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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anterior ischemic optic neuropathy is a well-recognized clinical syndrome that has been described in patients after an episode of migraine with visual aura (classic migraine) and, less commonly, after an episode of visual aura without headache (acephalgic migraine). Little emphasis, however, has been placed on migraine-associated retrobulbar or posterior ischemic optic neuropathy. We report two cases of visual loss presumed to be due to posterior ischemic optic neuropathy that occurred in the setting of otherwise typical migraine episodes. We review the English language literature on ischemic optic neuropathy associated with migraine. Although most cases of ischemic optic neuropathy associated with migraine are of the anterior variety, posterior ischemic optic neuropathy should be considered in the differential diagnosis of any patient with acute loss of vision and evidence for a retrobulbar optic neuropathy, during or after an attack of migraine headache or following an otherwise typical episode of visual aura without headache (acephalgic migraine).
Headache 1996 Sep
PMID:Posterior ischemic optic neuropathy associated with migraine. 882 7

Headache is the most frequent symptom for which a patient with giant cell arteritis (GCA) presents to a neurologist. Amaurosis fugax and ischemic optic neuropathy are well recognized complications. Less commonly recognized neurologic complications include transient ischemic attacks, cerebral infarctions, acute confusional states, multi-infarct dementia, ischemic cervical myelopathy, and ischemic mononeuropathies. Because patients with GCA generally respond well to corticosteroid therapy, prompt diagnosis can minimize neurologic damage.
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PMID:Giant cell (temporal) arteritis. 936 71

A case of ischemic optic neuropathy resulting from uterine hemorrhage is reported in which a 37-year-old white woman, gravida 1, para 0, was diagnosed at 8 weeks' gestation with a ruptured ectopic pregnancy. After diagnostic laparoscopy the patient underwent a minilaparotomy, cornual wedge resection, and right salpingectomy with a total estimated blood loss of 3000 ml. Her postoperative course was uneventful until postoperative day 4, when the patient complained of vision loss for the last 1 to 2 days, total body edema, and headache. Ophthalmologic examination revealed findings consistent with ischemic optic neuropathy. Multiple studies of the cerebrospinal fluid were negative, as were computed tomography studies and magnetic resonance imaging of the head. Ischemic optic neuropathy, whose pathogenesis is still unclear, is a rare complication of massive hemorrhage and may cause permanent vision loss.
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PMID:Ischemic optic neuropathy after hemorrhage from a cornual ectopic gestation. 942 71

We report a case of a 31 year-old man who presented a bilateral ischemic optic neuropathy associated with headaches and severe systemic hypertension. This episode appeared after administration of ergotamine tartrate and macrolides. This medication probably led to a vasospasm which occurs in patients with hypertension. The cardiovascular and serum lipid evaluations were normal. A migraine optic neuropathy can be evoked.
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PMID:[Bilateral ischemic optic neuropathy secondary to acute ergotism]. 975 93

A 70-year-old man presented with a history of headache and sudden loss of vision of the left eye. Funduscopic examination showed sector retinal edema and hemorrhage as well as optic disc swelling consistent with anterior ischemic optic neuropathy. The Westergren sedimentation rate was 66 mm/h. Temporal artery biopsy was consistent with giant cell arteritis. Routine transcranial Doppler testing performed on a Pioneer 2020 instrument (Nicolet Vascular, Inc., Golden, CO) equipped with special software for microembolus detection showed a microembolic signal in the left ophthalmic artery. During a subsequent monitoring study, microembolic signals were detected in the anterior and middle cerebral arteries, bilaterally. Microembolism can occur in giant cell arteritis. Ophthalmic artery microembolism can be detected in vivo by transcranial Doppler ultrasonography. This new imaging capability can potentially be useful when evaluating patients with vascular disorders of the eye.
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PMID:Ophthalmic artery microembolism in giant cell arteritis. 1113 Jul 57

A 12-year-old girl developed headaches and bilateral optic disk edema due to malignant hypertension. Optic disk edema in most of these cases is probably on the spectrum of ischemic optic neuropathy rather than increased intracranial pressure.
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PMID:Acute bilateral optic disk edema with a macular star figure in a 12-year-old girl. 1243 1

A 43-year-old man with fever, headache, and skin rash developed unilateral acute anterior ischemic optic neuropathy. The indirect immunofluorescence test was positive for Rickettsia conorii. Although retinal lesions have been described in Rickettsia conorii infection, this is the first reported case of ischemic optic neuropathy. This infection should be considered in a patient with nonarteritic anterior ischemic optic neuropathy with high fever or skin rash who inhabits or travels from an endemic area.
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PMID:Anterior ischemic optic neuropathy associated with rickettsia conorii infection. 1614 31

Cervicocranial arterial dissection (CCAD) occurs when there is a tear in the intimal layer of the carotid or vertebral arteries with subsequent extravasation of blood into the subintimal layers. The dissection may be extradural, intradural, or extend over both segments. The contents of the subintimal layers are highly thrombogenic, and thus, embolism, vessel stenosis, or occlusion may follow. Symptoms of dissection may be caused by local injury to the blood vessel or by ischemia to the retina or brain. Thus, dissection should always be considered in patients who present with Horner syndrome associated with ipsilateral headache, carotidynia, ocular pain, or amaurosis fugax. Rare neuro-ophthalmologic presentations of dissection include anterior and posterior ischemic optic neuropathy; central retinal artery occlusion; ophthalmic artery occlusion; transient ophthalmoparesis; and third, fourth, or sixth cranial nerve palsy. The most common serious complication of dissection is ischemic stroke. No randomized controlled trials have evaluated therapies for patients presenting with CCAD. Thus, treatment is essentially empiric and often varies by region. Medical management is first line in most patients. Given the propensity for thrombus formation and early embolization or occlusion, acute anticoagulation using intravenous heparin or low-molecular-weight heparinoids followed by short-term, dose-adjusted warfarin is the treatment of choice for most patients with extradural CCAD who present early after symptom onset. The risk of cerebral ischemia is greatest in the first few weeks after dissection; thus, it is reasonable to recommend antiplatelet agents for patients who present late and have not had evidence of ischemia. Intradural dissection is rare but is associated with a meaningful risk of subarachnoid hemorrhage (SAH). As a result, anticoagulants and antiplatelet agents should not be used if SAH is suspected or confirmed. Endovascular intervention may be necessary in a small minority of cases with recurrent events despite anticoagulation or SAH due to intradural dissection. Of special note, CCAD is not considered a contraindication for tissue plasminogen activator use in acute stroke patients who are otherwise eligible for treatment.
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PMID:Cervicocranial arterial dissection. 1728 90

Spontaneous dissection of the cervical internal carotid artery (sICAD) causes, in more than 90% of patients, carotid territory ischemia, local signs and symptoms on the side of dissection, or both, whereas the remaining sICAD remain clinically asymptomatic. Local signs and symptoms include head, facial, or neck pain, Horner syndrome, pulsatile tinnitus, and cranial nerve palsy. Head, facial, or neck pain occurs in 64-74% and is the presenting symptom in up to 58.5%, and the only manifestation in 2.2-4.5%. Headache is observed in 65-68%, facial pain in 34-53%, and neck pain in 9-26%. Horner syndrome consisting essentially of miosis and ptosis is detected in 28-41%. Cranial nerve palsy is reported in 8-16%; the lower cranial nerves IX-XII are most commonly affected, in particular the hypoglossal nerve. The facial nerve may also be involved; dysgeusia results mainly from involvement of the chorda tympani (0.5-7.0%) or the glossopharyngeal nerve. Transient pareses of the ocular motor (III, IV and VI) and trigeminal nerves have been observed. Pulsatile tinnitus is reported in 16-27%. About three quarters of sICAD cause ischemic events, which include ischemic stroke in 80-84%, transient ischemic attack in 15-16%, amaurosis fugax in 3%, ischemic optic neuropathy in 4%, and retinal infarct in 1%. Patients with sICAD causing ischemia show a lower prevalence of Horner syndrome and palsy of the caudal cranial nerves than patients with sICAD causing no ischemic events, whereas headache, neck pain, and pulsatile tinnitus are equally frequent in both groups. After an ischemic stroke, independency defined by a moderate Rankin scale score of 0-2 occurs in 63-90%, whereas the outcome of retinal infarct and ischemic optic neuropathy are not well known.
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PMID:Clinical manifestations of carotid dissection. 1729 Jan 13

In this prospective study, we report fifty consecutive cases of bilateral papilledema without neurosurgical or obvious ophthalmologic etiology, referred to our institution between January 2005 and March 2007. Lumbar puncture with opening CSF pressure measurement distinguished two groups of patients: Group 1 (n=39) with and Group 2 (n=11) without intracranial hypertension. In Group 1, 9/39 patients presented secondary intracranial hypertension mainly due to cerebral venous thrombosis. In 30 patients, after complete investigations, a diagnosis of idiopathic intracranial hypertension was made: as commonly reported, patients were predominantly overweight (96.7% with body mass index>25kg/m2) young (mean age=27.6 years) and women (96.7%). Eleven patients with intracranial hypertension had no headaches. In Group 2, the most common diagnosis was bilateral non-arteritic anterior ischemic optic neuropathy, but rare causes have been identified.
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PMID:[Bilateral papilledema: prospective study of fifty patients]. 1834 56


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