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

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

Persistent aura symptoms in patients with migraine are rare but well documented. The International Headache Society defines persistent aura without infarction as when the aura symptoms persist for > 1 week without radiographic evidence of infarction. The visual aura of migraine attacks has been explained by cortical spreading depression. We describe a case of a 28-year-old Mexican woman, who presented with persistent aura symptoms, and a literature review. The patient had a 24-year history of migraine headache. In November 2005 the patient had an attack which started with scintillating scotomas bilaterally associated with photopsias and amaurosis followed by migraine headache. All imaging studies were negative. The episode lasted 35 days and probably resolved with nimodipine therapy. Persistent aura symptoms are rare entities. This is the first case documented of a Mexican patient with persistent aura without infarction and probably resolved with nimodipine therapy.
Cephalalgia 2007 May
PMID:Migraine with persistent aura in a Mexican patient: case report and review of the literature. 1738 4

The main symptoms of acute primary angle-closure glaucoma (PACG) include pain in the head and/or the eyes in addition to the characteristic halo and blurred vision. When loss of vision is accompanied by such pain, PACG is usually suspected. However, no information has been available regarding painless acute angle-closure glaucoma. Recently, we treated a patient with painless acute PACG mimicking amaurosis fugax as a type of transient ischemic attack. Generally, amaurosis fugax causes transient monocular loss of vision due to occlusion of the ophthalmic artery. The formation of microemboli derived from the heart or carotid artery and/or the occurrence of some hemodynamic abnormality due to arteriosclerosis is closely related to amaurosis fugax, and most cases are complicated by intracranial or extracranial arterial lesions. In the present case, we provisionally diagnosed transient amaurosis fugax which, however, was shown by additional ocular testing to be painless PACG. Herein we describe our diagnostic process and the outcome.
Headache
PMID:Painless transient monocular loss of vision resulting from angle-closure glaucoma. 1763 5

Antiphospholipid Antibodies (aPAs) are specific circulating immunoglobulins that lead to a hypercoagulant state and recurrent arterial and venous thromboembolic events. The cerebral circulation is the most common site of arterial occlusion in aPAs, and neurologic events include amaurosis fugax, migrainous cephalalgia, transient ischemic attacks (TIA), stroke, ischemic encephalopathy, and vascular dementia. A review of the literature yields numerous studies citing neurocognitive and neuropsychiatric symptoms associated with this syndrome in a much younger population than is seen in other cerebrovascular disorders. These associated features include focal and generalized cognitive deficits, early-onset vascular dementia, and neuropsychiatric symptoms such as affective and thought disorders. These neurocognitive and neurobehavioral manifestations may be underemphasized in this population and aPAs should be considered in a differential diagnosis. Largescale prospective studies are needed to quantify psychiatric and neuropsychological sequelae of this disorder.
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PMID:A review of neurological sequelae and cognitive deficits associated with antiphospholipid antibodies. 1789 70

Wegener's granulomatosis is a systemic necrotizing vasculitis that affects medium size and small vessels. Neurological involvement occurs in 22% to 54% of patients, mainly in the form of mononeuritis multiplex. Central nervous system involvement is reported in only 2% to 8% of the cases. We report a 42-year-old male who presented with headache, diplopia, third and sixth cranial nerve palsies and left eye amaurosis associated to mass located in the Meckel cavum and diffuse meningeal involvement. A biopsy of the mass disclosed a chronic granulomatous necrotizing inflammation with Langhans giant cells. A chest CAT scan showed three cavitated lung nodules and ANCA antibodies were positive in a titer of 1:80. Treatment with steroid and cyclophosphamide was started and cranial nerve palsies resolved and the number and size of lung nodules decreased. The patient was lost from follow up.
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PMID:[Neurological involvement in Wegener's granulomatosis: report of one case]. 1791 49

Case report of a 66-year-old woman with episodes of amaurosis fugax and hemicranic headache with otherwise normal ophthalmologic and neurological examinations and normal imaging. While ESR was in the normal range for patient's age, acute phase proteins (C-reactive protein and fibrinogen) were elevated. Giant cell arteritis was proved by temporal artery biopsy. Giant cell arteritis should be considered as an important differential diagnosis of amaurosis fugax even in patients with normal ESR. Acute phase protein testing can give relevant diagnostic information.
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PMID:[Amaurosis fugax with elevated acute phase proteins]. 1798 30

There is no doubt that ocular migraine also known as retinal migraine or ophthalmic migraine should not to be confused with ophthalmoplegic migraine. The hallmark of ocular migraine is the unilateral visual loss or "monocular transient loss of vision" associated or followed by the headache. Better safe than sorry, therefore an ophthalmologic examination during the migraine attack is the most diagnostic method. age with typical history for ocular migraine. Importantly supportive data sustain that different neuro-ophthalmologic manifestations as amaurosis fugax, retinal vascular thrombosis and optic neuropathy, may be considered as the ocular hallmarks of the Hughes's syndrome. Clues for the evaluating of antiphospholipid antibodies include recurrent thrombosis especially in young people, recurrent fetal loss, and thrombocytopenia. There are no studies that focus exclusively on the prophylaxis of ocular migraine. Ocular features due to antiphospholipid antibodies - induced thrombosis or Hughes's syndrome should be treated with anticoagulant therapy.
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PMID:Ocular migraine and antiphospholipid antibodies--where we stand? 1806 48

Several cases of hypothyroidism have been reported to develop idiopathic intracranial hypertension not directly precisely linked with cerebral venous sinus thrombosis (CVT). A 31-year-old Chinese woman presented with bilateral blurred vision and paroxysmal amaurosis for about 6 months without headache. Neurological examination revealed normal expect for the sixth cranial nerve palsy and bilateral papilledema. Laboratory tests showed pronounced hypothyroidism and greatly increased serum triglyceride. Cerebral spinal fluid showed the increased opening and closing pressure. Digital subtraction angiography (DSA) disclosed a filling defect in the adjunction of bilateral transverse sinuses and sigmoid sinuses. Her symptoms gradually improved with levothyroxine, mannitol and anticoagulants treatment. In presenting the rare case of lateral sinus thrombosis associated with primary hypothyroidism, we wish to alert physicians that patients presenting with papilledema and hypothyroidism may require investigations of DSA for CVT, even in the absence of headache.
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PMID:Lateral sinus thrombosis and intracranial hypertension associated with primary hypothyroidism: case report. 1828 54

Medical statements from previous epidemiologic studies consider temporal arteritis as extremely rare or absent in Hispanic patients. A probable genetic protective condition was proposed as an explanation for this. We performed a descriptive observational, retrospective, comparable and not randomized study in the southern region of Puerto Rico (Ponce Area). The period for recollection of data was July/2002 to March/2004. We reviewed all the information of the clinical charts of patients diagnosed with temporal arteritis who were seen in the medical offices of one internist and two rheumatologists of the teaching staff of Damas Hospital. The subjects of our study consisted of 11 patients (8 female and 3 male), between the ages of 70 to 90, all of Hispanic origin, with a diagnosis of temporal arteritis. Frequencies and percentages were used to describe the data of the study. Headache was the most common symptom. Other symptoms included the presence of fatigue, malaise, anorexia, scalp tenderness, amaurosis fugax and decreased vision. Laboratory results showed the presence of a mild leukocytosis and anemia in most of the patients. Renal and liver functions were observed to be well-preserved, and serum electrolyte levels were within normal limits. The increase of the ESR and C Reactive Protein values and positive unilateral and bilateral biopsy studies were statistically significant. All of the above characterization of Hispanic population with temporal arteritis cited in our study correlates well with the classic description of the disease in previous epidemiological studies conducted on non-Hispanic subjects. Our study confirmed the presence of temporal arteritis in a Hispanic population. The disease was more prevalent in women than men, with a female to male ratio of 2:6, which is the lowest ratio found for this disease compared to previous epidemiological studies. In our study group, the disease was found in patients over 70 years of age, with a mean age of 75.7. Arterial hypertension was the most commonly associated condition in our patients, probably due to its high prevalence in our community. The clinical characteristics of our patients correlate closely with the previous data from other ethnic groups.
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PMID:Temporal arteritis in Puerto Rico Hispanics. 1961 May 72


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