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CEREBROVASCULAR DISORDERS OF OPHTHALMOLOGIC IMPORTANCE

Vascular Insufficiency & Occlusion of the Internal Carotid Artery

Amaurosis fugax is a fleeting or transient loss of vision that is usually associated clinically with carotid occlusive disease, though it can occur with any microembolic or thrombotic disorder, including cardiac valvular disease, cardiac arrhythmia, temporal arteritis, migraine, severe hypotension or shock, papil-ledema, orbital tumors, and hyperviscosity states. Antiphospholipid antibodies have been associated with transient and permanent cerebral and retinal vascular occlusions in patients younger than the usual stroke population. These antibodies may be the key determinant in patients with existing structural lesions of the carotid artery, mitral valve, etc. In embolization, vision can be suddenly lost or slowly disappear like a curtain rising or falling. In hypotension, the visual field constricts from the periphery to the center.

Perhaps 95% of episodes of amaurosis fugax occur as a result of atherosclerotic lesions of the ipsilateral internal carotid artery. Cerebral and retinal disturbances occur as a result of small emboli breaking loose from the sclerotic plaque and lodging in cerebral or retinal arterioles (occlusion of the central retinal artery or a major branch can occur). Cholesterol emboli (Hollenhorst plaques) may be visible with the ophthalmoscope as small, glistening, yellow-red crystals situated at bifurcations of the retinal arteries. The nonreflective gummy white plugs filling retinal vessels, which characterize platelet-fibrin emboli, are less commonly seen because they quickly disperse and traverse the retinal circulation. In patients with amaurosis fugax, high-grade (70-99%) stenosis of the internal carotid artery, as determined by ultrasound or angiographic studies, is an indication for carotid endarterectomy to reduce the risk of cerebral hemisphere stroke. Low-grade (0-29%) and probably medium-grade (30-69%) stenosis are best treated medically, usually with low-dose (81 mg/d) aspirin. Incidentally noted cholesterol retinal emboli in asymptomatic individuals are associated with a tenfold increased risk of cerebral infarction, but the role of carotid endarterectomy in such individuals is uncertain.

Retinal arterial occlusions occur from calcific or platelet-fibrin emboli. (Cholesterol emboli lodge in retinal vessels but do not usually occlude them.) Calcific emboli, which originate from damaged cardiac valves, have a duller, white-gray appearance compared with cholesterol emboli. In the acute stages of embolic retinal arterial occlusion, treatment with ocular massage, anterior chamber paracentesis, rebreathing into a paper bag to increase inhaled CO₂ level, and intravenous acetazolamide may lead to displacement of the embolus and recovery of vision. After 12 hours, the clinical picture is usually irreversible, though many exceptions to this rule have been reported. Visual acuity better than counting fingers on presentation has a better prognosis with vigorous treatment. Central retinal or branch artery occlusion, especially when due to Hollenhorst plaques, has a poorer 5-year survival rate due to attendant cardiac disease or stroke than does occlusion due to thrombotic disease.

Slow flow (venous stasis) retinopathy is a sign of internal carotid artery occlusion. It is characterized by venous dilation and tortuosity, retinal hemorrhages, macular edema, and eventual neovascular proliferation. It resembles diabetic retinopathy, but the changes occur more in the retinal midperiphery than the posterior pole. In more severe cases, there may be vasodilation of the conjunctiva, iris neovascularization, neovascular glaucoma, and frank anterior segment ischemia with corneal edema, anterior uveitis, and cataract. Diagnosis is most easily confirmed by demonstration of reversal of blood flow in the ipsilateral ophthalmic artery using orbital ultrasound, but further investigation by angiography is usually required to determine the full extent of arterial disease. Carotid endarterectomy may be indicated but carries a risk of precipitating or exacerbating intraocular neovascularization. The role of panretinal laser photocoagulation in treating intraocular neovascularization is uncertain.

Occlusion of the Middle Cerebral Artery

This disorder may produce severe contralateral hemiplegia, hemianesthesia, and homonymous hemianopia. The lower quadrants of the visual fields (upper radiations) are most apt to be involved. Aphasia may be present if the dominant hemisphere is involved.

Vascular Insufficiency of the Vertebrobasilar Arterial System

Brief episodes of transient bilateral blurring of vision commonly precede a basilar artery stroke. An attack seldom leaves any residual visual impairment, and the episode may be so minimal that the patient or doctor does not heed the warning. The blurring is described as a graying of vision just as if the house lights were being dimmed at a theater. Episodes seldom last more than 5 minutes (often only a few seconds) and may be associated with other transient symptoms of vertebrobasilar insufficiency. Antiplatelet drugs can decrease the frequency and severity of vertebrobasilar symptoms.

Occlusion of the Basilar Artery

Complete or extensive thrombosis of the basilar artery nearly always causes death. With partial occlusion or basilar "insufficiency" due to arteriosclerosis, a wide variety of brainstem and cerebellar signs may be present. These include nystagmus, supranuclear oculomotor signs, and involvement of cranial nerves III, IV, VI, and VII.

Prolonged anticoagulant therapy has become the accepted treatment of partial basilar artery thrombotic occlusion.

Occlusion of the Posterior Cerebral Artery

Occlusion of the posterior cerebral artery seldom causes death. Occlusion of the cortical branches (most common) causes homonymous hemianopia, usually superior quadrantic (the artery supplies primarily the inferior visual cortex). Lesions on the left in right-handed persons can cause aphasia, agraphia, and alexia if extensive with parietal and occipital involvement. Involvement of the occipital lobe and splenium of the corpus callosum can cause alexia (inability to read) without agraphia (inability to write); such a patient would not be able to read his or her own writing. Occlusion of the proximal branches may produce the thalamic syndrome (thalamic pain, hemiparesis, hemianesthesia, choreoathetoid movements) and cerebellar ataxia.

Subdural Hemorrhage

Subdural hemorrhage results from tearing or shearing of the veins bridging the subdural space from the pia mater to the dural sinus. It leads to an encapsulated accumulation of blood in the subdural space, usually over one cerebral hemisphere. It is nearly always caused by head trauma. The trauma may be minimal and may precede the onset of neurologic signs by weeks or even months.

In infants, subdural hemorrhage produces progressive enlargement of the head with bulging fontanelles. The diagnosis is established by the finding of bloody spinal fluid on tapping the subdural space and by enlarged head measurements. Ocular signs include strabismus, pupillary changes, papilledema, and retinal hemorrhages.

In adults, the symptoms of chronic subdural hematoma are severe headache, drowsiness, and mental confusion, usually appearing hours to weeks (even months) after trauma. Symptomatology is similar to that of cerebral tumors. Papilledema is present in 30-50% of cases. Retinal hemorrhages occur in association with papilledema. Ipsilateral dilation of the pupil is the most common and most serious pupillary sign and is an urgent indication for immediate surgical evacuation of blood. Unequal, miotic, or mydriatic pupils can occur, or there may be no pupillary signs. Other signs, including vestibular nystagmus and cranial nerve palsies, also occur. Many of these signs result from herniation and compression of the brainstem and therefore often appear late with stupor and coma.

Skull films may show a shift of a calcified pineal gland. CT scan or MRI frequently confirms the diagnosis.

Treatment of acute large subdural hematoma consists of surgical evacuation of the blood; small hematomas may be treated with steroids or simply followed with careful observation. Without treatment, the course of large hematomas is progressively downhill to coma and death. With early and adequate treatment, the prognosis is good.

Subarachnoid Hemorrhage

Subarachnoid hemorrhage most commonly results from ruptured congenital berry aneurysms of the circle of Willis in the subarachnoid space. It may also result from trauma, birth injuries, intracranial hem- orrhage, hemorrhage associated with tumors, arteriovenous malformations, or systemic bleeding disorders.

The most prominent symptom of subarachnoid hemorrhage is sudden, severe headache, usually occipital and often associated with signs of meningeal irritation (eg, stiff neck). Drowsiness, loss of consciousness, coma, and death may occur rapidly once an aneurysm ruptures and produces a subarachnoid hemorrhage. Ocular symptoms are not always present. A posterior communicating artery aneurysm may produce a third nerve palsy with pupillary involvement by distention of an aneurysmal sac before the aneurysm ruptures and produces a subarachnoid hemorrhage. Oculomotor palsy with associated numbness and pain in the distribution of the ipsilateral trigeminal nerve is pathognomonic of a supraclinoid, internal carotid, or posterior communicating artery aneurysm. Papilledema usually appears late when it does occur and after there has been a subarachnoid hemorrhage. Various types of intraocular hemorrhage occur infrequently (preretinal hemorrhages are the most common-Terson's syndrome) and carry a poor prognosis for life when they are both early and extensive, since they reflect rapid severe elevation of intracranial pressure.

Exophthalmos may occur as a result of extravasation of blood into orbital tissues. Pressure of an aneurysm on the optic nerve may cause blindness in one eye.

Arteriography following injection of radiopaque substances may help to demonstrate and localize the aneurysms. Blood is present in the cerebrospinal fluid.

Ligation of aneurysmal vessels or of parent arterial trunks may be advisable. Supportive treatment, including control of blood pressure, is all that can be offered during the acute phase of subarachnoid hemorrhage. Thus, it is important to diagnose the posterior communicating artery aneurysm when it first produces a third nerve palsy with pupillary involvement.

Migraine

Migraine is a common episodic illness of unknown cause and varied symptomatology characterized by severe unilateral headache (which alternates sides), visual disturbances, nausea, and vomiting. The neurologic symptoms that usually precede the headache occur in the vasoconstrictive phase; the headache follows in the vasodilative phase. There is usually a family history of a similar disorder. The disease usually becomes manifest between ages 15 and 30 years. It is more common and more severe in women. Many factors, particularly emotional ones, may predispose or contribute to the attacks. Prodromal symptoms are common and include drowsiness, paresthesias, "scintillating" scotomas, blurred vision, and other symptoms. In some patients, homonymous hemianopia can be accurately recorded on the tangent screen during attacks. There are no other objective findings. Visual symptoms usually last only 15-30 minutes. Antiphospholipid antibodies have been associated with migrainous headaches and severe atypical migraine.

Ergotamine tartrate, when given early in an attack, is often effective. Once the attack is well under way, treatment is of little value. Sumatriptan is effective in the acute and well-established migraine attack. The headaches last several hours to several days. Bed rest is often helpful and sometimes essential for relief of discomfort.

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