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Traumatic Injury to the Posterior Fossa
Tra u m a t i c I n j u r y t o t h e Posterior Fossa Menarvia Nixon, MD, Sudheer Ambekar, MD, Shihao Zhang, MD, Cory Markham, BS, Hesam Akbarian-Tefaghi, BS, Kevin Morrow, Anil Nanda, MD, FACS, Bharat Guthikonda, MD*
BS,
KEYWORDS Traumatic brain injury Posterior fossa Intra-axial lesions Extra-axial lesions Vascular injuries KEY POINTS Traumatic injury to the posterior fossa is a complex pathologic condition because of the great heterogeneity of lesions present. As with all traumatic brain injuries, treatment of primary brain injuries and prevention of secondary brain injuries is the mainstay of management. It is imperative to recognize traumatic lesions of the posterior fossa early because of the occurrence of rapid neurologic decline. The decision regarding whether or not to proceed with surgical intervention depends on the patient’s clinical condition, neurologic status, and imaging findings. In general, nonoperative management should be considered only if the patient is fully conscious and the associated posterior fossa lesions are small with little or no mass effect. Posterior fossa traumatic vascular injuries should also be managed either by an open surgical or endovascular approach.
INTRODUCTION
It is estimated that more than 1.7 million cases of traumatic brain injury (TBI) occur in the United States each year and nearly 3% of these cases result in fatality. Although the leading cause of TBI in the United States is injury from falls, motor vehicle accidents are the leading cause of TBI that results in mortality.1 Trauma to the posterior cranial fossa is a subset of TBI that affects the parts of the brain located inferior to the tentorium cerebelli including the cerebellum, brainstem, major cranial blood vessels, and parts of cranial nerves III-XII (Fig. 1).2 However, most studies do not distinguish between trauma to the posterior fossa and other types of TBI. Major injuries within the posterior fossa are reported in 3.3% of all head trauma.3 Despite having
Department of Neurosurgery, LSU HSC Shreveport, 1501 Kings Highway, Shreveport, LA 71130, USA * Corresponding author. E-mail address: [email protected] Neurol Clin 32 (2014) 943–955 http://dx.doi.org/10.1016/j.ncl.2014.07.010 neurologic.theclinics.com 0733-8619/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
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Fig. 1. Midsagittal view of human brain. The approximate location of posterior cranial fossa is shaded. The ring represents the location of foramen magnum. (Courtesy of John Beal, PhD, Department of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center.)
a lower rate of occurrence, trauma to this area is associated with a higher rate of morbidity compared with supratentorial trauma. By definition, TBI is the result of an external force impacting the head and causing a sudden change in acceleration of the brain. Anatomically, the posterior fossa is the largest of the three fossa (anterior, middle, and posterior), located along the floor of the cranial cavity. Its boundaries are marked by aspects of the sphenoid, occipital, parietal, and temporal bones, with a roof formed from reflections of the dura mater called the tentorium cerebelli that houses the clinically important transverse venous sinuses.4 Although it is the largest fossa, the amount of space that is allowed for expansion is the smallest of the three fossa. Thus, the presence of critical structures that are contained within the posterior fossa combined with minimal compliance leads to significant morbidity from any mass-occupying lesions.5 Trauma to the posterior fossa may impair the function of cerebellum and/or the brainstem. When trauma affects the structures of the posterior fossa, the supratentorial region also may be affected. Studies have shown that more favorable outcomes were achieved when the supratentorial region was spared.6 Skull fractures could further complicate the management of patients with TBI, especially if a fracture is open. TBI is divided into primary and secondary brain injury. Primary brain injury refers to damage suffered as a direct result of the initial event, whereas secondary brain injury refers to the indirect insult to the brain as a result of the sequelae of the traumatic event. Primary traumatic injuries are commonly subdivided into blunt and penetrating injuries. Mass lesions from TBI are usually categorized as either intra- or extra-axial lesions. Intra-axial brain lesions are defined by intraparenchymal cerebellar or brainstem damage caused by hematoma, diffuse axonal injury from shearing forces, or delayed posttraumatic intracerebellar hematomas. Extra-axial injuries include epidural hematomas (EDH), subdural hematoma (SDH), and subarachnoid hemorrhage (SAH).7
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INTRA-AXIAL LESIONS
Intraparenchymal cerebellar hemorrhage secondary to trauma constitutes about 3% of all the traumatic head injuries and about 25% of all the traumatic injuries to the posterior fossa.3,8,9 Liu10 reported the incidence of traumatic cerebellar hemorrhage to be 3.7% among all head injuries. Cerebellar hemorrhage may occur in patients of all age groups, although it may more commonly be observed in young patients because this age group is more commonly involved in motor vehicle accidents. Pathophysiology
The exact mechanism of cerebellar contusion is unclear. They may be caused by blunt or penetrating trauma. Takeuchi and colleagues11 proposed three mechanisms of injury in the pathogenesis of cerebellar hematoma. The first is coup injury, where the posterior fossa is the first site of impact. This type of injury typically results in contusion of one of the cerebellar hemispheres with a concomitant contusion of the frontal or temporal lobes. Typically, in a coup injury of the cerebellum, there is evidence of an overlying injury, such as an epidural or a SDH or a fracture of the occipital bone. The second is contrecoup injury, where the site of first impact is other than the posterior fossa. Commonly, frontal or the temporal region is the first site of impact in this mechanism of injury. Again, in this type of injury, the cerebellar hemispheres are more commonly involved than the midline structures. However, in a contrecoup injury of the cerebellum, other traumatic lesions of the posterior fossa are rarely present. The third is shear-related injury, caused by acceleration-deceleration forces. This type of injury is frequently associated with diffuse axonal injury. Differential movements of one portion of the brain with respect to the other lead to the development of shear-strain forces. The most common locations where these forces develop are the gray-white matter junction, brain-pia mater interface, cerebrospinal fluid–brain interface, and skull-dura interface. In the posterior fossa, these lesions are usually seen in the dorsolateral brainstem and in the cerebellar hemispheres. In addition to the previously mentioned three mechanisms of injury, a fourth type of injury is also commonly observed. This is the delayed cerebellar hematoma, which develops secondary to cerebellar contusion as a result of secondary insult. The exact mechanism of this injury is unknown; however, this occurs more commonly in elderly people with underlying coagulopathy or hypertension.12 Delayed intracerebellar hemorrhage develops a few hours to days after trauma. It may progress rapidly and lead to brainstem compression. Various mechanisms, such as increased endothelial permeability of small vessels in the posterior fossa and hyperoxidation within the endothelial cells, have been hypothesized in its development.13,14 Therefore, it is essential to monitor the patients with posterior fossa trauma with serial imaging. As the size of the hematoma grows, the cerebellar parenchyma is destroyed and the hematoma causes mass effect. This may result in fourth ventricular compression leading to obstructive hydrocephalus. Edema of the cerebellar parenchyma around the hematoma adds to the mass effect. In later stages, there may be direct compression of the brainstem resulting in alteration of mental status, stupor, coma, and ultimately death. This sequence of events corresponds to the medullary stage of transtentorial herniation as described by Plum and Posner.15 Herniation may occur when the cerebellar tonsils are forced through the foramen magnum (tonsillar herniation) or when the vermis is forced upward through the tentorial incisura (upward or reverse transtentorial herniation). The latter condition may occur when the supratentorial compartment is suddenly decompressed in the
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presence of a large posterior fossa lesion. It is fortunately a rare condition. There is upward displacement of the vermis through the tentorial incisura causing compression of brainstem and death. Clinical Presentation
Traumatic parenchymal lesions of the cerebellum range from completely asymptomatic to coma and death. The variety and extent of signs and symptoms depend on the site of hemorrhage, size of the hemorrhage, presence of perilesional edema, and mass effect on surrounding structures. Clinical features may be classified into the following stages and usually correlate with the progression of the underlying pathophysiologic process (secondary injury). Stage I: asymptomatic or mild symptoms (dizziness, headache, vertigo); no cerebellar signs, no mass effect, no hydrocephalus, no brainstem compression; detected on imaging; the lesion is usually small, less than 2 cm; usually involving the cerebellar hemispheres Stage II: symptomatic; cerebellar signs present (axial or appendicular or both); mild mass effect over fourth ventricle, no hydrocephalus, no brainstem compression; the lesion is usually greater than 2 cm Stage III: symptomatic; cerebellar signs present, moderate mass effect on fourth ventricle, mild hydrocephalus, mild brainstem compression; the lesion is about 3 to 4 cm Stage IV: symptomatic; cerebellar signs present, severe mass effect over fourth ventricle, severe hydrocephalus, brainstem compression, and altered mental status; the lesion is usually greater than 4 cm Stage V: symptomatic; severe brainstem compression; coma and death; lesion over 4 cm Imaging Studies
As with other acute traumatic hemorrhagic lesions, acute cerebellar hemorrhage appears hyperdense on computed tomography (CT) scan (Fig. 2) and isointense on T1weighted and hypointense on T2-weighted magnetic resonance images. The following features should be observed on imaging while assessing a patient with cerebellar hemorrhage following trauma. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Location of hemorrhage (hemispheric, vermis, both) Presence of perilesional edema Associated posterior fossa traumatic lesions (EDH, SDH, fracture) Mass effect over fourth ventricle Ventricle size to assess for hydrocephalus Compression of brainstem Tonsillar herniation Effacement of basal cisterns Configuration of basal cisterns (“inverted smile” sign seen in upward herniation) Presence of associated diffuse axonal injury or supratentorial traumatic lesions Dissection of the hematoma into the brainstem through the fourth ventricle
Management Goals
The general management algorithm of a patient with TBI is beyond the scope of this article and is well described in the literature. In this section we discuss the specific management of focal cerebellar parenchymal hemorrhage. Conservative management of cerebellar contusion and hematoma may be considered in a fully alert patient
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Fig. 2. Cerebellar hematoma. Traumatic vermian hematoma in a patient. The hematoma has extended into the fourth ventricle and compressed it. There is also edema around the hematoma.
with a small lesion. Close monitoring is required to detect early signs of deterioration, which mandates surgical evacuation. Surgical evacuation for intraparenchymal cerebellar hemorrhage is usually indicated in the following situations: (1) contusion or hematoma greater than 3 cm in maximum dimension, (2) effacement of the basal cisterns, (3) moderate to severe mass effect over fourth ventricle causing hydrocephalus, (4) signs of tonsillar or upward herniation, and (5) moderate to severe brainstem compression. EXTRA-AXIAL LESIONS
External forces that give rise to TBI first stop at the skull and are then transmitted to the underlying structures in a linear fashion. This causes a vertical force on the brain tissue adjacent to the inner table of the skull at the site of the impact.16 As a result, the formation of intracranial, extra-axial hematomas after head injury is a common occurrence.17 Pathophysiology
EDH occurs in 2% to 5% of head-injured patients and posterior fossa EDH constitutes 4% to 13% of all EDH.18 EDHs are located between the outer (periosteal) layer of the dura mater and the inner table of the skull (Fig. 3). They typically develop at the moment of impact at the coup site. They are often associated with overlying occipital fractures.7 In comparison with the supratentorium EDH, posterior fossa EDHs are more frequently of venous rather than arterial origin. They are most often caused by transverse sinus injury from direct occipital trauma. Clival EDHs are an even rarer variant of posterior fossa EDHs and may occur by hyperflexion or extension cervical injuries or basilar clival fractures.19 SDHs are located between the inner (meningeal) layer of the dura mater and the arachnoid. SDHs are not always a result of the direct impact in head trauma but can result from shearing of bridging veins and venous sinuses. They occur in approximately 11% of head-injured patients. SDHs are associated with the highest mortality rate of all traumatic intracranial injuries. The rate is more than four times higher in
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Fig. 3. Noncontrast computer tomography scan of a 23-year-old man with an epidural hematoma of the posterior fossa located between the outer layer of the dura mater and the inner table of the skull. Note the characteristic hyperdense, biconvex appearance of the lesion. Arrowhead showing biconvex hyperdense collection consistent with an epidural hematoma. (From Maschke M, Morsdorf MM, Timman D, et al. Posterior fossa trauma. In: Manto M, Gruol D, Schmahmann J, et al, editors. Handbook of cerebellum and cerebellar disorders. New York: Springer Science1Business Media, 2013; with permission.)
patients older than 65 years. SDHs are more likely to be associated with moderate to severe underlying parenchymal injury, which is considered to be a contributor to the overall poor outcome of patients with SDHs.20 Traumatic SAH, like EDH of the posterior fossa, usually occurs because of rupture of venous structures. Despite its venous origin, traumatic SAH of the posterior fossa can occasionally lead to vasospasm of intracerebral arteries. The two most common types of fractures to the skull are linear and depressed fractures. Linear fractures are more common and have better patient outcomes compared with depressed fractures.10 Fractures to the occipital bone are of special concern because it is the major bone of the posterior cranial fossa and transmits many important anatomic structures including the vertebral arteries, hypoglossal nerves (cranial nerve XII), meningeal branches of ascending pharyngeal artery, transverse sinus, sigmoid sinus, and vagus nerves (Fig. 4). Clinical Findings
The classic “lucid” interval described in EDH occurs in 15% to 30% of patients and even less commonly in EDHs occurring in the posterior fossa. It consists of a brief loss of consciousness, caused by impact, followed by an awake period and late deterioration caused by mass effect and increasing intracranial pressure (ICP). With compressive lesions of the posterior fossa, including EDHs and SDHs, patients usually present with headache, nausea, and vomiting followed by loss of consciousness. Because of the limited size of the posterior fossa, early detection is imperative to avoid rapid and life-threatening neurologic deterioration.
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Fig. 4. Both (A) and (B) are noncontrast computed tomography scans of the head showing the crescentic or concave shape of an acute subdural hematoma. (A) shows the lower compartment of the the posterior fossa whereas (B) shows a higher cut at the the superior poles of the cerebellum depicting the crescentic nature of an acute subdural hematoma. (From Maschke M, Morsdorf MM, Timman D, et al. Posterior fossa trauma. In: Manto M, Gruol D, Schmahmann J, et al, editors. Handbook of cerebellum and cerebellar disorders. New York: Springer Science1Business Media, 2013; with permission.)
Clinical Examination
Pupillary examination by assessment of pupil size and reactivity to light is imperative in posterior fossa trauma, especially in patients with suspected mass lesions (eg, EDH, SDH). Sluggish or no pupillary reactivity may indicate compression of the fourth ventricle or brainstem and/or hydrocephalus. Downward deviation of the eyes may also be associated with unreactive pupils and possible hydrocephalus. The Glascow Coma Scale (GCS) is used to assess level of consciousness. Consciousness has two components: arousal and content. Impairment of arousal can vary from drowsiness to obtundation to coma. Coma is the most severe form of arousal impairment, and is defined as the inability to follow commands, speak, or open eyes to pain.21 Cranial nerve III and VI palsies may indicate impending herniation or increased ICP, respectively. Motor examination should evaluate muscle tone, reflexes, coordination, and motor strength. Imaging Studies
CT scanning is the imaging modality of choice for evaluation of head-injured patients. It allows rapid assessment of the location, extent, and type of intracranial lesions caused by the head injury.19 According to Pascual and Prieto22 three major findings should be evaluated on a head-injured patient’s CT: (1) presence of intracranial hematomas, (2) appearance of basal cisterns, and (3) presence of traumatic SAH. Studies have indicated a relationship between status of basal cisterns and outcome. Compressed or absent basal cisterns indicate a threefold risk of increased ICP.19
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The characteristic CT appearance of acute EDH is hyperdense, biconvex lesions adjacent to the skull. Mass effect is common.23 Occasionally, EDHs may appear heterogeneous with hyperdense and isodense areas, which may indicate active bleeding. Acute SDH appears as hyperdense, crescentic collections between the dura and brain parenchyma on CT (Fig. 5). In contrast with acute EDHs, acute SDHs are more diffuse, less uniform, and concave over the brain surface.24 CT scan is more sensitive than magnetic resonance imaging to disclose SAH at the acute stage, showing hyperdense fluid within the cisterns and sulci, around the falx of cerebellum, or in ventricles (Fig. 6).7 Management Goals
There are no class I or II guidelines for specific management of posterior fossa traumatic injuries. Factors that determine surgical versus nonsurgical management of injuries to the posterior fossa are discussed next.24,25 Acute epidural hematomas
Volume greater than 30 cm3 and compression or obliteration of the fourth ventricle regardless of GCS score should undergo surgical evacuation as soon as possible. Volume less than 30 cm3, thickness less than 15 mm, no compression or mild compression of the fourth ventricle, GCS greater than 8, and no focal deficit can be managed with serial CT scans and close neurologic examinations. Acute subdural hematoma
Thickness greater than 10 mm and/or compression of the fourth ventricle regardless of GCS score should undergo surgical decompression as soon as possible. Thickness less than 10 mm, GCS score less than 9 with decrease in greater than 2 points between injury and hospital admission, and asymmetric or fixed pupils should undergo surgical decompression. GCS score less than 9 should undergo ICP monitoring. Skull fractures
Open skull fractures, closed depressed skull fracture greater than 1 cm, and fractures with significant underlying intracranial hematoma should undergo surgical intervention.
Fig. 5. Noncontrast computer tomography scan depicting a depressed occipital bone fracture abutting the right transverse sinus.
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Fig. 6. Noncontrast computed tomography scan of a 43-year-old woman with sudden-onset severe headache following trauma. There is subarachnoid hemorrhage in the basal cisterns.
Open skull fractures depressed greater than the thickness of the cranium should undergo surgical debridement to prevent infection. Nondepressed cranial fractures, fractures without clinical or radiographic evidence of violation of the dura, depression less than 1 cm, and fractures without significant intracranial hematomas do not require surgical intervention. Simple linear skull fractures do not require surgical intervention. Surgical Intervention
The general principles of craniotomy and craniectomy in the posterior fossa apply. In general, a large craniectomy is preferred to provide adequate decompression. The foramen magnum rim should be removed to provide adequate room for the tonsils and prevent tonsillar herniation. Placement of an external ventricular drain before performing posterior fossa decompression is recommended in light of the risk of obstructive hydrocephalus. Earlier literature warned against such intervention to avoid the possibility of upward herniation; however, to circumvent this occurrence, care should be taken to allow for minimal drainage of cerebrospinal fluid on placement of the ventricular drain. It is also important not to chase the hematoma beyond the fourth ventricle and into the brainstem because the risk of causing inadvertent injury to the surrounding normal brainstem parenchyma is very high. The goal of surgery in posterior fossa traumatic lesions is to reduce the intracranial tension and the mass effect on the fourth ventricle. Meticulous hemostasis is of great importance as in any neurosurgery. The dura should not be closed under tension and if there is any difficulty, a dural graft should be used. VASCULAR INJURIES
Arterial dissections are possible but rare in trauma to the posterior fossa. Damage to the arteries of the posterior fossa are usually associated with fractures but can occur without bony injury. Studies suggest that the vertebral artery (VA) is less commonly
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injured in all traumatic events compared with the carotid arteries (internal, external, and common carotid). The exception to this is when there is cervical spinal trauma affecting the foramen transversarium.26 Transverse fracture of the petrous bone can extend into the occipital bone leading to laceration of major venous sinuses, such as the sigmoid sinus.27 These venous sinus injuries could lead to venous EDH. Other vascular injuries usually involve the posteroinferior cerebellar artery (PICA). Pathophysiology
Rapid acceleration-deceleration causing rotation and hyperextension of the neck is a mechanism causing VA injuries (VAI).28 This injury has the potential to cause posterior circulation or cerebellar/brainstem stroke. Degree of VAI is classified into five grades. Grade I injury is described as arterial dissections with less than 25% luminal narrowing. Grade II injury is arterial dissection with more than 25% luminal narrowing. Grade III injury is when there is pseudoaneurysm of the VA. Grade IV injury occurs when there is occlusion of the VA. Grade V injury is a VA transsection.29 The most common cause of SAH is trauma. Traumatic SAH in the posterior fossa has been associated with rupture or dissection of VA or its branches, and formation of true or pseudoaneurysms.30 Clinical Findings
Most patients that suffer VAI are asymptomatic initially after trauma. The symptomfree period can range from 10 to 72 hours, which makes early diagnosis difficult.28 CT angiography (CTA) is recommended as the screening tool in patients after blunt trauma for suspected VAI.29 VAI may cause neurologic deterioration from distal thromboembolic events causing ischemic stroke in the posterior fossa. The gold standard for diagnosis of VAI is digital subtraction angiography (DSA).31 However, CTA can be incorporated into the trauma CT scan of the entire body. Current CT scans can effectively image large segments of the body in a short period of time.32 CTA with three-dimensional reconstruction has quality that matches the imaging of DSA. On CTA, double-lumen appearance with eccentric round-shaped hyperdensity of the true lumen and a surrounding crescentic hypodensity corresponding to the false lumen is an indication of VA dissection. Another radiographic feature suggesting VA dissection is seen when the vessel has an increased overall diameter but poor visualization of the lumen.31 CTA excels in identifying occlusion of vessel lumen, intimal flap, and pseudoaneuysms. VAI is a dynamic process, with gradual progression, spontaneous improvement, or immediate deterioration. No single imaging modality is definite for diagnosis because of this fact. If CTA is not conclusive on diagnosis, DSA is performed. Classic findings on angiogram include pearl and string sign, a double lumen, or a fusiform dilatation of the dissected segment (Fig. 7). False lumen of the dissected vessel is seen when there is delayed contrast clearance.32 Definite diagnosis is often made by combination of clinical findings, CTA, and/or DSA. Traumatic intradural VA and PICA aneurysm may result from blunt or penetrating head trauma. Direct trauma with compression of the artery against the fixed edges of the falx or tentorium may cause vascular injury leading to the formation of dissection or pseudoaneurysm.33 Rupture of these aneurysms causes severe morbidity and mortality. Patients after head trauma with posterior fossa SAH or fourth ventricular intraventricular hemorrhage should be fully evaluated for vascular lesions. Management and Treatment
Traumatic VAI may cause ischemic stroke in the posterior fossa. Anticoagulation or antiplatelet therapy is used to reduce the risk of stroke. VAI usually occurs in the
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Fig. 7. (Left image) Right vertebral injection anteroposterior view showing fusiform enlargement of the V4 segment of the vertebral artery followed by abrupt narrowing. This string sign is characteristic of subarachnoid hemorrhage. (Right image) Right vertebral injection lateral view showing enlargement of the V4 segment of the vertebral artery with abrupt narrowing. The posterior inferior cerebellar artery arises from the segment that has dissection.
setting of patients with severe traumatic brain, spine, or intra-abdominal injury. In those patients, anticoagulation or antiplatelet therapy could be contraindicated because of increased risk of bleeding.29 Surgical options involve proximal ligation of the dissected vessels, clipping or wrapping of associated pseudoaneuysms, and extracranial to intracranial bypass.32 Open surgery has been shown to have high rates of morbidity and mortality. More recently, advances in endovascular intervention have provided alternative management strategies often with lower associated morbidity. Endovascular therapy offers minimal invasive technique, decreased operative time, and eliminates the need for donor vessel for bypass procedure. Also, when angiogram is performed for diagnosis, intervention could immediately be performed. In the setting of multisystem trauma, the diseased vessel could be accessed from a distal site away from patient injuries. Treatments include use of detachable balloons, coils, and liquid emobolic agents to completely eliminate the blood flow over the diseased vessel or obliterate dissecting aneurysms.32 The choice of therapy for patients with VAI should be determined on an individual basis, taking into account the type and severity of vascular injury, associated traumatic injuries, and the risk of bleeding associated with anticoagulation or antiplatelet therapy.29 Treatment of traumatic PICA aneurysm is usually by surgical clipping or endovascular obliteration when the patient is stable for such a procedure. Although traumatic PICA aneurysms are uncommon, they can cause significant morbidity because of risk of hemorrhage. Surgical approaches to PICA aneurysm depend on the specific location of the aneurysm. Combined subtemporal presigmoid transtentorial, far lateral suboccipital, midline suboccipital, and combined lateral and medial suboccipital are some of the approaches for clipping of PICA aneurysm. Endovascular treatment of PICA aneurysms can be achieved with good success rate and low morbidity.34 However, the best treatment option is determined on a case-by-case basis depending on the location and type of pathology and the patient’s associated comorbidities.
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SUMMARY
Traumatic injury to the posterior fossa is a complex pathologic condition because of the great heterogeneity of lesions present. As with all TBI, treatment of primary brain injuries and prevention of secondary brain injuries is the mainstay of management. It is imperative to recognize traumatic lesions of the posterior fossa early because of the occurrence of rapid neurologic decline. Overall, the decision regarding whether or not to proceed with surgical intervention depends on the patient’s clinical condition, neurologic status, and imaging findings. In general, nonoperative management should be considered only if the patient is fully conscious and the associated posterior fossa lesions are small with little or no mass effect. Posterior fossa traumatic vascular injuries should also be managed either by an open surgical or endovascular approach.19
REFERENCES
1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States: emergency department visits, hospitalizations and deaths 2002–2006. Atlanta (GA): Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2010. 2. Snell RS. Clinical neuroanatomy. 7th edition. Philadelphia: Wolters Kluwer Health/ Lippincott Williams & Wilkins; 2010. 3. Tsai FY, Teal JS, Itabashi HH, et al. Computed tomography of posterior fossa trauma. J Comput Assist Tomogr 1980;4:291–305. 4. (editor-in-chief). In: Standring S, editor. Gray’s anatomy: the anatomical basis of clinical practice. 39th edition. Spain: Elsevier Publishing; 2005. p. 1549. 5. Atkinson JL. Acute epidural hematoma. In: Batjer HH, Loftus CM, editors. Textbook of neurological surgery: principles and practice. Philadelphia: Lippincott Williams and Wilkins; 2005. p. 2843. 6. Hashimoto T, Nakamura N, Richard KE, et al. Primary brain stem lesions caused by closed head injuries. Neurosurg Rev 1993;16:291–8. 7. Maschke M, Morsdorf M, Timmann D, et al. Posterior fossa trauma. In: Manto M, Schmahmann DJ, Rossi F, et al, editors. Handbook of cerebellum and cerebellar disorders. New York: Springer Science; 2013. p. 2055–78. 8. Karasawa H, Furuya H, Naito H, et al. Acute hydrocephalus in posterior fossa injury. J Neurosurg 1997;86:629–32. 9. Wright RL. Traumatic hematomas of the posterior cranial fossa. J Neurosurg 1966;25:402–9. 10. Liu K. Characteristics of diagnosis and treatment of traumatic intracerebellar hemorrhage. Zhonghua Wai Ke Za Zhi 1997;35:166–7 [in Chinese]. 11. Takeuchi S, Takasato Y, Masaoka H, et al. Traumatic intra-cerebellar haematoma: study of 17 cases. Br J Neurosurg 2011;25:62–7. 12. d’Avella D, Servadei F, Scerrati M, et al. Traumatic intracerebellar hemorrhage: clinicoradiological analysis of 81 patients. Neurosurgery 2002;50:16–25. 13. Evans JP, Scheinker IM. Histologic studies of the brain following head trauma; post-traumatic petechial and massive intracerebral hemorrhage. J Neurosurg 1946;3:101–13. 14. Tsubokawa T, Yamada J, Tomizawa N, et al. Classification of traumatic intracerebral hematoma by repeated CT-scan and clinical course (author’s transl). Neurol Med Chir (Tokyo) 1979;19:1127–37 [in Japanese]. 15. Posner J, Saper C, Schiff N, et al. Plum and Posner’s Diagnosis of Stupor and Coma. New York: Oxford University Press; 2007.
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16. Denny-Brown D, Russell WR. Experimental cerebral concussion. J Physiol 1940; 99:153. 17. Saatman KE, Duhaime AC, Bullock R, et al. Classification of traumatic brain injury for targeted therapies. J Neurotrauma 2008;25(7):719–38. 18. Balik V, Lehto H, Sulla I, et al. Posterior fossa extradural haematomas. Cent Eur Neurosurg 2010;71(4):167–72. 19. Quinones-Hinojosa A, editor. Schmidek and sweet operative neurosurgical techniques. 6th edition. Philadelphia: Elsevier; 2012. 20. Gulsen S, Sonmez E, Yilmaz C, et al. Traumatic acute subdural hematoma extending from the posterior cranial fossa to the cerebellopontine angle. J Korean Neurosurg Soc 2009;46(3):277–80. 21. Greenberg M. Handbook of neurosurgery. 7th edition. New York: Thieme; 2010. 22. Pascual JM, Prieto R. Surgical management of severe closed head injury in adults. In: Quinones-Hinojosa A, editor. Schmidek and sweet operative neurosurgical techniques. 6th edition. Philadelphia: Elsevier; 2012. p. 1513–38. 23. Servadei F, Compagnone C, Sahuquillo J. The role of surgery in traumatic brain injury. Curr Opin Crit Care 2007;13:163–8. 24. Bullock MR, Chesnut R, Ghajar J, et al. Guidelines for the surgical management of traumatic brain injury. Neurosurgery 2006;58(S2):1–62. 25. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons. Guidelines for the management of severe traumatic brain injury. J Neurotrauma 2007;24:S1–106. 26. Desouza RM, Crocker MJ, Haliasos N, et al. Blunt traumatic vertebral artery injury: a clinical review. Eur Spine J 2011;20(9):1405–16. 27. Samii M, Tatagiba M. Skull base trauma: diagnosis and management. Neurol Res 2002;24:147–56. 28. Majidi S, Hassan A, Adil M, et al. Incidence and outcome of vertebral artery dissection in trauma setting: analysis of national trauma data base. Neurocrit Care 2014. [Epub ahead of print]. 29. Harrigan M, Hadley M, Dhall S, et al. Management of vertebral artery injuries following non-penetrating cervical trauma. Neurosurgery 2013;72:234–43. 30. Schuster J, Santiago P, Elliott J, et al. Acute traumatic posteroinferior cerebellar artery aneurysms: report of three cases. Neurosurgery 1999;45:1465–7. 31. Soper J, Parker G, Hallinan J. Vertebral artery dissection diagnosed with CT. AJNR Am J Neuroradiol 1995;16:952–4. 32. Ali M, Amenta P, Starke R, et al. Intracranial vertebral artery dissections: evolving perspectives. Interv Neuroradiol 2012;18:469–83. 33. Nishioka T, Maeda Y, Tomogane Y, et al. Unexpected delayed rupture of the vertebral-posterior inferior cerebellar artery aneurysms following closed head injury. Acta Neurochir (Wien) 2002;144:839–45. 34. Chalouhi N, Jabbour P, Starke R, et al. Endovascular treatment of proximal and distal posterior inferior cerebellar artery aneurysms. J Neurosurg 2013;118: 991–9.
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KEYWORDS Traumatic brain injury Posterior fossa Intra-axial lesions Extra-axial lesions Vascular injuries KEY POINTS Traumatic injury to the posterior fossa is a complex pathologic condition because of the great heterogeneity of lesions present. As with all traumatic brain injuries, treatment of primary brain injuries and prevention of secondary brain injuries is the mainstay of management. It is imperative to recognize traumatic lesions of the posterior fossa early because of the occurrence of rapid neurologic decline. The decision regarding whether or not to proceed with surgical intervention depends on the patient’s clinical condition, neurologic status, and imaging findings. In general, nonoperative management should be considered only if the patient is fully conscious and the associated posterior fossa lesions are small with little or no mass effect. Posterior fossa traumatic vascular injuries should also be managed either by an open surgical or endovascular approach.
INTRODUCTION
It is estimated that more than 1.7 million cases of traumatic brain injury (TBI) occur in the United States each year and nearly 3% of these cases result in fatality. Although the leading cause of TBI in the United States is injury from falls, motor vehicle accidents are the leading cause of TBI that results in mortality.1 Trauma to the posterior cranial fossa is a subset of TBI that affects the parts of the brain located inferior to the tentorium cerebelli including the cerebellum, brainstem, major cranial blood vessels, and parts of cranial nerves III-XII (Fig. 1).2 However, most studies do not distinguish between trauma to the posterior fossa and other types of TBI. Major injuries within the posterior fossa are reported in 3.3% of all head trauma.3 Despite having
Department of Neurosurgery, LSU HSC Shreveport, 1501 Kings Highway, Shreveport, LA 71130, USA * Corresponding author. E-mail address: [email protected] Neurol Clin 32 (2014) 943–955 http://dx.doi.org/10.1016/j.ncl.2014.07.010 neurologic.theclinics.com 0733-8619/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
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Fig. 1. Midsagittal view of human brain. The approximate location of posterior cranial fossa is shaded. The ring represents the location of foramen magnum. (Courtesy of John Beal, PhD, Department of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center.)
a lower rate of occurrence, trauma to this area is associated with a higher rate of morbidity compared with supratentorial trauma. By definition, TBI is the result of an external force impacting the head and causing a sudden change in acceleration of the brain. Anatomically, the posterior fossa is the largest of the three fossa (anterior, middle, and posterior), located along the floor of the cranial cavity. Its boundaries are marked by aspects of the sphenoid, occipital, parietal, and temporal bones, with a roof formed from reflections of the dura mater called the tentorium cerebelli that houses the clinically important transverse venous sinuses.4 Although it is the largest fossa, the amount of space that is allowed for expansion is the smallest of the three fossa. Thus, the presence of critical structures that are contained within the posterior fossa combined with minimal compliance leads to significant morbidity from any mass-occupying lesions.5 Trauma to the posterior fossa may impair the function of cerebellum and/or the brainstem. When trauma affects the structures of the posterior fossa, the supratentorial region also may be affected. Studies have shown that more favorable outcomes were achieved when the supratentorial region was spared.6 Skull fractures could further complicate the management of patients with TBI, especially if a fracture is open. TBI is divided into primary and secondary brain injury. Primary brain injury refers to damage suffered as a direct result of the initial event, whereas secondary brain injury refers to the indirect insult to the brain as a result of the sequelae of the traumatic event. Primary traumatic injuries are commonly subdivided into blunt and penetrating injuries. Mass lesions from TBI are usually categorized as either intra- or extra-axial lesions. Intra-axial brain lesions are defined by intraparenchymal cerebellar or brainstem damage caused by hematoma, diffuse axonal injury from shearing forces, or delayed posttraumatic intracerebellar hematomas. Extra-axial injuries include epidural hematomas (EDH), subdural hematoma (SDH), and subarachnoid hemorrhage (SAH).7
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INTRA-AXIAL LESIONS
Intraparenchymal cerebellar hemorrhage secondary to trauma constitutes about 3% of all the traumatic head injuries and about 25% of all the traumatic injuries to the posterior fossa.3,8,9 Liu10 reported the incidence of traumatic cerebellar hemorrhage to be 3.7% among all head injuries. Cerebellar hemorrhage may occur in patients of all age groups, although it may more commonly be observed in young patients because this age group is more commonly involved in motor vehicle accidents. Pathophysiology
The exact mechanism of cerebellar contusion is unclear. They may be caused by blunt or penetrating trauma. Takeuchi and colleagues11 proposed three mechanisms of injury in the pathogenesis of cerebellar hematoma. The first is coup injury, where the posterior fossa is the first site of impact. This type of injury typically results in contusion of one of the cerebellar hemispheres with a concomitant contusion of the frontal or temporal lobes. Typically, in a coup injury of the cerebellum, there is evidence of an overlying injury, such as an epidural or a SDH or a fracture of the occipital bone. The second is contrecoup injury, where the site of first impact is other than the posterior fossa. Commonly, frontal or the temporal region is the first site of impact in this mechanism of injury. Again, in this type of injury, the cerebellar hemispheres are more commonly involved than the midline structures. However, in a contrecoup injury of the cerebellum, other traumatic lesions of the posterior fossa are rarely present. The third is shear-related injury, caused by acceleration-deceleration forces. This type of injury is frequently associated with diffuse axonal injury. Differential movements of one portion of the brain with respect to the other lead to the development of shear-strain forces. The most common locations where these forces develop are the gray-white matter junction, brain-pia mater interface, cerebrospinal fluid–brain interface, and skull-dura interface. In the posterior fossa, these lesions are usually seen in the dorsolateral brainstem and in the cerebellar hemispheres. In addition to the previously mentioned three mechanisms of injury, a fourth type of injury is also commonly observed. This is the delayed cerebellar hematoma, which develops secondary to cerebellar contusion as a result of secondary insult. The exact mechanism of this injury is unknown; however, this occurs more commonly in elderly people with underlying coagulopathy or hypertension.12 Delayed intracerebellar hemorrhage develops a few hours to days after trauma. It may progress rapidly and lead to brainstem compression. Various mechanisms, such as increased endothelial permeability of small vessels in the posterior fossa and hyperoxidation within the endothelial cells, have been hypothesized in its development.13,14 Therefore, it is essential to monitor the patients with posterior fossa trauma with serial imaging. As the size of the hematoma grows, the cerebellar parenchyma is destroyed and the hematoma causes mass effect. This may result in fourth ventricular compression leading to obstructive hydrocephalus. Edema of the cerebellar parenchyma around the hematoma adds to the mass effect. In later stages, there may be direct compression of the brainstem resulting in alteration of mental status, stupor, coma, and ultimately death. This sequence of events corresponds to the medullary stage of transtentorial herniation as described by Plum and Posner.15 Herniation may occur when the cerebellar tonsils are forced through the foramen magnum (tonsillar herniation) or when the vermis is forced upward through the tentorial incisura (upward or reverse transtentorial herniation). The latter condition may occur when the supratentorial compartment is suddenly decompressed in the
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presence of a large posterior fossa lesion. It is fortunately a rare condition. There is upward displacement of the vermis through the tentorial incisura causing compression of brainstem and death. Clinical Presentation
Traumatic parenchymal lesions of the cerebellum range from completely asymptomatic to coma and death. The variety and extent of signs and symptoms depend on the site of hemorrhage, size of the hemorrhage, presence of perilesional edema, and mass effect on surrounding structures. Clinical features may be classified into the following stages and usually correlate with the progression of the underlying pathophysiologic process (secondary injury). Stage I: asymptomatic or mild symptoms (dizziness, headache, vertigo); no cerebellar signs, no mass effect, no hydrocephalus, no brainstem compression; detected on imaging; the lesion is usually small, less than 2 cm; usually involving the cerebellar hemispheres Stage II: symptomatic; cerebellar signs present (axial or appendicular or both); mild mass effect over fourth ventricle, no hydrocephalus, no brainstem compression; the lesion is usually greater than 2 cm Stage III: symptomatic; cerebellar signs present, moderate mass effect on fourth ventricle, mild hydrocephalus, mild brainstem compression; the lesion is about 3 to 4 cm Stage IV: symptomatic; cerebellar signs present, severe mass effect over fourth ventricle, severe hydrocephalus, brainstem compression, and altered mental status; the lesion is usually greater than 4 cm Stage V: symptomatic; severe brainstem compression; coma and death; lesion over 4 cm Imaging Studies
As with other acute traumatic hemorrhagic lesions, acute cerebellar hemorrhage appears hyperdense on computed tomography (CT) scan (Fig. 2) and isointense on T1weighted and hypointense on T2-weighted magnetic resonance images. The following features should be observed on imaging while assessing a patient with cerebellar hemorrhage following trauma. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Location of hemorrhage (hemispheric, vermis, both) Presence of perilesional edema Associated posterior fossa traumatic lesions (EDH, SDH, fracture) Mass effect over fourth ventricle Ventricle size to assess for hydrocephalus Compression of brainstem Tonsillar herniation Effacement of basal cisterns Configuration of basal cisterns (“inverted smile” sign seen in upward herniation) Presence of associated diffuse axonal injury or supratentorial traumatic lesions Dissection of the hematoma into the brainstem through the fourth ventricle
Management Goals
The general management algorithm of a patient with TBI is beyond the scope of this article and is well described in the literature. In this section we discuss the specific management of focal cerebellar parenchymal hemorrhage. Conservative management of cerebellar contusion and hematoma may be considered in a fully alert patient
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Fig. 2. Cerebellar hematoma. Traumatic vermian hematoma in a patient. The hematoma has extended into the fourth ventricle and compressed it. There is also edema around the hematoma.
with a small lesion. Close monitoring is required to detect early signs of deterioration, which mandates surgical evacuation. Surgical evacuation for intraparenchymal cerebellar hemorrhage is usually indicated in the following situations: (1) contusion or hematoma greater than 3 cm in maximum dimension, (2) effacement of the basal cisterns, (3) moderate to severe mass effect over fourth ventricle causing hydrocephalus, (4) signs of tonsillar or upward herniation, and (5) moderate to severe brainstem compression. EXTRA-AXIAL LESIONS
External forces that give rise to TBI first stop at the skull and are then transmitted to the underlying structures in a linear fashion. This causes a vertical force on the brain tissue adjacent to the inner table of the skull at the site of the impact.16 As a result, the formation of intracranial, extra-axial hematomas after head injury is a common occurrence.17 Pathophysiology
EDH occurs in 2% to 5% of head-injured patients and posterior fossa EDH constitutes 4% to 13% of all EDH.18 EDHs are located between the outer (periosteal) layer of the dura mater and the inner table of the skull (Fig. 3). They typically develop at the moment of impact at the coup site. They are often associated with overlying occipital fractures.7 In comparison with the supratentorium EDH, posterior fossa EDHs are more frequently of venous rather than arterial origin. They are most often caused by transverse sinus injury from direct occipital trauma. Clival EDHs are an even rarer variant of posterior fossa EDHs and may occur by hyperflexion or extension cervical injuries or basilar clival fractures.19 SDHs are located between the inner (meningeal) layer of the dura mater and the arachnoid. SDHs are not always a result of the direct impact in head trauma but can result from shearing of bridging veins and venous sinuses. They occur in approximately 11% of head-injured patients. SDHs are associated with the highest mortality rate of all traumatic intracranial injuries. The rate is more than four times higher in
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Fig. 3. Noncontrast computer tomography scan of a 23-year-old man with an epidural hematoma of the posterior fossa located between the outer layer of the dura mater and the inner table of the skull. Note the characteristic hyperdense, biconvex appearance of the lesion. Arrowhead showing biconvex hyperdense collection consistent with an epidural hematoma. (From Maschke M, Morsdorf MM, Timman D, et al. Posterior fossa trauma. In: Manto M, Gruol D, Schmahmann J, et al, editors. Handbook of cerebellum and cerebellar disorders. New York: Springer Science1Business Media, 2013; with permission.)
patients older than 65 years. SDHs are more likely to be associated with moderate to severe underlying parenchymal injury, which is considered to be a contributor to the overall poor outcome of patients with SDHs.20 Traumatic SAH, like EDH of the posterior fossa, usually occurs because of rupture of venous structures. Despite its venous origin, traumatic SAH of the posterior fossa can occasionally lead to vasospasm of intracerebral arteries. The two most common types of fractures to the skull are linear and depressed fractures. Linear fractures are more common and have better patient outcomes compared with depressed fractures.10 Fractures to the occipital bone are of special concern because it is the major bone of the posterior cranial fossa and transmits many important anatomic structures including the vertebral arteries, hypoglossal nerves (cranial nerve XII), meningeal branches of ascending pharyngeal artery, transverse sinus, sigmoid sinus, and vagus nerves (Fig. 4). Clinical Findings
The classic “lucid” interval described in EDH occurs in 15% to 30% of patients and even less commonly in EDHs occurring in the posterior fossa. It consists of a brief loss of consciousness, caused by impact, followed by an awake period and late deterioration caused by mass effect and increasing intracranial pressure (ICP). With compressive lesions of the posterior fossa, including EDHs and SDHs, patients usually present with headache, nausea, and vomiting followed by loss of consciousness. Because of the limited size of the posterior fossa, early detection is imperative to avoid rapid and life-threatening neurologic deterioration.
Posterior Fossa Trauma
Fig. 4. Both (A) and (B) are noncontrast computed tomography scans of the head showing the crescentic or concave shape of an acute subdural hematoma. (A) shows the lower compartment of the the posterior fossa whereas (B) shows a higher cut at the the superior poles of the cerebellum depicting the crescentic nature of an acute subdural hematoma. (From Maschke M, Morsdorf MM, Timman D, et al. Posterior fossa trauma. In: Manto M, Gruol D, Schmahmann J, et al, editors. Handbook of cerebellum and cerebellar disorders. New York: Springer Science1Business Media, 2013; with permission.)
Clinical Examination
Pupillary examination by assessment of pupil size and reactivity to light is imperative in posterior fossa trauma, especially in patients with suspected mass lesions (eg, EDH, SDH). Sluggish or no pupillary reactivity may indicate compression of the fourth ventricle or brainstem and/or hydrocephalus. Downward deviation of the eyes may also be associated with unreactive pupils and possible hydrocephalus. The Glascow Coma Scale (GCS) is used to assess level of consciousness. Consciousness has two components: arousal and content. Impairment of arousal can vary from drowsiness to obtundation to coma. Coma is the most severe form of arousal impairment, and is defined as the inability to follow commands, speak, or open eyes to pain.21 Cranial nerve III and VI palsies may indicate impending herniation or increased ICP, respectively. Motor examination should evaluate muscle tone, reflexes, coordination, and motor strength. Imaging Studies
CT scanning is the imaging modality of choice for evaluation of head-injured patients. It allows rapid assessment of the location, extent, and type of intracranial lesions caused by the head injury.19 According to Pascual and Prieto22 three major findings should be evaluated on a head-injured patient’s CT: (1) presence of intracranial hematomas, (2) appearance of basal cisterns, and (3) presence of traumatic SAH. Studies have indicated a relationship between status of basal cisterns and outcome. Compressed or absent basal cisterns indicate a threefold risk of increased ICP.19
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The characteristic CT appearance of acute EDH is hyperdense, biconvex lesions adjacent to the skull. Mass effect is common.23 Occasionally, EDHs may appear heterogeneous with hyperdense and isodense areas, which may indicate active bleeding. Acute SDH appears as hyperdense, crescentic collections between the dura and brain parenchyma on CT (Fig. 5). In contrast with acute EDHs, acute SDHs are more diffuse, less uniform, and concave over the brain surface.24 CT scan is more sensitive than magnetic resonance imaging to disclose SAH at the acute stage, showing hyperdense fluid within the cisterns and sulci, around the falx of cerebellum, or in ventricles (Fig. 6).7 Management Goals
There are no class I or II guidelines for specific management of posterior fossa traumatic injuries. Factors that determine surgical versus nonsurgical management of injuries to the posterior fossa are discussed next.24,25 Acute epidural hematomas
Volume greater than 30 cm3 and compression or obliteration of the fourth ventricle regardless of GCS score should undergo surgical evacuation as soon as possible. Volume less than 30 cm3, thickness less than 15 mm, no compression or mild compression of the fourth ventricle, GCS greater than 8, and no focal deficit can be managed with serial CT scans and close neurologic examinations. Acute subdural hematoma
Thickness greater than 10 mm and/or compression of the fourth ventricle regardless of GCS score should undergo surgical decompression as soon as possible. Thickness less than 10 mm, GCS score less than 9 with decrease in greater than 2 points between injury and hospital admission, and asymmetric or fixed pupils should undergo surgical decompression. GCS score less than 9 should undergo ICP monitoring. Skull fractures
Open skull fractures, closed depressed skull fracture greater than 1 cm, and fractures with significant underlying intracranial hematoma should undergo surgical intervention.
Fig. 5. Noncontrast computer tomography scan depicting a depressed occipital bone fracture abutting the right transverse sinus.
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Fig. 6. Noncontrast computed tomography scan of a 43-year-old woman with sudden-onset severe headache following trauma. There is subarachnoid hemorrhage in the basal cisterns.
Open skull fractures depressed greater than the thickness of the cranium should undergo surgical debridement to prevent infection. Nondepressed cranial fractures, fractures without clinical or radiographic evidence of violation of the dura, depression less than 1 cm, and fractures without significant intracranial hematomas do not require surgical intervention. Simple linear skull fractures do not require surgical intervention. Surgical Intervention
The general principles of craniotomy and craniectomy in the posterior fossa apply. In general, a large craniectomy is preferred to provide adequate decompression. The foramen magnum rim should be removed to provide adequate room for the tonsils and prevent tonsillar herniation. Placement of an external ventricular drain before performing posterior fossa decompression is recommended in light of the risk of obstructive hydrocephalus. Earlier literature warned against such intervention to avoid the possibility of upward herniation; however, to circumvent this occurrence, care should be taken to allow for minimal drainage of cerebrospinal fluid on placement of the ventricular drain. It is also important not to chase the hematoma beyond the fourth ventricle and into the brainstem because the risk of causing inadvertent injury to the surrounding normal brainstem parenchyma is very high. The goal of surgery in posterior fossa traumatic lesions is to reduce the intracranial tension and the mass effect on the fourth ventricle. Meticulous hemostasis is of great importance as in any neurosurgery. The dura should not be closed under tension and if there is any difficulty, a dural graft should be used. VASCULAR INJURIES
Arterial dissections are possible but rare in trauma to the posterior fossa. Damage to the arteries of the posterior fossa are usually associated with fractures but can occur without bony injury. Studies suggest that the vertebral artery (VA) is less commonly
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injured in all traumatic events compared with the carotid arteries (internal, external, and common carotid). The exception to this is when there is cervical spinal trauma affecting the foramen transversarium.26 Transverse fracture of the petrous bone can extend into the occipital bone leading to laceration of major venous sinuses, such as the sigmoid sinus.27 These venous sinus injuries could lead to venous EDH. Other vascular injuries usually involve the posteroinferior cerebellar artery (PICA). Pathophysiology
Rapid acceleration-deceleration causing rotation and hyperextension of the neck is a mechanism causing VA injuries (VAI).28 This injury has the potential to cause posterior circulation or cerebellar/brainstem stroke. Degree of VAI is classified into five grades. Grade I injury is described as arterial dissections with less than 25% luminal narrowing. Grade II injury is arterial dissection with more than 25% luminal narrowing. Grade III injury is when there is pseudoaneurysm of the VA. Grade IV injury occurs when there is occlusion of the VA. Grade V injury is a VA transsection.29 The most common cause of SAH is trauma. Traumatic SAH in the posterior fossa has been associated with rupture or dissection of VA or its branches, and formation of true or pseudoaneurysms.30 Clinical Findings
Most patients that suffer VAI are asymptomatic initially after trauma. The symptomfree period can range from 10 to 72 hours, which makes early diagnosis difficult.28 CT angiography (CTA) is recommended as the screening tool in patients after blunt trauma for suspected VAI.29 VAI may cause neurologic deterioration from distal thromboembolic events causing ischemic stroke in the posterior fossa. The gold standard for diagnosis of VAI is digital subtraction angiography (DSA).31 However, CTA can be incorporated into the trauma CT scan of the entire body. Current CT scans can effectively image large segments of the body in a short period of time.32 CTA with three-dimensional reconstruction has quality that matches the imaging of DSA. On CTA, double-lumen appearance with eccentric round-shaped hyperdensity of the true lumen and a surrounding crescentic hypodensity corresponding to the false lumen is an indication of VA dissection. Another radiographic feature suggesting VA dissection is seen when the vessel has an increased overall diameter but poor visualization of the lumen.31 CTA excels in identifying occlusion of vessel lumen, intimal flap, and pseudoaneuysms. VAI is a dynamic process, with gradual progression, spontaneous improvement, or immediate deterioration. No single imaging modality is definite for diagnosis because of this fact. If CTA is not conclusive on diagnosis, DSA is performed. Classic findings on angiogram include pearl and string sign, a double lumen, or a fusiform dilatation of the dissected segment (Fig. 7). False lumen of the dissected vessel is seen when there is delayed contrast clearance.32 Definite diagnosis is often made by combination of clinical findings, CTA, and/or DSA. Traumatic intradural VA and PICA aneurysm may result from blunt or penetrating head trauma. Direct trauma with compression of the artery against the fixed edges of the falx or tentorium may cause vascular injury leading to the formation of dissection or pseudoaneurysm.33 Rupture of these aneurysms causes severe morbidity and mortality. Patients after head trauma with posterior fossa SAH or fourth ventricular intraventricular hemorrhage should be fully evaluated for vascular lesions. Management and Treatment
Traumatic VAI may cause ischemic stroke in the posterior fossa. Anticoagulation or antiplatelet therapy is used to reduce the risk of stroke. VAI usually occurs in the
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Fig. 7. (Left image) Right vertebral injection anteroposterior view showing fusiform enlargement of the V4 segment of the vertebral artery followed by abrupt narrowing. This string sign is characteristic of subarachnoid hemorrhage. (Right image) Right vertebral injection lateral view showing enlargement of the V4 segment of the vertebral artery with abrupt narrowing. The posterior inferior cerebellar artery arises from the segment that has dissection.
setting of patients with severe traumatic brain, spine, or intra-abdominal injury. In those patients, anticoagulation or antiplatelet therapy could be contraindicated because of increased risk of bleeding.29 Surgical options involve proximal ligation of the dissected vessels, clipping or wrapping of associated pseudoaneuysms, and extracranial to intracranial bypass.32 Open surgery has been shown to have high rates of morbidity and mortality. More recently, advances in endovascular intervention have provided alternative management strategies often with lower associated morbidity. Endovascular therapy offers minimal invasive technique, decreased operative time, and eliminates the need for donor vessel for bypass procedure. Also, when angiogram is performed for diagnosis, intervention could immediately be performed. In the setting of multisystem trauma, the diseased vessel could be accessed from a distal site away from patient injuries. Treatments include use of detachable balloons, coils, and liquid emobolic agents to completely eliminate the blood flow over the diseased vessel or obliterate dissecting aneurysms.32 The choice of therapy for patients with VAI should be determined on an individual basis, taking into account the type and severity of vascular injury, associated traumatic injuries, and the risk of bleeding associated with anticoagulation or antiplatelet therapy.29 Treatment of traumatic PICA aneurysm is usually by surgical clipping or endovascular obliteration when the patient is stable for such a procedure. Although traumatic PICA aneurysms are uncommon, they can cause significant morbidity because of risk of hemorrhage. Surgical approaches to PICA aneurysm depend on the specific location of the aneurysm. Combined subtemporal presigmoid transtentorial, far lateral suboccipital, midline suboccipital, and combined lateral and medial suboccipital are some of the approaches for clipping of PICA aneurysm. Endovascular treatment of PICA aneurysms can be achieved with good success rate and low morbidity.34 However, the best treatment option is determined on a case-by-case basis depending on the location and type of pathology and the patient’s associated comorbidities.
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SUMMARY
Traumatic injury to the posterior fossa is a complex pathologic condition because of the great heterogeneity of lesions present. As with all TBI, treatment of primary brain injuries and prevention of secondary brain injuries is the mainstay of management. It is imperative to recognize traumatic lesions of the posterior fossa early because of the occurrence of rapid neurologic decline. Overall, the decision regarding whether or not to proceed with surgical intervention depends on the patient’s clinical condition, neurologic status, and imaging findings. In general, nonoperative management should be considered only if the patient is fully conscious and the associated posterior fossa lesions are small with little or no mass effect. Posterior fossa traumatic vascular injuries should also be managed either by an open surgical or endovascular approach.19
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