Intracranial Hemorrhage · 487 11

possible during surgery, and by therapeutically induced hypertension. These measures usually suffice to prevent the development of vasospastic infarcts, a much-feared complication. Vasospasm is a serious impediment to the effective diagnosis and treatment of aneurysmal subarachnoid hemorrhage.

Rebleeding, if it occurs, is more often lethal (50%) than the initial subarachnoid hemorrhage. The risk of rebleeding is 20% in the first 14 days after the initial SAH, and 50% in the first six months, if the aneurysm has not been obliterated. Unlike the initial SAH, rebleeds often produce large intraparenchymal hematomas, because the subarachnoid space around the aneurysm is partly sealed by adhesions resulting from the initial bleed. In such cases, the clinical manifestations and course of the aneurysmal rebleed are as described above for spontaneous intracerebral hemorrhage.

Subdural and Epidural Hematoma

Subdural Hematoma

In subdural hematoma, the collection of blood lies in the normally only virtual space between the dura mater and the arachnoid. The cause is usually trauma.

Acute Subdural Hematoma

Acute subdural hematoma (Fig. 11.35) is found in severe head trauma. It carries a poor prognosis, not because of the subdural blood itself but because it is very often associated with an underlying parenchymal injury. Its lethality may be as high as 50%. Its clinical manifestations are determined by the site and extent of the associated parenchymal injury.

Fig. 11.35 Acute subdural hematoma. The spaceoccupying lesion is concave in shape and poorly demarcated from the underlying brain tissue. There is a pronounced mass effect with midline shift.

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11 488 · 11 Blood Supply and Vascular Disorders of the Central Nervous System

Treatment is directed both at the hematoma itself and at the associated parenchymal injury. If open neurosurgical removal of the hematoma is necessary, contused brain tissue must often be resected as well. At surgery, a duraplasty may be performed, and the bone plate may be left out, rather than put back in its original position, in order to provide room for the swollen brain and prevent potentially lethal intracranial hypertension—a similar procedure to decompressive craniectomy for massive ischemic stroke. The current trend in neurosurgery is to perform such decompressions more frequently, both for stroke and for head trauma.

Chronic Subdural Hematoma

The etiology of chronic subdural hematoma remains incompletely understood. There is often an antecedent history of one or more minor traumatic episodes. The fluid collection lies between the inner dural membrane and the arachnoid and is probably derived from an initial hemorrhage of the bridging veins. In the chronic phase, granulation tissue is found in the wall of the hematoma. This tissue is thought to be the source of repeated, secondary bleeding into the fluid collection, so that it slowly expands, rather than being resorbed.

The manifestations of chronic subdural hematoma are produced by pressure on the underlying brain tissue and depend on the site of the hematoma. A chronic subdural hematoma overlying the central region may be clinically indistinguishable from an infarct.

The treatment consists of operative removal or percutaneous drainage. There is a relatively high recurrence rate. The presence of a subdural hematoma contraindicates therapeutic anticoagulation, which may cause additional bleeding into the hematoma cavity, producing mass effect.

Epidural Hematoma

In epidural hematoma, the blood collection lies between the dura mater and the periosteum (Fig. 11.36). It is classically produced by traumatic laceration of a meningeal artery. Because the dura mater is tightly attached to the inner surface of the skull, a great deal of pressure is required to create a fluid collection at this site. The cause is almost always a skull fracture with a tear in the middle meningeal artery, the largest of the meningeal vessels. Such fractures often occur without producing any serious injury to the brain; thus, many patients with epidural hematoma remain awake immediately after the traumatic event and do not lose consciousness until some time later (after the so-called “lucid interval”). They may then die from the rapidly rising intracranial pressure un-

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Vascular Syndromes of the Spinal Cord · 489 11

Fig. 11.36 Acute epidural hematoma, left. The hematoma is convex. The central hypodensity is due to blood that has not yet clotted. There is a pronounced mass effect with midline shift.

less the hematoma is rapidly diagnosed and operatively removed. Prompt treatment affords a good prognosis.

Vascular Syndromes of the Spinal Cord

Arterial Hypoperfusion

Spinal cord infarcts are much rarer than cerebral infarcts because of the extensive anastomotic network linking the arteries of the spinal cord. Large emboli cannot lodge in the small arteries of the cord, and the very small particles that can do so cause no clinically significant damage. Even aortic aneurysms or occlusions rarely cause damage to the spinal cord.

The symptoms of spinal cord infarction depend on the vascular territory involved.

Infarction in the territory of the anterior spinal artery. The clinical manifestations depend on the segmental level of the lesion. An infarct in the upper cervical spinal cord produces the following deficits: damage to the anterior horns and anterior roots causes flaccid paresis of the arms; damage to the decussating fibers of the lateral spinothalamic tract causes analgesia and thermanesthesia in the upper limbs; and damage to the corticospinal tracts causes spastic paraparesis. Bladder and bowel dysfunction are common. Because the posterior columns lie outside the territory of the anterior spinal artery, there may be no deficit of epicritic and proprioceptive sensation. The deficits typically appear suddenly and are accompanied by pain.

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Infarction in the territory of the posterolateral spinal artery produces deficits resulting from damage to the posterior columns, posterior roots, and posterior horns. The corticospinal tracts may also be damaged. There is thus an impairment of epicritic sense and proprioception below the level of the lesion. At the level of the lesion, damage to the posterior roots causes an additional segmental sensory deficit. If the corticospinal tracts are involved as well, spastic paraparesis results.

Diagnostic evaluation. The diagnosis of spinal cord infarction is usually difficult. Even with MRI, infarcts often cannot be reliably distinguished from other types of myelopathy. An important clue to the presence of a spinal cord infarct, in addition to the typical history and physical findings, is the radiological demonstration of ischemic changes in a vertebral body, because the spinal cord and the vertebral body are supplied by the same radicular artery. The blood­CNS barrier is not demonstrably disrupted within the lesion until a few days after the acute event (that is, the lesion is not contrast-enhancing until this time). The final step of the diagnostic evaluation is a lumbar puncture to rule out an infectious process.

For technical reasons, diffusion-weighted MRI, which reliably demonstrates acute ischemia in the brain, is difficult to perform in the spinal cord.

Impaired Venous Drainage

The most common cause of elevated venous pressure in the spinal veins is a dural arteriovenous fistula.

Congestive Myelopathy

Etiology. The cause of congestive myelopathy (Foix­Alajouanine disease), a disorder that mainly affects elderly men, was first recognized in the 1980s: an arteriovenous fistula, usually located on a spinal nerve root. Arterial blood passes through the fistula directly into the intradural veins. The fistula remains clinically silent as long as the excess flow of blood into the veins (the shunt volume) does not exceed their drainage capacity. As soon as it does, however, the venous pressure rises, and the spinal cord, which is very sensitive to such increases, is damaged.

Manifestations. The initial manifestations are unsteady gait and spastic paraparesis, sometimes accompanied by radicular pain. If the disease progresses, autonomic deficits appear, including bladder, bowel, and sexual dysfunction. The sensory deficit at first mainly concerns the protopathic modalities; later, epicritic sensation and proprioception are also affected. Further progression

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Vascular Syndromes of the Spinal Cord · 491 11

Case Presentation 11: Spinal Dural Arteriovenous Fistula

This 53-year-old woman noticed increasing weakness of both legs for several months. She had no pain, but complained of a “woolly” feeling in the legs, and also had increasing difficulty with urination and defecation. Peripheral neuropathy was diagnosed at first, but, when her leg weakness continued to progress, an MRI scan of the spinal cord was ordered (Fig. 11.37). This was performed in an outlying hospital and was initially interpreted as showing a tumor of the spinal cord.

The patient was transferred to the neurosurgical service. The patient’s clinical history and MRI findings were considered to be more consistent with a spinal dural arteriovenous fistula than with an intramedullary tumor. This suspicion was confirmed by angiography, and the fistula was surgically excised. The patient’s signs and symptoms resolved completely, except for residual bladder dysfunction.

a

b

Fig. 11.37 Spinal arteriovenous (AV) fistula. a Sagittal T2-weighted image. Intramedullary edema is seen in the lower portion of the spinal cord, including the conus medullaris. Dilated epimedullary veins appear as dark, rounded structures. b In this T1-weighted image obtained after the administration of intravenous contrast, some vessels appear bright, others dark. There is no contrast enhancement within the spinal cord.

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