuries. Lacerations may extend partially or entirely through all five layers of the scalp (skin, subcutaneous fibrofatty tissue, galea aponeurotica, loose areolar connective tissue, and periosteum) to the skull (2-1).

Focal discontinuity, soft tissue swelling, and subcutaneous air are commonly identified in scalp lacerations. Scalp lacerations should be carefully evaluated for the presence of any foreign bodies. If not removed during wound debridement, foreign bodies can be a potential source of substantial morbidity and are very important to identify on initial imaging studies. Wood fragments are often hypodense, whereas leaded glass, gravel, and metallic shards are variably hyperdense (2-2).

Scalp lacerations may or may not be associated with scalp hematomas. There are two distinctly different types of scalp hematomas: Cephalohematomas and subgaleal hematomas. The former are usually of no clinical significance, whereas the latter can cause hypovolemia and hypotension.

Cephalohematomas are subperiosteal blood collections that lie in the potential space between the outer surface of the calvarium and the pericranium, which serves as the periosteum of the skull (2-3). The pericranium continues medially into cranial sutures and is anatomically contiguous with the outer (periosteal) layer of the dura.

Cephalohematomas are the extracranial equivalent of an intracranial epidural hematoma (EDH). Cephalohematomas do not cross suture lines and are typically unilateral. Because they are anatomically constrained by the tough fibrous periosteum and its insertions, cephalohematomas rarely attain a large size.

Cephalohematomas occur in 1% of newborns and are more common following instrumented delivery. They are often diagnosed clinically but imaged only if they are unusually prominent or if intracranial injuries are suspected. NECT scans show a somewhat lens-shaped soft tissue mass that overlies a single bone (usually the parietal or occipital bone) (2-4). If more than one bone is affected, the two collections are separated by the intervening suture lines.

Subgaleal hematomas are subaponeurotic collections and are common findings in traumatized patients of all ages. Here, blood collects under the aponeurosis (the “galea”) of the occipitofrontalis muscle (2-5). Because a subgaleal hematoma lies deep to the scalp muscles and galea aponeurotica but external to the periosteum, it is not anatomically limited by suture lines.

Bleeding into the subgaleal space can be very extensive. Subgaleal hematomas are usually bilateral lesions that often spread diffusely around the entire calvarium. NECT scans show a heterogeneously hyperdense crescentic scalp mass that crosses one or more suture lines (2-6). In contrast to benign self-limited cephalohematomas, expanding subgaleal hematomas in infants and small children can cause significant blood loss.

Skull Fractures

Noticing a scalp “bump” or hematoma on initial imaging in head trauma is important, as calvarial fractures rarely—if ever—occur in the absence of overlying soft tissue swelling or scalp laceration. Skull fractures are present on initial CT scans in ~ 2/3 of patients with moderate head injury, although 25-35% of severely injured patients have no identifiable fracture, even with thin-section bone reconstructions.

Several types of acute skull fracture can be identified on imaging studies: Linear, depressed, and diastatic fractures (2-7). Fractures can involve the calvarium, skull base, or both.

Linear Skull Fractures

A linear skull fracture is a sharply marginated linear defect that typically involves both the inner and outer tables of the calvarium (2-8).

Most linear skull fractures are caused by relatively low-energy blunt trauma that is delivered over a relatively wide surface area. Linear skull fractures that extend into and widen a suture become diastatic fractures. When multiple complex fractures are present, 3D shaded surface display (SSD) can be very helpful in depicting their anatomy and relationships to cranial sutures (2-9).

Patients with an isolated linear nondisplaced skull fracture (NDSF), no intracranial hemorrhage or pneumocephalus, normal neurologic examination, and absence of other injuries are at a very low risk for delayed hemorrhage or other life-threatening complication. Hospitalization is not necessary for many children with NDSFs.

Depressed Skull Fractures

A depressed skull fracture is a fracture in which the fragments are displaced inward (2-9). Comminution of the fracture fragments starts at the point of maximum impact and spreads centrifugally. Depressed fractures are most often caused by high-energy direct blows to a small surface with a blunt object (e.g., hammer, baseball bat, or metal pipe).

Depressed skull fractures typically tear the underlying dura and arachnoid and are often associated with cortical contusions and potential leakage of CSF into the subdural space. Fractures extending to a dural sinus or the jugular bulb are associated with venous sinus thrombosis in 40% of cases (2-12A).

Diastatic Skull Fractures

A diastatic skull fracture is a fracture that widens (“diastases” or “splits open”) a suture or synchondrosis. Diastatic skull fractures usually occur in association with a linear skull fracture that extends into an adjacent suture (2-10).

Imaging

General Features

Both bone and soft tissue reconstruction algorithms should be used when evaluating patients with head injuries. Soft tissue reconstructions should be viewed with both narrow (“brain”) and intermediate (“subdural”) windows. Coronal and sagittal reformatted images obtained using the MDCT axial source data are helpful additions. SSDs can be useful in depicting complex and depressed fractures.

CT Findings

NECT scans demonstrate linear skull fractures as sharply marginated lucent lines. Depressed fractures are typically comminuted and show inward implosion of fracture fragments. Diastatic fractures appear as widened sutures or synchondroses (2-10)(2-8) and are usually associated with linear skull fractures.

MR Findings

MR is rarely used in the setting of acute head trauma because of the high cost, limited availability, and lengthy time required. Compared with CT, bone detail is poor, although parenchymal injuries are better seen. Adding T2* sequences, particularly SWI, is especially helpful in identifying hemorrhagic lesions.

Angiography

If a fracture crosses the site of a major vascular structure, such as the carotid canal or a dural venous sinus (2-11), CTA is recommended. Sagittal, coronal, and MIP reconstructions help delineate the site and extent of vascular injuries.

Clival and skull base fractures are strongly associated with neurovascular trauma, and CTA/CTV should always be obtained in these cases (2-12). Cervical fracture dislocations, distraction injuries, and penetrating neck trauma also merit further investigation. Uncomplicated asymptomatic soft tissue injuries of the neck rarely result in significant vascular injury.

Extraaxial Hemorrhages

Preamble

Extraaxial hemorrhages and hematomas are common manifestations of head trauma. They can occur in any intracranial compartment, within any space (potential or actual), and between any layers of the cranial meninges. Only the subarachnoid spaces exist normally; all the other spaces are potential spaces and occur only under pathologic conditions.

Epidural hematomas (EDHs) arise between the inner table of the skull and outer (periosteal) layer of the dura. Subdural hematomas (SDHs) are located between the inner (meningeal) layer of the dura and the arachnoid. Traumatic subarachnoid hemorrhage (tSAH) is found within the sulci and subarachnoid cisterns, between the arachnoid and the pia.

To discuss extraaxial hemorrhages, we work our way from the outside to the inside. We therefore begin this section with a discussion of EDHs (classic arterial as well as venous variants), then move deeper inside the cranium to the more common SDHs. We conclude with a consideration of tSAH.

Arterial Epidural Hematoma

EDHs are uncommon but potentially lethal complications of head trauma. If an EDH is promptly recognized and appropriately treated, mortality and morbidity can be minimized.

Terminology

An EDH is a collection of blood between the calvarium and outer (periosteal) layer of the dura.

Etiology

Most EDHs arise from direct trauma to the skull that lacerates an adjacent blood vessel (2-13). The vast majority (90%) are caused by arterial injury, most commonly to the middle meningeal artery. Approximately 10% of EDHs are venous, usually secondary to a fracture that crosses a dural venous sinus.

Pathology

Location

Over 90% of EDHs are unilateral and supratentorial. Between 90-95% are found directly adjacent to a skull fracture. The squamous portion of the temporal bone is the most common site.

Gross Pathology

EDHs are biconvex in shape. Adherence of the periosteal dura to the inner calvarium explains this typical configuration. As EDHs expand, they strip the dura away from the inner table of the skull, forming the classic lens-shaped hematoma (2-13). Because the dura is especially tightly attached to sutures, EDHs in adults rarely cross suture lines (10% of EDHs in children do cross sutures, especially if a fracture traverses the suture or sutural diastasis is present).

The typical gross or intraoperative appearance of an acute EDH is a dark purple (“currant jelly”) lentiform clot.

Clinical Issues

Epidemiology

EDHs are much less common than either tSAH or SDH. Although EDHs represent up to 10% of fatal injuries in autopsy series, they are found in only 1-4% of patients imaged for craniocerebral trauma.

Demographics

EDHs are uncommon in infants and older adults. Most are found in older children and young adults. The M:F ratio is 4:1.

Presentation

The prototypical “lucid interval,” during which a traumatized patient has an initial brief loss of consciousness followed by an asymptomatic period of various length prior to the onset of coma &/or neurologic deficit, occurs in only 50% of EDH cases. Headache, nausea, vomiting, symptoms of intracranial mass effect (e.g., pupil-involving third cranial nerve palsy) followed by somnolence and coma are common.

Natural History

Outcome depends on size and location of the hematoma, whether the EDH is arterial or venous, and whether there is active bleeding. In the absence of other associated traumatic brain injuries (TBIs), overall mortality rate with prompt recognition and appropriate treatment is < 5%.

Delayed development or enlargement of an EDH occurs in 10-15% of cases, usually within 24-36 hours following trauma.

Treatment Options

Many EDHs are now treated conservatively. Most traumatic EDHs are not surgical lesions at initial presentation, and the rate of conversion to surgery is low. Most venous and small classic hyperdense EDHs that do not exhibit a swirl sign and have minimal or no mass effect are managed conservatively with close clinical observation and follow-up imaging (2-16). Significant clinical predictors of EDH progression requiring conversion to surgical therapy are coagulopathy and younger age.

Imaging

General Features

EDHs, especially in adults, typically do not cross sutures unless a fracture with sutural diastasis is present. In children, 10% of EDHs cross suture lines, usually the coronal or sphenosquamous suture.

Look for other comorbid lesions, such as contrecoup injuries, tSAH, and secondary brain herniations, all of which are common findings in patients with EDHs.

CT Findings

NECT scan is the procedure of choice for initial imaging in patients with head injury. Both soft tissue and bone reconstruction algorithms should be obtained. Multiplanar reconstructions are especially useful in identifying vertex EDHs, which may be difficult to detect if only axial images are obtained.

The classic imaging appearance of arterial EDHs is a hyperdense (60-90 HU) biconvex extraaxial collection (2-14). Presence of a hypodense component (swirl sign) is seen in ~ 1/3 of cases and indicates active, rapid bleeding with unretracted clot (2-15).

EDHs compress the underlying subarachnoid space and displace the cortex medially, “buckling” the gray matter-white matter interface inward.

Air in an EDH occurs in ~ 20% of cases and is usually—but not invariably—associated with a sinus or mastoid fracture.

Patients with mixed-density EDHs tend to present earlier than patients with hyperdense hematomas and have lower Glasgow Coma Scale (GCS) scores, larger hematoma volumes, and poorer prognosis.

Imaging findings associated with adverse clinical outcome are thickness > 1.5 cm, volume > 30 mL, pterional (lateral aspect of the middle cranial fossa) location, midline shift > 5 mm, and the presence of a swirl sign within the hematoma on imaging.

Small, unoperated EDHs reduce in size and density with time and eventually resolve completely (2-16).

MR Findings

Acute EDHs are typically isointense with underlying brain, especially on T1WI. The displaced dura can be identified as a displaced “black line” between the hematoma and the brain.

Angiography

DSA may show a lacerated middle meningeal artery with “tram-track” fistulization of contrast from the middle meningeal artery into the paired middle meningeal veins. Mass effect with displaced cortical arteries and veins is seen.

Venous Epidural Hematomas

Not all EDHs are the same!Venous EDHs are often smaller, under lower pressure, and develop more slowly than their arterial counterparts. Most venous EDHs are caused by a skull fracture that crosses a dural venous sinus and therefore occur in the posterior fossa near the skull base (transverse/sigmoid sinus) (2-17) or the vertex of the brain [superior sagittal sinus (SSS)]. In contrast to their arterial counterparts, venous EDHs can “straddle” intracranial compartments, crossing both sutures and lines of dural attachment (2-18) and compressing or occluding the adjacent venous sinuses.

Venous EDHs can be subtle and easily overlooked. Coronal and sagittal reformatted images are key to the diagnosis and delineation of these variant EDHs. Several anatomic subtypes of venous EDHs, each with different treatment implications and prognosis, are recognized.

Vertex EDH

“Vertex” EDHs are rare. Usually caused by a linear or diastatic fracture that crosses the SSS, they often accumulate over hours or even days with slow, subtle onset of symptoms. “Vertex” hematomas can be subtle and are easily overlooked unless coronal and sagittal reformatted images are obtained (2-20).

Anterior Temporal EDH

Anterior temporal EDHs are a unique subgroup of hematomas that occur in the anterior tip of the middle cranial fossa (2-21). Anterior temporal EDHs are caused either by an isolated fracture of the adjacent greater sphenoid wing or by an isolated zygomaticomaxillary complex (“tripod”) facial fracture. The sphenoparietal dural venous sinus is injured as it curves medially along the undersurface of the lesser sphenoid wing, extravasating blood into the epidural space. Limited anatomically by the sphenotemporal suture laterally and the orbital fissure medially, anterior temporal EDHs remain stable in size and do not require surgical evacuation (2-22).

Clival EDH

Clival EDHs usually develop after a hyperflexion or hyperextension injury to the neck and are possibly caused by stripping of the tectorial membrane from attachments to the clivus. Less commonly, they have been associated with basilar skull fractures that lacerate the clival dural venous plexus.

Clival EDHs most often occur in children and present with multiple cranial neuropathies. The abducens nerve is the most commonly affected followed by the glossopharyngeal and hypoglossal nerves. They are typically limited in size by the tight attachment of the dura to the basisphenoid and tectorial membrane.

Management of a clival EDH is dictated by the severity and progression of the neurologic deficits and stability of the atlantoaxial joint. In patients with minor cranial nerve involvement, the clinical course is usually benign, and treatment with a cervical collar is typical.

NECT scans show a hyperdense collection between the clivus and tectorial membrane. Sagittal MR of the craniocervical junction shows the hematoma elevating the clival dura and extending inferiorly between the basisphenoid and tectorial membrane anterior to the medulla (2-23).

Acute Subdural Hematoma

Acute SDHs (aSDHs) are one of the leading causes of death and disability in patients with severe TBI. Older adult patients with ground-level falls (GLFs) are especially prone to developing SDHs. Anticoagulation may lead to especially rapid expansion of an aSDH.

SDHs are much more common than EDHs. Most do not occur as isolated injuries; the vast majority of SDHs are associated with tSAH as well as significant parenchymal injuries, such as cortical contusions, brain lacerations, and DAIs.

Terminology

An aSDH is a collection of acute blood products that lies in or between or within the inner border cell layer of the dura and the arachnoid (2-24).

Etiology

Trauma is the most common cause of aSDH. Both direct blows to the head and nonimpact injuries may result in formation of an aSDH. Tearing of bridging cortical veins as they cross the arachnoid and dural border cell layer to enter a dural venous sinus (usually the SSS) is the most common etiology. Cortical vein lacerations can occur with either a skull fracture or the sudden changes in velocity and brain rotation that occur during nonimpact CHI.

Blood from ruptured vessels spreads quickly through the potential space between the dura and the arachnoid. Large SDHs may spread over an entire hemisphere, also extending into the interhemispheric fissure and along the tentorium.

Tearing of cortical arteries or a venous sinus from a skull fracture may also give rise to an aSDH. The arachnoid itself may also rupture, creating a pathway for leakage of CSF into the subdural space that results in a subdural hygroma (SDHy) (pure CSF) or an admixture of both blood and CSF.

Less common causes of aSDH include aneurysm rupture, skull/dura-arachnoid metastases from vascular extracranial primary neoplasms, and spontaneous hemorrhage in patients with severe coagulopathy.

Pathology

Gross Pathology

The gross appearance of an aSDH is that of a soft, purplish, “currant jelly” clot beneath a tense, bulging dura (2-25). More than 95% are supratentorial. Most aSDHs spread diffusely over the affected hemisphere and are therefore typically crescent-shaped (2-26).

Clinical Issues

Epidemiology

An aSDH is the second most common extraaxial hematoma, exceeded only by tSAH. An aSDH is found in 10-20% of all patients with head injury and is observed in 30% of autopsied fatal injuries.

An aSDH may occur at any age from infancy to older adulthood. There is no sex predilection.

Presentation

Even relatively minor head trauma, especially in older adult patients who are often anticoagulated, may result in an aSDH. In such patients, a definite history of trauma may be lacking.

Clinical findings vary from none to loss of consciousness and coma. Most patients with aSDHs have low GCS scores on admission. Delayed deterioration, especially in older anticoagulated patients, is common.

Natural History

An aSDH may remain stable, grow slowly, or rapidly increase in size, causing mass effect and secondary brain herniations. Prognosis varies with hematoma thickness, midline shift, and the presence of associated parenchymal injuries. An aSDH that is thicker than 2 cm correlates with poor outcome (35-90% mortality). An aSDH that occupies more than 10% of the total available intracranial volume is usually lethal.

Treatment Options

The majority of patients with small SDHs are initially treated conservatively with close clinical observation and follow-up imaging. Small isolated falcine or tentorial SDHs typically do not increase in size and usually do not require short-term follow-up imaging.

Patients with larger SDHs, a lesion located at the convexity, alcohol abuse disorder, and repetitive falls are at the greatest risk for deterioration. Surveillance with follow-up CT scans is recommended until the SDH resolves or at least up to five weeks following the initial trauma.

Imaging

General Features

The classic finding of an aSDH is a supratentorial crescent-shaped extraaxial collection that displaces the gray matter-white matter interface and cortical veins medially (2-27). SDHs are typically more extensive than EDHs, easily spreading along the falx, tentorium, and around the anterior and middle fossa floors. SDHs may cross suture lines but generally do not cross dural attachments. Bilateral SDHs occur in 15% of cases. Contrecoup injuries, such as contusion of the contralateral hemisphere, are common.

Both standard soft tissue and intermediate (“subdural”) windows as well as bone algorithm reconstructions should be used in all trauma patients, as small, subtle aSDHs can be obscured by the density of the overlying calvarium (2-28). Coronal and sagittal reformatted images using the axial source data are especially helpful in visualizing small (“smear”) peritentorial and parafalcine aSDHs (2-29)(2-30).

CT Findings

NECT

Approximately 60% of aSDHs are hyperdense on NECT scans (2-27A). Mixed-attenuation lesions are found in 40% of cases. Pockets of hypodensity within a larger hyperdense aSDH usually indicate rapid bleeding (2-31). “Dots” or “lines” of CSF trapped within compressed, displaced sulci are often seen underlying an SDH (2-33).

Mass effect with an aSDH is common and expected. Subfalcine herniation should be proportionate to the size of the subdural collection. However, if the difference between the midline shift and thickness of the hematoma is 3 mm or more, then mortality is very high. This discrepancy occurs when underlying cerebral edema is triggered by the traumatic event. Early recognition and aggressive treatment for potentially catastrophic brain swelling are essential (2-32).

In other cases, especially in patients with repeated head injury, severe brain swelling with unilateral hemisphere vascular engorgement occurs very quickly. Here, the mass effect is greatly disproportionate to the size of the SDH, which may be relatively small.

Occasionally, an aSDH is nearly isodense with the underlying cortex. This unusual appearance is found in extremely anemic patients (Hgb < 8-10 g/dL) (2-33) and sometimes occurs in patients with coagulopathy. In rare cases, CSF leakage through a torn arachnoid may mix with—and dilute—the acute blood that collects in the subdural space.

CECT/CTA

CECT scans are helpful in detecting small isodense aSDHs. The normally enhancing cortical veins are displaced inward by the extraaxial fluid collection (2-27). CTA may be useful in visualizing a cortical vessel that is actively bleeding into the subdural space.

MR Findings

MR scans are rarely obtained in acutely brain-injured patients. In such cases, aSDHs appear isointense on T1WI and hypointense on T2WI. Signal intensity on FLAIR scans is usually iso- to hyperintense compared with CSF but hypointense compared with the adjacent brain. aSDHs are hypointense on T2* scans.

DWI shows heterogeneous signal within the hematoma but may show patchy foci of restricted diffusion in the cortex underlying the aSDH.

Differential Diagnosis

In the setting of acute trauma, the major differential diagnosis is EDH. Shape is a helpful feature, as most aSDHs are crescentic, whereas EDHs are biconvex. EDHs are almost always associated with skull fracture; SDHs frequently occur in the absence of skull fracture. EDHs may cross sites of dural attachment; SDHs do not cross the falx or tentorium.

Subacute Subdural Hematoma

With time, SDHs undergo organization, lysis, and neomembrane formation. Within 2-3 days, the initial soft, loosely organized clot of an aSDH becomes organized. Breakdown of blood products and the formation of organizing granulation tissue change the imaging appearance of subacute (sSDH) and chronic (cSDH) SDHs.

Terminology

An sSDH is between several days and several weeks old.

Pathology

A collection of partially liquified clot with resorbing blood products is surrounded on both sides by a “membrane” of organizing granulation tissue (2-34). The outermost membrane adheres to the dura and is typically thicker than the inner membrane, which abuts the thin, delicate arachnoid (2-36).

In some cases, repetitive hemorrhages of different ages arising from the friable granulation tissue may be present. In others, liquefaction of the hematoma over time produces serous blood-tinged fluid.

Clinical Issues

Epidemiology and Demographics

SDHs are common findings at imaging and autopsy. In contrast to aSDHs, sSDHs show a distinct bimodal distribution with children and older adults as the most commonly affected age groups.

Presentation

Clinical symptoms vary from asymptomatic to loss of consciousness and hemiparesis caused by sudden rehemorrhage into an sSDH. Headache and seizure are other common presentations.

Natural History and Treatment Options

Many sSDHs resolve spontaneously. In some cases, repeated hemorrhages may cause sudden enlargement and mass effect. Surgical drainage may be indicated if the sSDH is enlarging or becomes symptomatic.

Imaging

General Features

Imaging findings are related to hematoma age and the presence of encasing membranes. Evolution of an untreated, uncomplicated SDH follows a very predictable pattern on CT. Density of an extraaxial hematoma decreases ~ 1-2 HU each day (2-35). Therefore, an SDH will become nearly isodense with the underlying cerebral cortex within a few days following trauma.

CT Findings

sSDHs are typically crescent-shaped fluid collections that are iso- to slightly hypodense compared with the underlying cortex on NECT (2-37). Medial displacement of the gray matter-white matter interface (“buckling”) is often present, along with “dot-like” foci of CSF in the trapped, partially effaced sulci underlying the sSDH (2-38). Mixed-density hemorrhages are common.

Bilateral sSDHs may be difficult to detect because of their “balanced” mass effect. Sulcal effacement with displaced gray matter-white matter interfaces is the typical appearance.

CECT/CTV shows that the enhanced cortical veins are displaced medially (2-37). The encasing membranes, especially the thicker superficial layer, may enhance.

MR Findings

MR can be very helpful in identifying sSDHs, especially small lesions that are virtually isodense with underlying brain on CT scans.

Signal intensity varies with hematoma age but is less predictable than on CT, making precise “aging” of subdural collections more problematic. In general, early sSDHs are isointense with cortex on T1WI (2-39A) and hypointense on T2WI but gradually become more hyperintense as extracellular methemoglobin increases. Most late-stage sSDHs are T1/T2 “bright-bright.” A linear T2 hypointensity representing the encasing membranes that surround the SDH is sometimes present.

FLAIR is the most sensitive standard sequence for detecting sSDH, as the collection is typically hyperintense. Because FLAIR signal intensity varies depending on the relative contribution of T1 and T2 effects, early sSDHs may initially appear hypointense due to their intrinsic T2 shortening.

T2* scans are also very sensitive, as sSDHs show distinct “blooming”(2-39B).

Signal intensity on DWI also varies with hematoma age. DWI commonly shows a crescentic high-intensity area with a low-intensity rim closer to the brain surface (double-layer appearance) (2-39C). The low-intensity area corresponds to a mixture of resolved clot and CSF, whereas the high-intensity area correlates with solid clot.

T1 C+ scans demonstrate enhancing, thickened, encasing membranes. The membrane surrounding an sSDH is usually thicker on the dural side of the collection. Delayed scans may show gradual “filling in” and increasing hyperintensity of the sSDH.

Differential Diagnosis

The major differential diagnosis of an sSDH is an isodense aSDH. These are typically seen only in an extremely anemic or anticoagulated patient. A subdural effusion that follows surgery or meningitis or that occurs as a component of intracranial hypotension can also mimic an sSDH. An SDHy is typically isodense/isointense with CSF and does not demonstrate enhancing, encapsulating membranes.

Chronic/Mixed Subdural Hematoma

Terminology

A cSDH is an encapsulated collection of sanguineous or serosanguineous fluid confined within the subdural space. Recurrent hemorrhage(s) into a preexisting cSDH are common and produce a mixed-age (mSDH) or “acute-on-chronic” SDH.

Etiology

With continued degradation of blood products, an SDH becomes progressively more liquified until it is largely serous fluid tinged with blood products (2-40). Rehemorrhage from vascularized encapsulating membranes (2-42) or rupture of stretched cortical veins as they pass over the cSDH to enter the SSS (2-27) occurs in 5-10% of cSDHs and is considered “acute-on-chronic” SDH.

Pathology

Gross Pathology

Blood within the subdural space incites tissue reaction around its margins. Organization and resorption of the hematoma contained within the “membranes” of surrounding granulation tissue continue. These neomembranes have fragile, easily disrupted capillaries and easily rebleed, creating an mSDH. Multiple hemorrhages of different ages are common in mSDHs (2-41)(2-42).

Eventually, most of the liquified clot in a cSDH is resorbed. Only a thickened dura-arachnoid layer remains with a few scattered pockets of old blood trapped between the inner and outer membranes.

Clinical Issues

Epidemiology

Unoperated, uncomplicated sSDHs eventually evolve into cSDHs. Approximately 5-10% will rehemorrhage, causing multiloculated mSDHs (2-41).

Demographics

cSDHs may occur at any age. mSDHs are much more common in older adult patients.

Presentation

Presentation varies from no/mild symptoms (e.g., headache) to sudden neurologic deterioration if a preexisting cSDH rehemorrhages.

Natural History

In the absence of repeated hemorrhages, cSDHs gradually resorb and largely resolve, leaving a residue of thickened dura-arachnoid that may persist for months or even years. Older patients, especially those with brain atrophy, are subject to repeated hemorrhages.

Treatment Options

If follow-up imaging of an sSDH shows expected resorption and regression of the cSDH, no surgery may be required. Surgical drainage with evacuation of the cSDH and resection of its encapsulating membranes is performed if significant mass effect or repeated hemorrhages cause neurologic complications.

Imaging

General Features

cSDHs have a spectrum of imaging appearances. Uncomplicated cSDHs show relatively homogeneous density/signal intensity (2-43) with slight gravity-dependent gradation of their contents (“hematocrit effect”).

mSDHs with acute hemorrhage into a preexisting cSDH show a hematocrit level with distinct layering of the old (top) and new (bottom) hemorrhages. Sometimes, septated pockets that contain hemorrhages of different ages form (2-44A). Dependent layering of blood within the loculated collections may appear quite bizarre.

Extremely old, longstanding cSDHs with virtually complete resorption of all liquid contents are seen as pachymeningopathies with diffuse dura-arachnoid thickening.

CT Findings

NECT

A hypodense crescentic fluid collection extending over the surface of one or both cerebral hemispheres is the classic finding in cSDH. Uncomplicated cSDHs approach CSF in density (2-43). The hematocrit effect creates a slight gradation in density that increases from top to bottom.

Trabecular or loculated cSDHs show internal septations, often with evidence of repeated hemorrhages (2-44A). With age, the encapsulating membranes surrounding the cSDH become thickened and may appear moderately hyperdense. Eventually, some cSDHs show peripheral calcifications that persist for many years. In rare cases, a cSDH may densely calcify or even ossify, a condition aptly termed “armored brain.”

CECT

The encapsulating membranes around a cSDH contain fragile neocapillaries that lack endothelial tight junctions. Therefore, the membranes show strong enhancement following contrast administration.

MR Findings

As with all intracranial hematomas, signal intensity of a cSDH or mSDH is quite variable and depends on the age of the blood products. On T1 scans, uncomplicated cSDHs are typically iso- to slightly hyperintense compared with CSF. Depending on the stage of evolution, cSDHs are iso- to hypointense compared with CSF on T2 scans.

Most cSDHs are hyperintense on FLAIR and may show “blooming” on T2* scans if subacute-chronic blood clots are still present (2-39B). In ~ 1/4 of all cases, superficial siderosis can be identified over the gyri underlying a cSDH.

The encapsulating membranes of a cSDH enhance following contrast administration. Typically, the outer layer is thicker than the inner layer.

Uncomplicated cSDHs do not restrict on DWI. With cSDHs, a “double layer” effect—a crescent of hyperintensity medial to a nonrestricting fluid collection—indicates acute rehemorrhage (2-39C).

Differential Diagnosis

An mSDH is difficult to mistake for anything else. In older patients, a small uncomplicated cSDH may be difficult to distinguish from simple brain atrophy with enlarged bifrontal CSF spaces. However, cSDHs exhibit mass effect; they flatten the underlying gyri, often extending around the entire hemisphere and into the interhemispheric fissure. The increased extraaxial spaces in patients with cerebral atrophy are predominantly frontal and temporal.

A traumatic SDHy is an accumulation of CSF in the subdural space after head injury, probably secondary to an arachnoid tear. SDHys are sometimes detected within the first 24 hours after trauma; however, the mean time for appearance is nine days after injury. An SDHy or a hematohygroma in an infant or young child should be considered highly suspicious for abusive head trauma (AHT) (child abuse; see later discussion).

A classic uncomplicated SDHy is a hypodense, CSF-like, crescentic extraaxial collection that consists purely of CSF, has no blood products, lacks encapsulating membranes, and shows no enhancement following contrast administration. CSF leakage into the subdural space is also present in the vast majority of patients with cSDH. Therefore, many—if not most—cSDHs contain a mixture of both CSF and blood products.

A subdural effusion is an accumulation of clear fluid over the cerebral convexities or in the interhemispheric fissure. Subdural effusions are generally complications of meningitis; a history of prior infection, not trauma, is typical.

A subdural empyema (SDE) is a hypodense extraaxial fluid collection that contains pus. Most SDEs are secondary to sinusitis or mastoiditis, have strongly enhancing membranes, and often coexist with findings of meningitis. A typical SDE restricts strongly and uniformly on DWI. Look for underlying sulcal/cisternal hyperintensity on FLAIR and enhancement on T1 C+.

Traumatic Subarachnoid Hemorrhage

tSAH is found in virtually all cases of moderate to severe head trauma. Indeed, trauma—not ruptured saccular aneurysm—is the most common cause of intracranial subarachnoid hemorrhage (SAH).

Etiology

tSAH can occur with both direct trauma to the skull and nonimpact CHI. Tearing of cortical arteries and veins, rupture of contusions and lacerations into the contiguous subarachnoid space, and choroid plexus bleeds with intraventricular hemorrhage may all result in blood collecting within the subarachnoid cisterns.

Although tSAH occasionally occurs in isolation, it is usually accompanied by other manifestations of brain injury. Subtle tSAH may be the only clue on initial imaging studies that more serious injuries lurk beneath the surface.

Pathology

Location

tSAHs are predominantly found in the anteroinferior frontal and temporal sulci, perisylvian regions, and over the hemispheric convexities (2-45). In very severe cases, tSAH spreads over most of the brain. In mild cases, blood collects in a single sulcus or the dependent portion of the interpeduncular fossa.

Gross Pathology

With the exception of location and associated parenchymal injuries, the gross appearance of tSAH is similar to that of aneurysmal SAH (aSAH). Curvilinear foci of bright red blood collect in cisterns and surface sulci (2-46)(2-47).

tSAH typically occurs adjacent to cortical contusions. tSAH is also commonly identified under acute EDH and SDH.

Clinical Issues

Epidemiology

tSAH is found in most cases of moderate trauma and is identified in virtually 100% of fatal brain injuries at autopsy.

Natural History

Breakdown and resorption of tSAH occurs gradually. Patients with isolated tSAH have very low rates of clinical or radiographic deterioration and typically do well.

Imaging

General Features

With the exception of location, the general imaging appearance of tSAH is similar to that of aSAH, i.e., sulcal-cisternal hyperdensity/hyperintensity (2-48). tSAH is typically more focal or patchy than the diffuse subarachnoid blood indicative of aneurysmal hemorrhage.

CT Findings

Acute tSAH is typically peripheral, appearing as linear hyperdensities in sulci adjacent to cortical contusions or under EDHs or SDHs. Occasionally, isolated tSAH is identified within the interpeduncular fossa (2-49).

MR Findings

As acute blood is isointense with brain, it may be difficult to detect on T1WI. “Dirty” sulci with “smudging” of the perisylvian cisterns is typical. Subarachnoid blood is hyperintense to brain on T2WI and appears similar in signal intensity to cisternal CSF. FLAIR scans show hyperintensity in the affected sulci.

“Blooming” with hypointensity can be identified on T2* scans, typically adjacent to areas of cortical contusion. tSAH is recognized on GRE or SWI sequences as hypointense signal intensity surrounded by hyperintense CSF.

Angiography

Emergent CTA is usually unnecessary in cases with typical peripheral tSAH on NECT. Patients with suprasellar (“central”) SAH may harbor a ruptured aneurysm and should be screened with CTA regardless of mechanism of injury.

Differential Diagnosis

The major differential diagnosis of tSAH is nontraumatic SAH (ntSAH). Aneurysmal rupture causes 80-90% of all ntSAHs. In contrast to tSAH, aSAH is concentrated in the basal cisterns.

Sulcal-cisternal hyperintensity on FLAIR is nonspecific and can be caused by meningitis, neoplasm, artifact (incomplete CSF suppression), contrast leakage into the subarachnoid space (e.g., with renal failure), and high inspired oxygen during general anesthesia.

The term pseudo-SAH has been used to describe the CT appearance of a brain with severe cerebral edema. Hypodense brain makes circulating blood in arteries and veins look relatively hyperdense. The hyperdensity seen here is smooth and conforms to the expected shape of the vessels, not the subarachnoid spaces, and should not be mistaken for either tSAH or ntSAH.

Parenchymal Injuries

Preamble

Intraaxial traumatic injuries include cortical contusions and lacerations, diffuse axonal injury (DAI), subcortical injuries (SCIs), and intraventricular hemorrhages. In this section, we again begin with the most peripheral injuries—cortical contusions—and work our way inward, ending with the deepest (subcortical) injuries. In general, the deeper the abnormalities, the more serious the injury.

Cerebral Contusions and Lacerations

Cerebral contusions are the most common of the intraaxial injuries. True brain lacerations are rare and typically occur only with severe (often fatal) head injury.

Terminology

Cerebral contusions are basically “brain bruises.” They evolve with time and are often more apparent on delayed scans than at the time of initial imaging. Cerebral contusions are also called gyral “crest” injuries. The term “gliding” contusion is sometimes used to describe parasagittal contusions.

Etiology

Most cerebral contusions result from nonmissile or blunt head injury. CHI induces abrupt changes in angular momentum and deceleration. The brain is suddenly and forcibly impacted against an osseous ridge or the hard, knife-like edge of the falx cerebri and tentorium cerebelli. Less commonly, a depressed skull fracture directly damages the underlying brain.

Pathology

Location

Contusions are injuries of the brain surface that involve the gray matter and contiguous subcortical white matter (2-50)(2-51). They occur in very characteristic, highly predictable locations. Nearly 1/2 involve the temporal lobes. The temporal tips, as well as the lateral and inferior surfaces and the perisylvian gyri, are most commonly affected (2-53). The inferior (orbital) surfaces of the frontal lobes are also frequently affected (2-54).

Convexity gyri, the dorsal corpus callosum body, dorsolateral midbrain, and cerebellum are less common sites of cerebral contusions. The occipital poles are rarely involved, even with relatively severe CHI.

Size and Number

Cerebral contusions vary in size from tiny lesions to large confluent hematomas. They are almost always multiple and often bilateral (2-54) (2-55). Contusions that occur at 180° opposite the site of direct impact (the “coup”) are common and called contrecoup lesions (2-56).

Clinical Issues

Epidemiology and Demographics

Cerebral contusions account for ~ 1/2 of all traumatic parenchymal lesions. They occur at all ages, from infants to older adults. The peak age is 15-24 years, and the M:F ratio is 3:1.

Imaging

CT Findings

Initial scans obtained soon after a CHI may be normal. The most frequent abnormality is the presence of focal or petechial hemorrhages along gyral crests immediately adjacent to the calvarium (2-58B). A mixture of petechial hemorrhages surrounded by patchy ill-defined hypodense areas of edema is common (2-55) (2-56).

A lesion “blooming” over time is frequent and seen with progressive increase in hemorrhage, edema, and mass effect (2-57). Small lesions may coalesce, forming larger focal hematomas. Development of new lesions that were not present on initial imaging is also common.

MR Findings

MR is much more sensitive than CT in detecting cerebral contusions but is rarely obtained in the acute stage of TBI. T2 scans show patchy hyperintense areas (edema) surrounding hypointense foci of hemorrhage.

FLAIR scans are most sensitive for detecting cortical edema and associated tSAH, both of which appear as hyperintense foci on FLAIR (2-58D). T2* (GRE, SWI) is the most sensitive sequence for imaging parenchymal hemorrhages (2-58E). Significant “blooming” is typical in acute lesions. Complications, such as excitotoxic injury of the corpus callosum, may occur (2-58F).

Differential Diagnosis

The major differential diagnosis of cortical contusion is DAI. Both cerebral contusions and DAI are often present in patients who have sustained moderate to severe head injury. Contusions tend to be superficial, located along gyral crests. DAI is most commonly found in the corona radiata and along compact white matter tracts, such as the internal capsule and corpus callosum.

Severe cortical contusion with confluent hematomas may be difficult to distinguish from brain laceration on imaging studies. Brain laceration occurs when severe trauma disrupts the pia and literally tears the underlying brain apart (2-59). Parenchymal brain laceration (PBL) in infants and young children is typically associated with AHT.

A “burst lobe” is the most severe manifestation of frank brain laceration (2-60)(2-61). Here, the affected lobe is grossly disrupted with large hematoma formation and adjacent tSAH. In some cases, especially those with depressed skull fracture, the arachnoid is also lacerated, and hemorrhage from the burst lobe extends to communicate directly with the subdural space, forming a coexisting SDH.

Diffuse Axonal Injury

DAI is the second most common parenchymal lesion seen in TBI, exceeded only by cortical contusions. Patients with DAI often exhibit an apparent discrepancy between clinical status (often moderately to severely impaired) and initial imaging findings (often normal or minimally abnormal).

Etiology

Most DAIs are caused by high-velocity MVCs and are dynamic, deformative, nonimpact injuries resulting from the inertial forces of rotation generated by sudden changes in acceleration/deceleration. The cortex moves at a different speed relative to underlying deep brain structures (white matter, deep gray nuclei). This results in axonal stretching, especially where brain tissues of different density intersect, i.e., the gray matter-white matter interface.

Pathology

Location

DAI occurs in highly predictable locations. The cortex is typically spared; it is the subcortical and deep white matter that is most commonly affected. Lesions in compact white matter tracts, such as the corpus callosum, especially the genu and splenium, fornix, and internal capsule, are frequent. The midbrain and pons are less common sites of DAI (2-62)(2-63).

Gross Pathology

The vast majority of DAIs are microscopic and nonhemorrhagic. Tears of penetrating vessels (diffuse vascular injury) may cause small round to ovoid or linear hemorrhages that sometimes are the only gross indications of underlying axonal injury (2-64). These visible lesions are truly just the “tip of the iceberg.”

Clinical Issues

Epidemiology and Demographics

DAI is present in virtually all fatal TBIs and is found in almost 3/4 of patients with moderate or severe injury who survive the acute stage.

DAI may occur at any age, but peak incidence is in young adults (15-24 years old). Male patients are at least twice as often afflicted with TBI as female patients.

Presentation

DAI typically causes much more significant impairment compared with extracerebral hematomas and cortical contusions. DAI often causes immediate loss of consciousness, which may be transient (in the case of mild TBI) or progress to coma (with moderate to severe injury). In severe DAI, immediate coma from the moment of impact is typical. A very low GCS score, often < 6-8, is typical in patients who survive the initial impact.

Imaging

CT Findings

Initial NECT is often normal or minimally abnormal. Mild diffuse brain swelling with sulcal effacement may be present. A few small round or ovoid subcortical hemorrhages may be visible (2-65), but the underlying damage is typically much more diffuse and much more severe than these relatively modest abnormalities would indicate.

MR Findings

MR is much more sensitive in detecting changes of DAI. T2WI and FLAIR may show hyperintense foci in the subcortical white matter and corpus callosum (2-66A). Multiple lesions are the rule, and a combination of DAI and contusions or hematomas is very common.

T2* (GRE, SWI) scans are very sensitive to the microbleeds of DAI and typically show multifocal ovoid and linear hypointensities (2-66B)(2-66C). DWI may show multiple foci of restricted diffusion (2-66D).

Differential Diagnosis

Cortical contusions often coexist with DAI in moderate to severe TBI. Cortical contusions are typically superficial lesions, usually located along gyral crests.

Multifocal hemorrhages with “blooming” on T2* (GRE, SWI) scans can be seen in numerous pathologies, including DAI. Diffuse vascular injury appears as multifocal parenchymal black dots. Pneumocephalus may cause multifocal “blooming” lesions in the subarachnoid spaces. Parenchymal lesions are rare.

Subcortical (Deep Brain) Injury

Terminology

SCIs are traumatic lesions of deep brain structures, such as the brainstem, basal ganglia, thalami, and ventricles. Most represent severe shear-strain injuries that disrupt axons, tear penetrating blood vessels, and damage the choroid plexus of the lateral ventricles.

Pathology

Gross Pathology

Manifestations of SCI include deep hemorrhagic contusions, nonhemorrhagic lacerations, intraventricular bleeds, and tSAH (2-67). SCIs usually occur with other traumatic lesions, such as cortical contusions and DAI.

Clinical Issues

Epidemiology

Between 5-10% of patients with moderate to severe brain trauma sustain SCIs. SCIs are the third most common parenchymal brain injury after cortical contusions and DAI. As with most TBIs, SCIs are most common in male patients between 15-24 years of age.

Natural History

Prognosis is poor in these severely injured patients. Many do not survive; those who do typically have profound neurologic impairment with severe long-term disability.

PARENCHYMAL BRAIN INJURIES

Cerebral Contusions

• Most common intraaxial injury

 Brain impacts skull &/or dura

 Causes “brain bruises” in gyral crests

 Usually multiple, often bilateral

 Anteroinferior frontal, temporal lobes most common sites

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