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

It is important to establish the diagnosis of temporal arteritis because the disease is treatable; treatment may prevent blindness and even death. Temporal arteritis usually occurs in people older than 51 years of age, although very rarely, histologically documented disease occurs in younger people. The onset may be occult, so that there are few findings. A multitude of signs and symptoms may occur such as fever, headaches, malaise, weight loss, anemia, stroke, cranial nerve palsies, polymyalgia rheumatica, aortitis and other large vessel involvement. The eye may suffer from ischemic optic neuropathy (anterior or posterior), central or cilio-retinal arterial occlusion, ophthalmic artery ischemia, or extraocular muscle palsies. An arterial biopsy showing giant cell arteritis establishes the diagnosis. However, a negative biopsy does not rule out the disease because of the occasional presence of skip areas. Arteriography has only rarely yielded a positive temporal artery biopsy when the initial biopsy done elsewhere was negative. As a diagnostic parameter, the erythrocyte sedimentation rate is nonspecific, being elevated in diseases other than temporal arteritis and sometimes being falsely lowered by technical factors. Furthermore, the temporal artery biopsy is occasionally positive despite a normal erythrocyte sedimentation rate. Treatment is aimed at relieving the patient's symptoms and normalizing the erythrocyte sedimentation rate. Because of the wide spectrum of clinical and laboratory finding in temporal arteritis, no one specific treatment regimen with systemic corticosteroids works for all patients. Temporal arteritis is a well known disease of the elderly which ir rarely fatal but results in significant visual morbidity (Hinzpeter & Naumann, 1976; Spencer & Hoyt, 1960). Since Hutchinson's (1890) description, more than a thousand articles have been written on the subject (Cohen & Smith, 1974). Despite this, many unanswered questions and controversies remain concerning the diagnosis, prognosis and treatment of temporal arteritis. My goal is to review these questions and areas of controversy.
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PMID:Controversies regarding giant cell (temporal, cranial) arteritis. 39 20

A 49-year-old woman with a 6-year history of headaches was found to have a pale right optic disc with narrowed retinal arterioles and a congested left optic disc. Her visual acuity was 20/20 in each eye with normal visual fields in May 1983. These findings were attributed to a previous attack of non-arteritic anterior ischemic optic neuropathy (AION). She had a normal neurologic examination and a normal head computed tomographic (CT) scan performed 2 years prior to her initial ophthalmologic evaluation. She was followed over the next 2 years without change in her fundus examination. In December 1987, after a generalized tonic-clonic seizure, she was found to have a large right frontoparietal mass without direct impingement on the optic nerves, or chiasm on neuroradiological studies. At this time she developed marked papilledema in the left eye with a pale optic disc in the right eye remaining unchanged. Histopathological diagnosis of malignant glioma was made. Two diseases, ischemic optic neuropathy and glioma, in one patient represents a bizarre example of the pseudo-Foster Kennedy syndrome.
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PMID:Pseudo-Foster Kennedy syndrome in a patient with anterior ischemic optic neuropathy and a nonbasal glioma. 214 36

The Hemostasis and Thrombosis Laboratory at the Oregon Health Sciences University identified 80 patients with significantly elevated anticardiolipin antibody (ACLA) levels. We reviewed all of their available medical records and found that 25 of these patients had associated neurological symptoms or disorders. These symptoms and disorders could be grouped into four distinct clinical patterns comprising encephalopathy, multiple cerebral infarctions, migraine-like headaches, and visual abnormalities including amaurosis fugax and ischemic optic neuropathy. Cerebral ischemia best explained these neurological dysfunctions. There was no correlation between the presence or absence of neurological disease and ACLA levels, but ACLA levels were higher in patients with encephalopathy than in others with neurological involvement (p less than 0.05). How neurological dysfunction and the presence of these antiphospholipid antibodies are related remains to be clarified. Nevertheless, in patients with unexplained cerebral ischemia, establishing the presence of ACLA may have prognostic and therapeutic importance. In particular, acute immunosuppressive therapy and plasmapheresis may be useful in patients with acute ischemic encephalopathy.
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PMID:Neurological disease associated with antiphospholipid antibodies. 272 12

We report the case of a 26 year old obese woman who presented with intermittent headaches and blurred vision in her left eye (OS) and on clinical examination had an enlarged visual field blind spot OS with OS disc edema. After an extensive neurologic work up including two nondiagnostic lumbar punctures, a clinical diagnosis of OS anterior ischemic optic neuropathy was made. Gradual progression of visual field loss OS prompted reassessment of the diagnosis and intracranial pressure was confirmed to be markedly elevated by usage of a subarachnoid monitoring bolt, thus establishing the diagnosis of pseudotumour cerebri. An optic nerve sheath fenestration was performed OS with subsequent reversal of the progressive visual field loss.
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PMID:Asymmetric papilledema and visual loss in pseudotumour cerebri. 369 Apr 29

Two patients with histories of classic migraine developed ischemic optic neuropathy during a severe headache. Clinical and radiologic studies excluded other causes for the visual field loss. In both cases, the field loss was permanent. No further visual or neurologic disturbances have occurred in either patient during a 3 1/2- and 2 1/2-year period of follow-up, respectively.
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PMID:Migrainous optic neuropathy. 623 28

Giant-cell arteritis is a polysymptomatic disease of the elderly. Systemic symptomatology includes headaches, arthralgias, myalgias, tender temporal arteries, jaw claudication, low-grade fever, anemia, anorexia, malaise, and weight loss. Visual loss from anterior ischemic optic neuropathy and diplopia resulting from ischemia of the ocular muscles represents the major ocular manifestations of giant cell arteritis. When the diagnosis is suspected, blood for a sedimentation rate should be drawn, and, if it confirms the clinical impression, high dose prednisone should be started immediately and a temporal artery biopsy performed at a later date. Only by asking the proper questions and suspecting the diagnosis will this preventable form of blindness receive the prompt attention it deserves.
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PMID:Giant-cell arteritis. Signs and symptoms. 715 21

The clinical, laboratorial perimetric and fluorescein angiographic features of the arteritic type of the anterior ischemic optic neuropathy (A-AION) was studied in 25 patients (40 eyes) in order to characterize the profile of the disease and to allow the differential diagnosis with the non-arteritic anterior ischemic optic neuropathy (NA-AION) and other disorders of the optic nerve. The A-AION occurred in patients 60 to 88 years old (mean 74 years) and was highly predominant in females (64 per cent). Fifteen patients had both eyes involved, either simultaneously or usually within few days or weeks after the initial involvement. Headache and eye pain were the most commonly observed prodromic complaints whereas systemic symptoms of giant cell arteritis (GCA) were seen in all patients. The laboratorial abnormalities most commonly found were high values of reactive C protein, plasmatic fibrinogen and erythrocyte sedimentation rate. In the great majority of the patients visual acuity was severely affected. The optic disc was always abnormal, usually showing a pale edema. In addition to that retinal changes were commonly found. Goldmann perimetry disclosed a wide variety of visual fields abnormalities, the most common of them being inferior altitudinal defects. Fluorescein fundus angiography revealed delayed or absent disc fluorescence, or sectorial or diffuse hypofluorescence or hyperfluorescence of the optic disc. Choroidal filling delay was the most characteristic and frequent angiographic finding in the arteritc type of the disease.
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PMID:[The arteritic type of anterior ischemic optic neuropathy. Study of 25 cases]. 789 8

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 (due to 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:Neurologic aspects of giant cell (temporal) arteritis. 826 30

A 53-year-old right-handed woman presented with headaches and dizziness. She had been well for ten years following successful cadaveric renal transplantation and was taking prednisolone and azathioprine. Two months later she had more headaches with transient dominant hemisphere disturbances and then suffered a completed right hemisphere deficit. As this was recovering, she developed an ischemic optic neuropathy, Computerized tomography (CT) was then normal although CSF analysis showed lymphocytosis and high protein. Steroid trial led to dramatic symptomatic and clinical recovery. On tailing off steroids, progressive bilateral hemisphere disturbance occurred. She was bedbound, with fever, headache, incontinence and disturbed consciousness. New evidence of infarction in watershed territories on CT led to temporal lobe biopsy. Cortical arterioles and venules showed proliferation of lymphoid cells staining for leucocyte common antigen and B-cell markers characteristic of Neoplastic Angioendotheliomatosis (NAE). After chemotherapy she regained independence and mobility and CSF protein fell. This is the first case of NAE to our knowledge in association with immunosuppression for renal transplant and is further evidence that NAE is malignant lymphoma. Cerebrovascular disease is common in such patients, the simultaneous events in differing territories is typical of NAE. Response to chemotherapeutic agents occurred although the typical natural history was unchanged.
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PMID:Neoplastic angioendotheliomatosis: a treatable "vascular dementia" occurring in an immunosuppressed transplant patient. 847 50

Cranial nerve palsy was present in 23 of 190 consecutive adult patients (12%) with spontaneous dissection of the extracranial internal carotid artery. Ten patients (5.2%) had a syndrome of lower cranial nerve palsies (with invariable involvement of cranial nerve XII with or without additional involvement of cranial nerves XI, X, and IX), seven (3.7%) had palsy of cranial nerve V, and five (2.6%) had a syndrome of ocular motor palsies. Palsy of cranial nerve VIII and ischemic optic neuropathy occurred in one patient each. Three patients had dysgeusia without other cranial nerve involvement, presumably due to involvement of the chorda tympani nerve. Headache or face pain (often unilateral) was present in 83% of patients. Other associated manifestations were cerebral ischemic symptoms, bruits, or oculosympathetic palsy. In one patient, cranial nerve palsy was the only manifestation of internal carotid artery dissection, and in another patient, the disease presented only as a palsy of cranial nerve XII and oculosympathetic palsy. In six patients, a syndrome of hemicrania and ipsilateral cranial nerve palsy was the sole manifestation of internal carotid artery dissection. Cranial nerve palsy is not rare in internal carotid artery dissection. Compression or stretching of the nerve by the expanded artery may explain some but not all of the palsies. An alternative mechanism is likely interruption of the nutrient vessels supplying the nerve.
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PMID:Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery. 861 94


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