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-17-year-old man who sustained a basal skull fracture during a motor vehicle accident and developed rapidly progressive proptosis, chemosis, and visual loss in the right eye. A, Right internal carotid angiogram, lateral projection, shows a carotid-cavernous fistula associated with a large cavernous sinus vanx with drainage to the superior ophthalmic vein (curved arrow) and cortical venous drainage (straight arrow). B, Right internal carotid angiogram, lateral projection, shows complete closure of fistula with preservation of parent artery after balloon embolization.
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Interventional neuroradiology has made tremendous advances in the 28 years since Lussenhop and Spence [75] first reported occlusion of a cerebral AVM by embolization with radiologic guidance. This progress is largely attributable to continuing advances in imaging techniques, catheters, and embolic technology, coupled with an improved understanding...
Citations
A 46-year-old woman presented with a history of focal Scizures for 7 years, slowly progressive left-side weakness of the extremities and face, and gait disturbance beginning approximately 3 years prior to admission. She also had numbness of the left side of her body and face. Past medical history was otherwise remarkable only for occasional asthmatic attacks, relieved by nonprescription inhalers. She took no other medications. An allergy to shellfish was noted. On admission to the hospital, phenytoin (Dilantin®), dexamethasone (Decadron®), and ranitidine (Zantac®) were prescribed.
Interventional Neuroradiology (INR), a hybrid of traditional neurosurgery and neuroradiology, may be broadly defined as treatment of central nervous system (CNS) disease by endovascular access for the purpose of delivering therapeutic agents, including both drugs and devices (1–7). Development of novel materials and techniques has opened new therapeutic avenues and offered means to understanding CNS pathophysiology.
Interventional neuroradiologic procedures have become the preferred treatment for certain vascular disorders of the central nervous system as a result of the development of new catheters and embolic agents and improved imaging techniques. Whether these procedures are used preoperatively or as definitive treatment, the risk of embolization has decreased with increasing experience, and they compare favorably with the risk of surgery and other treatment modalities. Although devascularizing procedures decrease or eliminate the blood supply to vascular lesions, transluminal angioplasty and thrombolytic therapy increase blood flow to tissues and are effective treatments for symptomatic cerebral vasospasm and iatrogenic cerebral emboli, respectively.
Conscious sedation is the preferred anesthetic technique for therapeutic angioembolization because of the ability to perform repeated neurologic assessment. For the uncooperative, obtunded, and pediatric patient, general anesthesia is required for immobilization, control of the airway, and ventilation. Evoked-potential monitoring and preembolization testing with Amytal sodium have decreased the incidence of neurologic complications significantly.
Patients with cardiovascular instability and elevated intracranial pressure are at increased risk if controlled hypotension is necessary during embolization.
Complications associated with therapeutic embolization can result in stroke, paralysis, or death. An anaphylactic reaction to contrast media can produce airway obstruction and cardiopulmonary compromise. Resuscitation equipment and emergency drugs should always be available. Acute pulmonary embolism may occur if an arterial injection of embolizing material is carried through an AVM to the venous circulation and thence into the lung. Closure of a large AVM may result in acute systemic hypertension and pulmonary edema; this is a common complication of occlusion of a vein of Galen AVM in an infant.
Intracranial hemorrhage is another serious complication of neuroembolic procedures. Emergency management includes airway control, hyperventilation and barbiturate administration for elevated intracranial pressure, and maintenance of cardiovascular stability to preserve cerebral perfusion pressure.
Interventional neurovascular techniques for the treatment of cerebrovascular disorders and stroke have evolved rapidly during the past decade. Development of soft, atraumatic microcatheters and steerable microguidewires have now allowed the interventional neuroradiologist relatively safe access to all the larger intracranial vessels around the skull base and circle of Willis. Newer nonionic contrast media used to visualize the cerebral vessels have decreased adverse reactions. Digital subtraction angiography has allowed rapid interpretation and immediate visualization of the blood vessels during infusion therapy of thrombolytic agents. Magnetic resonance imaging and magnetic resonance angiography now allow noninvasive screening and follow-up of patients with cerebrovascular occlusive disease.
Neuroendovascular surgery/interventional neuroradiology is a relatively new subspecialty that has been evolving since the mid-1970s. During the last 2 decades, significant advances have been made in this field of minimally invasive therapy for the treatment of intracranial cerebral aneurysms; acute stroke therapy intervention; cerebral arteriovenous malformations; carotid-cavernous sinus fistulae; head, neck, and spinal cord vascular lesions; and other complex cerebrovascular diseases. Advanced postresidency fellowship programs have now been established in North America, Europe, and Japan, specifically for training in this new subspecialty. During a period of 14 years, from 1986 to the present, an ad hoc committee comprising senior executive committee members of the American Society of Interventional and Therapeutic Neuroradiology, the joint section of Cerebrovascular Neurosurgery, and the American Society of Neuroradiology met to establish general guidelines that were mutually agreeable to both societies for training physicians in this field. These training standard guidelines were unanimously endorsed by the executive committee of the joint section of cerebrovascular neurosurgery in April 1999, by the executive committee of the American Society of Interventional and Therapeutic Neuroradiology and the American Society of Neuroradiology in May 1999, and by the executive council of the American Association of Neurological Surgeons and the Congress of Neurological Surgeons in June 15999. The guidelines for residency/fellowship education have now been endorsed by the parent organizations of both the interventional and diagnostic neuroradiology communities, as well as both senior organizations representing neurosurgery in North America. These guidelines for training should be used as a reference and guide by any institution establishing a training program in neuroendovascular surgery/interventional neuroradiology.
The term idiopathic intracranial hypertension (IIH) has been used interchangeably in the literature with pseudotumor cerebri. Pseudotumor cerebri syndrome (PTCS) is now used to denote idiopathic and secondary etiologies of increased intracranial hypertension. Common symptoms of elevated intracranial pressure (ICP) are headache, transient visual obscurations, and pulsatile tinnitus. Visual acuity may range from normal to no light perception. The visual acuity is not related to the degree of papilledema, except for atrophic papilledema in which the vision would be invariably poor. Concentric enlargement of the blind spot is the most common defect, followed by isopter constriction and loss of the inferior nasal quadrant of the visual field with a nasal step. Color defects usually involve red-green abnormalities. No afferent pupillary defect is detected in most instances of bilateral papilledema. One-third of patients have horizontal diplopia. Papilledema is clinically defined as optic disc swelling resulting only from increased ICP, which is equal to or greater than 250 mmH2O in adults while in a lateral recumbent position. Optical coherence tomography (OCT) can be used as an adjunct to ophthalmoscopy to monitor the severity and evolution of papilledema.
The two major goals of therapy in PTCS, a term that includes idiopathic (IIH) and secondary etiologies of increased intracranial hypertension, are to prevent visual loss and treat and prevent headaches. The mainstay of medical treatment of PTCS is weight loss. The Idiopathic Intracranial Hypertension Treatment Trial is currently an ongoing prospective randomized, double-blinded, placebo-controlled trial to compare the efficacy of acetazolamide (up to 4 g/day) added to a low-sodium, weight reduction diet versus dieting alone or preventing or restoring visual loss. If headaches develop, then antimigraine medications may be added.
Indications for surgery include the following: (1) progressive visual loss despite maximal medical treatment, (2) severe or sudden visual loss at onset with an afferent pupillary defect or signs of advancing optic nerve dysfunction, and (3) severe papilledema causing macular edema or exudates. Optic nerve sheath decompression (ONSD) has been shown to be safe and effective in treating vision in PTCS. ONSD may not be the treatment of choice for those who have progressive visual loss and intractable headaches, which are better managed by ventriculoperitoneal (VP) or lumboperitoneal (LP) shunting. Because of the high rate of complications and failures following VP or LP shunting, bariatric surgery may be an effective alternative in severely obese patients with PTCS. Because of increasing evidence of nonthrombotic dural venous sinus stenosis, endovascular stenting may be an option for treatment of PTCS.
The management of PTCS in pregnancy is similar to that in nonpregnant adults. In children, the criteria for elevated CSF opening pressure are greater than 280 mmH2O. The management of PTCS otherwise is similar to that in adults.
