The term stroke includes cerebral ischemia (transient ischemic attacks and cerebral infarctions) and cerebral hemorrhage. A stroke is suspected when a patient presents with acute neurologic symptoms and signs (acute usually means that the mechanism is vascular). Stroke patients often have neuro-ophthalmic complaints, including visual loss, visual field defects, and diplopia. Retinal vascular disorders are equivalent to strokes involving various ocular vascular territories. Once the diagnosis of stroke is suspected, the first step is to determine whether the vascular event is ischemic or hemorrhagic. In the eye, this can be done by looking at the fundus; for the brain, it requires neuroimaging, usually a head computed tomographic (CT) scan without contrast (▶ Fig. 20.1 and ▶ Fig. 20.2) Fig. 20.1 Computed tomographic scan of the brain without contrast showing hypodensities at the level of both occipital lobes consistent with bilateral occipital infarctions. Fig. 20.2 Computed tomographic scan of the brain without contrast showing hyperdensities in the left frontal lobe and ventricles, consistent with intraparenchymal hemorrhages with ventricular extension. Questions to be answered in patients with suspected cerebrovascular disease (and retinal vascular diseases) include the following: Is it a vascular event? Where in the brain or the eye has the vascular event occurred (parenchymal and vascular topography)? What type of vascular event is it (pathology)? What has caused the vascular event (mechanism)? What are the consequences of the vascular event (impairments, disabilities, and handicap)? What other medical problems coexist? Once a stroke is confirmed and the mechanism (ischemic vs. hemorrhagic) is determined, the cause should be clarified to offer the best secondary prevention to the patient (▶ Fig. 20.3). Fig. 20.3 Mechanisms of cerebral and ocular ischemia. (From Schuenke M, Schulte E, Schumacher U, Ross LM, Lamperti ED, Voll M. THIEME Atlas of Anatomy; Head and Neuroanatomy. Stuttgart, Germany: Thieme; 2007. Illustration by Markus Voll.) Four main mechanisms can result in cerebral ischemia. Thrombosis of a vessel Large-vessel or macrovascular (arterial) disease Small-vessel or microvascular (arterial) disease Emboli Cardiac source of emboli Artery to artery Hypoperfusion Venous thrombosis Carotid disease (mostly interval carotid artery) often presents with ocular symptoms and signs. Asymptomatic retinal emboli Transient monocular visual loss Central or branch retinal artery occlusion Ophthalmic artery occlusion Episcleral artery dilation Venous stasis retinopathy Ocular ischemic syndrome Ischemic optic neuropathy (rare) Optic nerve compression (rare) Horner syndrome Ocular motor nerve paresis (rare) Referred pain The carotid artery can be affected by the following diseases: Arterial wall Atheroma Dissection Fibromuscular dysplasia Arteritis Infectious Noninfectious (Takayasu, giant cell arteritis) Trauma External radiation Tumors (carotid glomus) External compression Tumors Trauma Blood flow Coagulation disorders Emboli (heart, artery to artery) Dissections of the internal carotid artery commonly present with an ipsilateral acute Horner syndrome associated with orbital, face, or head pain. These patients are at risk for a cerebral infarction and should be evaluated and treated emergently (▶ Fig. 20.4 and ▶ Fig. 20.5) Fig. 20.4 a–c (a) Axial T1-weighted magnetic resonance imaging showing a hypersignal in the wall of the dissected right internal carotid artery (arrow). Note the normal black signal (flow void) of the normal left internal carotid artery. (b) Carotid ultrasound (sagittal view on the left and axial cut on the right) showing the residual normal flow in the dissected artery (in color) and the hematoma in the wall of the artery (arrows). (c) Magnetic resonance angiography of the head demonstrating decreased signal in the middle cerebral artery (arrows) ipsilateral to the dissected carotid artery. This finding suggests that the patient is at risk for hemodynamic cerebral infarction. This patient should be admitted to the hospital and maintained on strict bed rest until normal blood flow is restored (this is best seen with transcranial Doppler). Fig. 20.5 Axial T1-weighted magnetic resonance imaging showing hypersignals in the wall of the dissected internal carotid arteries (arrows). This patient presented with bilateral painful acute Horner syndrome. Dissections involve the extracranial carotid or vertebral arteries more often than the intracranial arteries. They may occur spontaneously or after cervical trauma (car accident, strangulation, chiropractic manipulation). There is often a symptom-free interval of a few days between the trauma and the first sign of the dissection. Pain is often present immediately after the trauma. The risk of cerebral emboli in cardiac disease is classically defined as “high” (needing urgent treatment) and “low or uncertain” (often not directly responsible for the cerebral infection) Atrial Atrial fibrillation Sustained atrial flutter Sick sinus syndrome Left atrial thrombus Left atrial appendage thrombus Left atrial myxoma Valvular disease Mitral stenosis Prosthetic valves Mechanical Bioprosthetic Endocarditis Infective Noninfective Marantic Liebman Sachs (systemic lupus erythematosus; antiphospholipid antibodies) Ventricular Recent anterior myocardial infarction Left ventricular thrombus Left ventricular myxoma Dilated cardiomyopathy Iatrogenic Cardiac catheterization Cardiac surgery Atrial Patent foramen ovale Atrial septal aneurysm Spontaneous echo contrast on transesophageal echocardiogram (TEE) Valvular disease Mitral annulus calcification Mitral valve prolapse Calcified aortic stenosis Fibroelastoma Giant Lambl excrescences Ventricular Akinetic/dyskinetic ventricular wall segment Subaortic hypertrophic cardiomyopathy Congestive heart failure Cerebral infarctions can be related to occlusion of a large intracranial vessel (such as posterior cerebral artery or middle cerebral artery), or can be related to diseases affecting small intracranial vessels. Small vessel diseases include abnormalities in the vessel content and vessel wall abnormalities. Hypercoagulable states Acute Vasculitis Noninflammatory vasculopathies Chronic Arteriolar sclerosis (“lacuna” due to hypertension) Cerebral amyloid angiopathy Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) Mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS) Vascular risk factors should be evaluated in all patients with cerebral or ocular ischemia. Aggressive treatment of modifiable risk factors is essential in secondary prevention. Risk factors for ischemic stroke include the following: Nonmodifiable Age Gender (men > women) Ethnicity (African Americans and Hispanics > Caucasians) Heredity Migraine Modifiable Elevated blood pressure Cardiovascular disease Diabetes Hyperlipidemia Cigarette smoking Alcohol abuse Obesity Sedentary lifestyle Obstructive sleep apnea Asymptomatic carotid stenosis Hyperhomocysteinemia Chronic infection Oral contraceptives Some tests are systematically obtained in the emergency department in patients with suspected strokes. Other tests are obtained based on the patient’s characteristics and risk factors. These tests include the following (* tests are indicated only for certain patients, depending on stroke type and clinical setting): Laboratory Complete blood count Platelet count Blood glucose level Serum electrolytes, including magnesium and calcium Serum creatinine level Prothrombin time and activated partial prothrombin time, international normalized ratio Urinalysis (may detect occult blood indicating embolic events in the kidney) Hepatic function tests* Toxicology screen* Blood alcohol determination* Pregnancy test* Other tests Electrocardiogram (or cardiac monitoring) Chest X-ray (helpful in assessing cardiac disease and aspiration pneumonia) Brain CT or magnetic resonance imaging (MRI)—often with computed tomographic angiography (CTA) or magnetic resonance angiography (MRA) of head and neck Carotid duplex ultrasound* (in anterior circulation infarctions when CTA or MRA are not performed immediately) Holter monitor* Transthoracic or transesophageal echocardiogram* Lumbar puncture* Hypercoagulable states can produce a cerebral or retinal infarction by occluding an artery. Many of these factors are congenital (thrombophilia), and the thrombotic episode is triggered by an acquired factor. For example, a woman born with congenital activated protein C resistance may have a normal childhood and may develop a cerebral venous thrombosis only when she starts an oral contraceptive pill or when she is pregnant. Hypercoagulable states are only rarely responsible for cerebral or ocular arterial ischemia. The workup should be obtained only in specific situations, such as the following: Younger patients No obvious risk factor for cerebral or ocular ischemia Family history of thrombophilia, or recurrent thrombosis Prior history of thrombosis Recurrent, unexplained episodes of thrombosis Venous thrombosis at unusual sites (e.g., cerebral venous thrombosis) Congenital factors Protein C defect/deficiency Protein S defect/deficiency Antithrombin III deficiency Activated protein C resistance (factor V Leiden) Prothrombin gene (factor II 20210A) mutation Heparin cofactor II deficiency Dysfibrinogenemia Plasminogen activator inhibitor (PAI-1) gene polymorphism Congenital plasminogen deficiency Thrombomodulin gene mutation Sickle cell disease Platelet defects Acquired factors Antiphospholipid syndrome Myeloproliferative disorder Paroxysmal nocturnal hemoglobinuria Thrombotic thrombocytopenic purpura Disseminated intravascular coagulation Malignancy Sepsis Hyperviscosity syndrome Trauma Immobilization Surgery Pregnancy Oral contraceptives Heparin-induced thrombocytopenia Combined risk (both acquired and genetic factors) Hyperhomocysteinemia Elevated factor VIII levels Elevated fibrinogen levels Pearls Multiple congenital thrombophilia often coexist in the same patient; therefore, all patients at risk should be screened for all types of thrombophilia. ▶ Table 20.1 lists angiopathies of the central nervous system associated with ocular manifestations. Mechanism of ocular disease Angiopathy Transmission Manifestations Homocystinuria and homocysteinemia Premature atherosclerotic occlusion of carotid arteries and large cerebral arteries Autosomal recessive Retinal ischemia Fabry disease (angiokeratoma corporis diffusum) Glycosphingolipid deposit in endothelial cells, cerebral aneurysms X-linked recessive Lens subluxation, whorl-like corneal opacification Neurofibromatosis 1 Arterial dissections, aneurysms, fistulae, moyamoya disease, ganglioneuromas, neurofibromas Autosomal dominant Tortuosity of vessels, neurofibromas, Lisch nodules, optic nerve gliomas, retinal hamartomas MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, strokelike episodes) syndrome Proliferation of mitochondria in smooth muscle cells of cerebral vessels Maternally inherited (point mutation in mitochondrial DNA) Optic atrophy, pigmentary retinopathy, chronic progressive external ophthalmoplegia von Hippel–Lindau disease Cerebellar, brainstem, and spinal cord hemangioblastoma Autosomal dominant Retinal angiomas Tuberous sclerosis (Bourneville disease) Intracranial aneurysms, moyamoya disease Autosomal dominant Retinal hamartomas Rendu–Osler–Weber syndrome (hereditary hemorrhagic telangiectasia) Arteriovenous malformations, venous angiomas, aneurysms, meningeal telangiectasia Autosomal dominant Retinal telangiectasia Ataxia-telangiectasia (Louis-Bar syndrome) Telangiectasia Autosomal recessive Oculocutaneous telangiectasia CADASIL (cerebral autosomal arteriopathy with subcortical infarcts and leukoencephalopathy) Nonatherosclerotic, nonamyloidotic angiopathy of leptomeningeal and small penetrating arteries Autosomal dominant Mild vascular retinopathy HERNS (Hereditary endotheliopathy with retinopathy, nephropathy, and stroke) Nonatherosclerotic arteriopathy of retina, small penetrating cerebral arteries, and kidneys Autosomal dominant Vascular retinopathy Menkes syndrome (kinky hair disease) Tortuosity, elongation, and occlusion of cerebral arteries X-linked recessive Ocular ischemia Marfan syndrome Aneurysms, aortic dissection Autosomal dominant Lens subluxation, retinal detachment Hereditary cerebral amyloid angiopathy Hereditary cerebral hemorrhage with amyloidosis (HCHWA)–Dutch type (beta-amyloid) HCHWA–Iceland type (cystatin C) Autosomal dominant None Fibromuscular dysplasia Arterial stenosis, arterial dissections, aneurysms, carotid cavernous fistulae May be autosomal dominant; mostly sporadic Retinal emboli Ehler–Danlos syndrome (type IV) Aneurysms, carotid cavernous fistulae, carotid or vertebral artery dissection Heterogeneous Ocular ischemia, angioid streaks Pseudoxanthoma elasticum (Grönblad–Strandberg syndrome) Premature atherosclerosis, aneurysms, carotid cavernous fistulae Angioid streaks, peau d’orange fundus Moyamoya disease Noninflammatory occlusive intracranial vasculopathy May be associated with other hereditary disorders Morning glory disc, ocular ischemia Sturge–Weber syndrome (encephalofacial angiomatosis) Leptomeningeal venous angioma, arteriovenous malformations, venous and dural sinus abnormalities Possibly autosomal dominant; mostly sporadic Skin, conjunctiva, episclera, uveal angiomas, glaucoma Wyburn-Mason syndrome Cerebral arteriovenous malformations (usually brainstem) Sporadic Retinal arteriovenous (racemose angioma) malformations Because a large part of the cerebrospinal fluid (CSF) drains into the venous sinuses and the internal jugular veins (▶ Fig. 20.6 and ▶ Fig. 20.7), thrombosis of an intracranial venous sinus usually results in raised intracranial pressure with headaches and papilledema. Ultimately, the thrombus may extend to the deep cerebral veins and the cortical veins, resulting in acute cerebral venous infarctions and hemorrhages. Fig. 20.6 a–c (a) Sagittal view of the intracranial venous system. (b) Anteroposterior drainage of the intracranial venous blood. ([a, b] From Schuenke M, Schulte E, Schumacher U, Ross LM, Lamperti ED, Voll M. THIEME Atlas of Anatomy; Head and Neuroanatomy. Stuttgart, Germany: Thieme. 2007. Illustrations by Markus Voll.) (c) Drainage of the CSF into the superior sagittal sinus. ([c] From Schuenke M, Schulte E, Schumacher U, Ross LM, Lamperti ED, Voll M. THIEME Atlas of Anatomy; Head and Neuroanatomy. Stuttgart, Germany: Thieme; 2007. Illustration by Karl Wesker.) Fig. 20.7 Intracranial venous sinuses. View from above. (From Schuenke M, Schulte E, Schumacher U, Ross LM, Lamperti ED, Voll M. THIEME Atlas of Anatomy; Head and Neuroanatomy. Stuttgart, Germany: Thieme; 2007:255, Fig. 8.5c). The cortical veins empty into the dural venous sinuses, which have an anteroposterior drainage into the transverse sinuses and the jugular veins. Occlusion of a sinus usually results in reversal of the flow in some veins, producing specific clinical manifestations based on the anatomical location of the thrombosed sinus (e.g., when the cavernous sinus is thrombosed, the orbital veins drain anteriorly instead of posteriorly, and there is orbital congestion with proptosis). In most cases, the CSF drainage is compromised, and there are symptoms and signs of raised intracranial pressure. Dilation and thrombosis of the cortical veins produce catastrophic venous infarctions that are often hemorrhagic. There are multiple veins draining the cerebellum and the brainstem (▶ Fig. 20.8). Thrombosis of some veins may result in dilation of these veins and compression or ischemia of the adjacent cranial nerves. This explains why petrosal sinus thrombosis can produce multiple cranial nerve palsies such as sixth, fifth, seventh, and third nerve palsies. Isolated diplopia with pain may rarely be the first sign of cerebral venous thrombosis. Fig. 20.8 Veins of the brainstem (anterior view). (From Schuenke M, Schulte E, Schumacher U, Ross LM, Lamperti ED, Voll M. THIEME Atlas of Anatomy; Head and Neuroanatomy. Stuttgart, Germany: Thieme; 2007. Illustration by Markus Voll). Classic clinical presentations of cerebral venous thrombosis include the following: Raised intracranial pressure (headache, papilledema, sixth nerve palsy) Seizures Altered mental status Neurologic deficit (hemiparesis, aphasia based on the location of cerebral infarctions) Deficits on alternating sides or occurring bilaterally (unlike in cerebral arterial ischemia) Urgent treatment is necessary to prevent multiple cerebral venous infarctions and death. Pearls Permanent visual loss from papilledema is a classic complication of cerebral venous thrombosis. Early treatment of intracranial hypertension is necessary. When possible, a lumbar puncture should be performed prior to anticoagulation to reduce the intracranial pressure and help preserve vision. MRI and magnetic resonance venography (MRV) usually allow very good noninvasive visualization of the intracranial venous sinuses (▶ Fig. 20.9 and ▶ Fig. 20.10). Artifacts are common, and CT venography often complements these tests. A catheter cerebral venogram is only rarely required. Fig. 20.9 Magnetic resonance venogram (sagittal, three quarter posterior view, and posterior view) showing the normal cerebral venous sinuses. Fig. 20.10 a, b (a) Sagittal T1-weighted magnetic resonance imaging of the brain showing a hyperintense signal in the right transverse sinus (arrow) in a patient with headaches and papilledema. This is suggestive of subacute thrombosis of the transverse sinus. (b) Magnetic resonance venogram (posterior view) showing the absence of signal in the thrombosed right transverse sinus (arrow). Intracranial hemorrhages are classified as follows (▶ Fig. 20.11): Fig. 20.11 a–c Classification of intracranial hemorrhages. (a) Epidural hematoma, (b) subdural hematoma, (c) subarachnoid hemorrhage (From Schuenke M, Schulte E, Schumacher U, Ross LM, Lamperti ED, Voll M. THIEME Atlas of Anatomy, Head and Neuroanatomy. Stuttgart, Germany: Thieme; 2007. Illustration by Markus Voll.) Epidural hemorrhage (between the skull and meninges): Usually results from skull fracture (temporal bone with rupture of the middle meningeal artery). There can be rapid expansion of the hematoma with uncal herniation, ipsilateral third nerve palsy, and death if the hematoma is not drained emergently. Subdural hemorrhage (between the dura and the subarachnoid space): Usually results from mild head trauma or may be spontaneous (rupture of the bridging veins). Particularly common in the elderly. There is relatively slow expansion of the hematoma with headaches and mass effect on the adjacent cerebral hemisphere. Visual field defects are common. Subdural hematoma can be subacute (over days) or chronic (over months). Subarachnoid hemorrhage (in the subarachnoid space): Usually results from aneurysmal rupture, or may be spontaneous or from head trauma. The blood in the subarachnoid space can produce arterial spasm with cerebral ischemia, or it may block CSF passage and cause obstructive hydrocephalus. Intraparenchymal hemorrhage (▶ Fig. 20.12 and ▶ Fig. 20.13): Intraparenchymal hemorrhages usually result from bleeding of the small perforating arteries and most often involve the basal ganglia. Superficial intracerebral hemorrhages are often associated with subarachnoid hemorrhage from aneurysmal or arteriovenous malformation rupture. Fig. 20.12 Axial computed tomographic scan of the brain without contrast showing a left occipital intraparenchymal hemorrhage (yellow arrow) and left subdural hematoma (red arrows) in a patient with bacterial endocarditis and multiple mycotic aneurysms. Fig. 20.13 Axial computed tomographic scan of the brain without contrast showing a left intraparenchymal hemorrhage in a patient with uncontrolled arterial hypertension. Cerebral hemorrhages may result from the following: Arterial hypertension Vascular malformations Arteriovenous malformations Cavernous hemangiomas Aneurysms Cerebral amyloid angiopathy Brain tumor/metastases Bleeding disorders Coagulopathies Thrombocytopenia Anticoagulants Thrombolytic treatment Head trauma Vasculitis Endocarditis Cerebral venous thrombosis Drugs (sympathomimetic agents) Alcohol use Low cholesterol When evaluating a patient with an acute intraparenchymal hemorrhage, it is important to determine the source of the hemorrhage. It is sometimes impossible acutely because the hemorrhage may hide an underlying lesion. Repeat brain imaging a few weeks later (once the blood has partially resolved) sometimes allows visualization of a cavernous hemangioma or a mass (▶ Fig. 20.14 and ▶ Fig. 20.15). Fig. 20.14 Axial T2-weighted brain magnetic resonance imaging showing bleeding of a cavernous hemangioma in the right pons (arrow). This patient had an acute right sixth nerve palsy. Fig. 20.15 Axial T2-weighted brain magnetic resonance imaging showing bleeding of a cavernous hemangioma of the left midbrain (arrow) producing a right fourth nerve palsy. Funduscopic examination is sometimes useful by revealing retinal vascular malformations (▶ Fig. 20.16 and ▶ Fig. 20.17). Fig. 20.16 a, b (a) Retinal cavernous hemangioma (grapelike hemangiomas) in a patient with familial cerebral and retinal cavernous hemangiomas. (b) Axial T2-weighted brain magnetic resonance imaging showing multiple cavernous hemangiomas (arrows). Fig. 20.17 a, b (a) Retinal vascular malformation (a true arteriovenous malformation) in the setting of Wyburn-Mason syndrome. Note additionally the diffusely tortuous vessels. (b) Sagittal T1-weighted magnetic resonance imaging of the brain without contrast showing a large intracranial vascular malformation (the areas in black correspond to dilated vascular flow voids). Bleeding in the subarachnoid space (▶ Fig. 20.18) is usually revealed by an acute, explosive headache. There may be a third nerve palsy if the subarachnoid hemorrhage is related to rupture of an aneurysm of the posterior communicating artery (▶ Fig. 20.19). Fig. 20.18 a, b (a) Axial T2-weighted magnetic resonance imaging of the brain in a patient with a left homonymous hemianopia, showing a large arteriovenous malformation in the right occipital lobe. (b) Sagittal catheter angiogram with selective catheterization of a vertebral artery showing the occipital arteriovenous malformation. Fig. 20.19 Most common sites of intracranial aneurysms. (From Schuenke M, Schulte E, Schumacher U, Ross LM, Lamperti ED, Voll M. THIEME Atlas of Anatomy, Head and Neuroanatomy. Stuttgart, Germany: Thieme; 2007. Illustration by Markus Voll). The prognosis of subarachnoid hemorrhage is poor. Immediate diagnosis and treatment are essential. Subarachnoid hemorrhage should be suspected in all patients presenting with a very severe headache. Other neurologic symptoms and signs depend on the cause of the subarachnoid hemorrhage and the location of the aneurysm (if related to an aneurysmal rupture). The most common complications are vasospasm with cerebral infarction and obstructive hydrocephalus. Visual fields often reveal a contralateral homonymous defect when the vascular malformation involves the retrochiasmal visual pathways (▶ Fig. 20.20). Fig. 20.20 Axial computed tomographic scan of the brain without contrast showing a subarachnoid hemorrhage. Note the hyperdensities filling the subarachnoid space (arrows). Aneurysm rupture Vascular malformation bleeding Bleeding diathesis Trauma Drug (cocaine, methamphetamine) Amyloid angiopathy Hypertension Brain tumors Spinal lesions Aneurysms Arteriovenous malformations Tumors Subarachnoid hemorrhage produces a very acute increase in intracranial pressure, sometimes associated with Terson syndrome (retinal and vitreous hemorrhages) (▶ Fig. 20.21 and ▶ Fig. 20.22). Terson syndrome is a classic cause of unilateral or bilateral visual loss in patients with subarachnoid hemorrhage. Because these patients are often unconscious, the diagnosis of Terson syndrome is typically delayed unless funduscopic examination is systematically performed. Fig. 20.21 a, b (a) Optic nerve edema and peripapillary hemorrhages in the right eye of a patient with aneurysmal rupture and subarachnoid hemorrhage, suggesting Terson syndrome. (b) There are multiple subhyaloid hemorrhages (dark hemorrhages) as well as intraretinal hemorrhages and disc edema in the left eye. Fig. 20.22 Vitreous hemorrhage in the left eye in a patient with aneurysmal rupture and subarachnoid hemorrhage (Terson syndrome). Note that the view of the fundus is blocked by the intravitreal blood. Classic findings include the following: Optic nerve head edema, often with hemorrhages Retinal hemorrhages Subhyaloid hemorrhages Vitreous hemorrhages The intraocular hemorrhages likely result from acute venous pressure secondary to the subarachnoid hemorrhages; they do not result from diffusion of the blood from the subarachnoid space into the eye. In many cases, the hemorrhages resolve spontaneously over a few weeks or months. Macular hemorrhages may result in permanent visual loss. Persistent vitreous hemorrhage may require a vitrectomy for removal of the blood. Traction retinal detachment may develop. Intracranial aneurysms represent the most common cause of subarachnoid hemorrhage. This is why catheter angiography is always performed immediately when a subarachnoid hemorrhage is diagnosed: early treatment of the ruptured aneurysm allows prevention of complications and rebleeding. All intracranial vessels are examined because about 20% of patients have more than one intracranial aneurysm. Intracranial aneurysms (▶ Table 20.2, ▶ Fig. 20.23) may manifest in various ways: Location of aneurysm Frequency % Neuro-ophthalmic manifestations Carotid-ophthalmic aneurysms Ophthalmic artery Superior hypophyseal artery 5 Compression, ischemia, hemorrhage of anterior visual pathways: Optic nerve (monocular visual loss, junctional scotoma) Chiasm (bitemporal hemianopia) Optic tract (homonymous hemianopia) Orbital pain Anterior communicating artery aneurysm 30 Compression, ischemia, hemorrhage of anterior visual pathways: Optic nerve (monocular visual loss, junctional scotoma) Chiasm (bitemporal hemianopia) Internal carotid artery bifurcation aneurysm 4 Compression, ischemia, hemorrhage of visual pathways: Optic nerve (monocular visual loss, junctional scotoma) Chiasm (bitemporal hemianopia) Optic tract (contralateral homonymous hemianopia) Cavernous sinus aneurysm 2 Sixth nerve palsy Horner syndrome Third, fourth, and fifth (V1 and V2) nerve palsies Compression of anterior visual pathways: Optic nerve (monocular visual loss) Chiasm (bitemporal hemianopia) Middle cerebral artery aneurysm 20 Compression, ischemia, hemorrhage of retrochiasmal visual pathways: Optic radiations (contralateral homonymous hemianopia) Posterior communicating artery aneurysm 35 Ipsilateral third nerve palsy Orbital pain, headache Basilar artery aneurysm 3–5 Ipsilateral third nerve palsy: uni- or bilateral Compression of the adjacent midbrain or pons: Horizontal gaze palsy, skew deviation, internuclear ophthalmoplegia, lid retraction nystagmus, sixth nerve palsy Posterior cerebral artery aneurysm < 3 Ipsilateral third nerve palsy Compression of the retrochiasmal visual pathways: Optic radiations (contralateral homonymous hemianopsia) Superior cerebellar artery aneurysm < 3 Ipsilateral third nerve palsy Occipital headache Anterior inferior cerebellar artery (AICA) aneurysm < 3 Ipsilateral sixth nerve palsy Occipital headache Posterior inferior cerebellar artery (PICA) aneurysm < 3 Ipsilateral sixth nerve palsy Occipital headache Vertebral artery aneurysm < 3 Ipsilateral sixth nerve palsy Occipital headache Rupture of the aneurysm (subarachnoid hemorrhage) Papilledema (raised intracranial pressure) Sudden headache Terson syndrome Sixth Nerve Palsy Fig. 20.23 a, b (a) Axial brain magnetic resonance imaging (diffusion-weighted) showing a right occipital infarction (as hyperintense) from an occlusion of the right posterior cerebral artery due to an embolus from the sac of a proximal aneurysm on the posterior cerebral artery. (b) Catheter angiogram (frontal view) showing a large aneurysm on the right posterior cerebral artery (arrow).
20.1.1 Cerebral Infarctions
Causes of Cerebral Infarction (see ▶ Fig. 20.3)
Ocular Manifestations of Carotid Disease
Differential Diagnosis of Carotid Artery Disease
Cervical Artery Dissections
Cardiac Sources of Embolism and Embolic Risk
High Risk
Low or Uncertain Risk
Classification of Small Vessel Disease
20.1.2 Abnormalities in the Vessel Content
20.1.3 Vessel Wall Abnormalities (Veins and Arteries)
Risk Factors for Ischemic Stroke
Laboratory and Diagnostic Tests Recommended for Patients with Suspected Stroke
Hypercoagulable States
Risk Factors for Thrombosis
Angiopathies of the Central Nervous System Associated with Ocular Manifestations
20.1.4 Cerebral Venous Thrombosis
Diagnosis of Cerebral Venous Thrombosis
20.1.5 Intracranial Hemorrhage
Risk Factors for Intraparenchymal Hemorrhage
Subarachnoid Hemorrhage
Etiologies of Subarachnoid Hemorrhage
Terson Syndrome
Intracranial Aneurysms
Orbital pain, headache
Orbital pain, headache
Orbital pain
Headache
Occipital headache
Occipital headache
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