Neurovascular Complications After Nonpenetrating Brain Injury

Sunil Kothari, Michael M. Green, and Ana Durand-Sanchez

INTRODUCTION

Although uncommon, neurovascular complications of traumatic brain injury (TBI) can have devastating consequences. This chapter will focus on three of the most often seen of these complications—arterial dissection, carotid-cavernous fistulas (CCFs), and traumatic aneurysms.

• Recognizing neurovascular sequelae of TBI is complicated by several factors:

Patients may be asymptomatic or may have nonspecific symptoms

Symptoms may be delayed in their presentation, sometimes for weeks to months

Symptoms (e.g., headache) may mistakenly be attributed to the TBI itself, rather than to a neurovascular problem

There is often no correlation between the severity of TBI and the development of neurovascular sequelae

• Clinicians need to maintain a high index of suspicion in order to expediently identify these conditions.

ARTERIAL DISSECTION

• Can occur as a result of stretch injury or direct trauma, resulting in a tear in the wall of an artery, which allows intrusion of blood within the layers of the arterial wall.

• The site of dissection may be either within the connective tissue and vasa vasorum of the media or, more commonly, intimal [1]. Intimal disruption can lead to thrombus formation, which can result in vascular obstruction in situ and/or result in distal embolization. Expansion of the subintimal blood causes luminal narrowing, sometimes resulting in obstruction. Involvement of the media or adventitia can result in aneurysms, pseudoaneurysms, or fistulae.

• Dissections can occur intracranially or extracranially, either in the internal carotid artery or the vertebral artery; they occur extracranially more commonly than intracranially.

Carotid artery dissections significantly outnumber vertebral artery dissections [2].

Dissections can be bilateral 30% to 40% of the time [3].

• Usually, there is no external evidence of trauma over the affected vessel.

Clinical Presentation

• Symptoms may be a result of local effects or due to ischemia.

• Often, but not always, local symptoms precede the development of ischemia. Therefore, early recognition of local symptoms and timely intervention may reduce the risk of the development of ischemia.

Extracranial Carotid Artery Dissection

Local Symptoms

• Headache and neck pain are usually the most prominent symptoms [1]. The pain is typically ipsilateral, sharp or constant, and affects the jaw and face or frontoparietal area.

• Patients may report pulsatile tinnitus or a subjective bruit.

• A partial Horner’s syndrome (miosis and ptosis) can be seen on the ipsilateral side as a result of involvement of the sympathetic fibers that travel along the internal carotid artery.

• Ipsilateral cranial nerve palsies can also be seen. The lower cranial nerves are more often involved, with taste disturbance and tongue weakness being the most common manifestations [1].

Ischemic Symptoms

• Ischemic symptoms (cerebral or retinal) are common in carotid dissections, occurring in the majority of patients [4] and resulting in either transient ischemic attacks or infarctions.

• Ischemic symptoms usually follow local symptoms by hours or days.

• Specific symptoms are referable to the vascular territories of the involved vessel and can include visual loss (e.g., amaurosis fugax), aphasia, hemiparesis, and so on.

Extracranial Vertebral Artery Dissection

Local Symptoms

• Neck pain, often severe, is the most prominent local symptom. The pain is primarily located in the ipsilateral occipitocervical region.

Ischemic Symptoms

• Ischemic symptoms may not occur if there is adequate collateral circulation.

• When ischemic symptoms occur, symptoms usually reflect involvement of brainstem or cerebellar structures and can include ataxia, vertigo, dysarthria, and diplopia.

Intracranial Dissections

• Ischemic symptoms, not local symptoms, are usually the first manifestation. Ischemic symptoms tend to be more severe than in extracranial dissection.

• Intracranial dissections are much more likely to rupture, resulting in subarachnoid hemorrhage [1].

Imaging

• Although catheter angiography remains the gold standard, noninvasive options are frequently used, at least for the initial diagnosis. These include CT angiography (CTA), MR angiography (MRA), and Doppler ultrasound.

• Choice of modality should take into consideration issues such as degree of suspicion, accessibility of modality, contraindications to modality (e.g., to contrast or magnetic fields), and so on.

Treatment

• Treatment is broadly divided into medical and interventional treatments.

• Medical treatment consists either of antiplatelet therapy or anticoagulation. Although anticoagulation has generally been viewed as the primary therapeutic approach, a recent study found that there is currently not enough evidence to definitively recommend one modality over another [5].

• Interventional treatment includes surgery as well as procedures such as stenting or balloon occlusion.

• Choice of treatment depends on many factors including the patient’s symptoms, time course of symptom progression, nature of lesion, etiology of ischemia (e.g., embolic vs. vessel occlusion), patient’s overall neurological status, contraindications to certain treatments (e.g., anticoagulation), and availability of newer interventional modalities.

• Most patients will require follow-up imaging to monitor status of the dissection, especially if being treated medically.

CAROTID-CAVERNOUS FISTULAS

Description

• Although fistulas can occur in any artery after dissection or occlusion, the most common posttraumatic fistula occurs between the internal carotid artery and the cavernous sinus [4].

• The cavernous sinuses contain a number of venous channels. They are located on either side of the sella turcica and posterior to the orbits.

• A number of important structures pass through the cavernous sinus, including the internal carotid artery and cranial nerves III, IV, V, and VI.

• Although there are several different types of CCFs, by far the most common after trauma is one in which a fistula develops directly between the internal carotid artery and the cavernous sinus. These traumatic CCFs are known as Barrow type A CCF or direct CCF [6]. Traumatic CCFs represent high-flow shunts because there is shunting of blood between a high-flow arterial system and a low-flow venous system. The high-flow shunt created by the CCF increases venous resistance, which impedes the venous drainage into the cavernous sinus.

• Although traumatic CCFs can develop at the time of or shortly after the initial injury, they can also develop much later, when an initially injured internal carotid artery finally erodes or ruptures into the cavernous sinus.

• Bilateral traumatic CCFs have been reported [7].

Clinical Presentation

• The symptoms of traumatic CCF are a result of vascular congestion in the regions that are normally drained by the cavernous sinus.

• Orbital and periorbital manifestations are the most common and include ipsilateral chemosis, scleral injection, proptosis (sometimes pulsatile), and pain.

• An orbital or facial bruit may be auscultated [8,9].

• Extraocular palsy (especially of CN VI) and diminished visual acuity can also occur.

• Increased intraocular pressure (because of impaired aqueous humor drainage through the canals of Schlemm) may result in glaucoma and loss of vision (ischemic optic neuropathy) [8].

• In addition to orbital and ophthalmic symptoms, patients may complain of headache, epistaxis, upper facial numbness, and tinnitus (often described as buzzing or “swishing”) [7].

• The possibility of significant or even complete visual loss (from retinal hypoxia and/or ischemic optic neuropathy) warrants early detection and management of a traumatic CCF [7]. Other serious complications include cerebral ischemia (because of “vascular steal”) and hemorrhage, both subarachnoid as well as parenchymal.

Imaging

The gold standard modality is four-vessel digital subtraction angiography (DSA). However, the use of CT (with contrast) and MRI/MRA has also been described [7].

Treatment

• Traumatic CCFs are most often treated with endovascular techniques [4,7]. These include the use of balloons and coils to achieve occlusion or embolization.

• Direct surgical repair may be indicated in some cases [4].

• Although closure of the fistula usually results in resolution of most symptoms, visual function may not return because of permanent injury to the optic nerve [9].

TRAUMATIC INTRACRANIAL ANEURYSMS

Description

• Traumatic intracranial aneurysms (TICA), although uncommon, are associated with significant morbidity and mortality rates of 50% after rupture [10].

• Although more often associated with severe TBI, they can occur after even mild head trauma [10].

• Traumatic aneurysms can be classified both by histological type and location. Histologically, TICA fall into one of three main categories:

True aneurysms involve disruption of the intima and media with preservation of the adventitia, which forms the aneurysm wall.

In false aneurysms (or pseudoaneurysms), all three layers (intima, media, and adventitia) are disrupted and the extravasated blood is contained only by arachnoid, brain parenchyma, or the hematoma itself.

Mixed aneurysms represent false aneurysms that are formed after the contained rupture of a true aneurysm.

• TICA are also classified by their anatomic location. In particular, they can be distinguished by whether they arise proximal or distal to the circle of Willis.

Aneurysms that arise proximal to the circle of Willis can involve the carotid artery (either the supraclinoid or intraclinoid segment) or the vertebrobasilar arteries.

Aneurysms that arise distal to the circle of Willis involve cortical or subcortical arteries (or their branches).

Clinical Presentation

• The clinical presentation depends on whether the aneurysm has ruptured or not. Unfortunately, most aneurysms are asymptomatic until rupture, thereby minimizing the possibility of early detection.

• Patients with supraclinoid carotid artery aneurysms can present with headache, memory disturbance, and visual changes before rupture. Patients with unruptured infraclinoid carotid artery aneurysms can present with cranial nerve deficits, diabetes insipidus, recurrent epistaxis, or symptoms of a CCF [10,11].

• Most traumatic aneurysms present after rupturing, resulting in subdural, subarachnoid, or intraparenchymal hemorrhages. Symptoms of a ruptured aneurysm typically include decreased level of consciousness, focal neurological deficit, and/or seizure.

• The average time from initial trauma to aneurysmal hemorrhage is approximately 21 days, although rupture can be delayed for months or even years [10].

Imaging

• Unruptured aneurysms are difficult to detect with routine, noncontrast CT or MRI scans. CT or MR angiography may be considered, especially given the cost and risk of complications associated with DSA, the diagnostic gold standard [10].

• After rupture, CT or MRI will demonstrate intracranial hemorrhage. DSA should be performed as soon as possible in order to identify the underlying lesion.

Treatment

• The goal of treatment is to exclude the aneurysm from the circulation by surgical or endovascular methods.

• Endovascular procedures are more difficult with traumatic aneurysms because of the lack of an aneurismal neck, the extent of the arterial wall involved, the fragile nature of these aneurysms, and the lack of a defined wall in cases of pseudoaneurysm. Despite this, endovascular techniques utilizing balloons or embolization with detachable coils have been used with some success [10].

• Surgical clipping has advantages in that it allows for removal of the hematoma, provides definitive isolation of the aneurysm, and allows for the reconstruction of the parent artery, if needed [10].

• Ultimately, considerations such as aneurysm structure, location, clinical status of the patient, and availability of appropriately skilled personnel will dictate the optimal treatment method.

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