Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 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

Basilar migraine has been studied by Bickerstaff who considers that there is a vasoconstriction in the basilar territory resulting in transient ischemia with the corresponding neurological symptoms including vertigo, and followed by the vasodilatation causing the headache. Three cases, treated in neurology, have had an audiovestibular investigation with an E.N.G. and an audiogram and are described herein. Nystagmus and hearing loss have been observed in one of these cases and it is suggested that the internal auditory artery participates in the basilar migrainous processes. The diagnosis of basilar migraine is impossible to prove and the investigation is very limited. Finally it is the evolution of the patient which helps in establishing the diagnosis of basilar migraine.
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PMID:[Basilar migraine]. 61 47

Older people often describe their headaches as starting with vague neck discomfort and eventually moving to the temples and forehead. These are muscle-tension headaches, by far the most common type in the elderly. Although cervical osteoarthritis often is at fault, depression can be a significant factor, patricularly when headaches are chronic. There is no sure cure for tension headache, and often, several of the many remedies-ethyl chloride spray, moist heat, massage, antidepressant drugs, analgesics, local anesthetics, etc.-must be tried before an effective one is found. But just as important to successful therapy are concern, compassion, and a willingness to listen on the part of the physician. True migraine headaches are rare in the elderly. More prevalent is the type of vascular headache associated with giant cell arteritis, which is severe and resistant to any form of analgesic except the strongest narcotics. Vascular headaches also may result from congestive heart failure (which produces venous congestion in the cranial cavity), transient ischemia, increased intracranial pressure, and a variety of metabolic disturbances.
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PMID:The types of headache that affect the elderly. 95 13

Severe extremity ischemia developed in four patients who had ingested methysergide maleate or ergot for the relief of headache. Symptoms involved the upper extremity in two patients and the lower extremity in two. Spontaneous reversal of the ischemic picture was obtained by simple discontinuation of ergot in most instances, although intra-arterial vasodilators were used in one case. Angliography disclosed arterial spasm and was a useful adjunct in confirming the cause of ischemia in each of the patients. It was especially useful when a history or ergot ingestion was not immediately available.
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PMID:Ergotism. 115 59

Acetazolamide, a carbonic anhydrase inhibitor, has proved to be useful in the assessment of "vasodilatory capacity" in cerebrovascular disease. To obtain further information on the nature of interictal low-flow regions in migraine, we reinvestigated 20 asymptomatic patients suffering from migraine with aura (n = 15) or without aura (n = 5) and who had either minor (n = 12) or marked (n = 8) regional hypoperfusion when examined in a previous 99mTc-HMPAO SPECT investigation. These patients received acetazolamide IV prior to tracer application. In 14/20 cases regional hypoperfusion resolved. Three patients with migraine with aura had less pronounced regional hypoperfusion compared to baseline. No change in baseline hypoperfusion was detectable in three older patients. No further decreases in flow were measured. In contrast to patients with cerebrovascular ischemia, in whom acetazolamide usually enhances low-flow regions, vasodilatory capacity appears intact in most migraine patients with interictal regional hypoperfusion. Thus, the "acetazolamide test" might be useful in the differential diagnosis of migraine with aura from transient cerebrovascular ischemia.
Cephalalgia 1992 Oct
PMID:The influence of acetazolamide on cerebral low-flow regions in migraine--an interictal 99mTc-HMPAO SPECT study. 142 58

Internal carotid artery dissection is a major cause of ischemic stroke in the young. Pain is the leading symptom and is associated with other focal signs such as Horner's syndrome and painful tinnitus or with signs of cerebral or retinal ischemia. We report two patients with angiographically confirmed extracranial internal carotid artery dissection presenting with cephalic pain as the only manifestation. The first patient had a diffuse headache and a latero-cervical pain lasting for 12 days, reminiscent of carotidynia. The second patient experienced an exploding headache suggestive of subarachnoid hemorrhage, which was ruled out by computed tomography of the head and cerebrospinal fluid study. These patients demonstrate that recognition of carotid artery dissection as a cause of carotidynia and headache suggestive of subarachnoid hemorrhage may permit an earlier diagnosis and possibly the prevention of a stroke through the use of anticoagulation.
Cephalalgia 1992 Oct
PMID:Pain as the only manifestation of internal carotid artery dissection. 142 63

Forty-six migraineurs and 69 age- and sex-matched controls referred for MRI scans of the brain were evaluated for the incidence of intracranial pathology. Axial long TR/short TE and long TR/long TE and sagittal short TR/short TE scans were performed in all patients. Enhancement with Gd-DTPA was performed in all controls and in nine migraineurs. Six of 46 (13%) of the migraineurs had white matter lesions versus three of 69 (4.3%) of the controls. The white matter lesions in migraineurs were seen in a younger age group than in the controls. These findings agree with recent MRI studies. Ischemia or an immune-based white matter demyelination are possible mechanisms for the white matter lesions.
Headache 1992 Nov
PMID:MRI in migraineurs. 146 10

Two hypotheses have dominated attempts to understand the etiology of migraine with aura or classic migraine; the vascular spasm model proposed by Wolff and colleagues, and the spreading cortical depression hypothesis. Neither can provide a fully satisfactory explanation for the syndrome, however. We propose that classic migraine is both spreading cortical depression and localized ischemia linked in a vicious cycle by potassium induced vasoconstriction. The cycle can be initiated by any event which raises the local cortical ECF potassium concentration to approximately 20 mM. Such an event could be a localized burst of activity of a group of cells, localized metabolic impairment, or a transient reduction in blood flow to a region of the cortex. Once this level of potassium concentration is reached, it may result in localized depolarization of neurons, releasing more potassium into the ECF. Glial siphoning can distribute the potassium preferentially toward the blood vessels in the area, leading to an elevation in potassium concentration in the ECF surrounding the vascular smooth muscle of the arterioles. Above approximately 15 mM, vascular smooth muscle increases its tension in response to elevations in potassium. Therefore, as cortical ECF potassium concentration rises above 15 to 20 mM, localized vasoconstriction occurs, thereby reducing both the supply of oxygen for aerobic metabolism and the removal of potassium in the blood. Under these conditions, the effectiveness of the mechanisms which control potassium concentration is impaired and unable to prevent additional elevations in potassium. As the concentration continues to rise, vasoconstriction becomes more intense, perpetuating the cycle that results in localized depression of cortical neuronal activity and ischemia. The condition is propagated to adjacent regions of the cortex by diffusion and glial-mediated spread of potassium. In many respects, the hypothesis unites the vascular spasm and spreading depression models. If verified, it may provide insight into the causes of classic migraine as well as give direction toward development of effective therapies.
Headache 1992 Jan
PMID:Migraine with aura: a vicious cycle perpetuated by potassium-induced vasoconstriction. 155 28

Three cases of bilateral deafness with cytologically-demonstrated meningeal carcinomatosis are reported. The first patient, a 64-year old man, presented with bilateral deafness, gait disturbances, and bilateral facial paresis. The second patient, a 78-year-old man, had bilateral deafness, unsteady gait and fluctuations in consciousness. The last patient, a 69-year-old man, complained of bilateral deafness and severe headache, and presented with right facial paresis and left laterodeviation while walking. All three patients had abnormal cochleo-vestibular findings and brainstem auditory evoked responses (BAER) that suggested peripheral lesions with absent or very delayed I waves. The brain CT scans with an without contrast enhancement were entirely normal, and the diagnosis was established by lumbar puncture. From our own cases and a review of the literature, deafness in meningeal carcinomatosis may start unilaterally but becomes bilateral in less than a week. Vestibular disturbances may not be apparent, but they can be demonstrated in almost all cases. Facial paresis or plegia is also a very frequent finding. The destruction of the eighth and seventh cranial nerves is probably due to direct infiltration by neoplastic cells as well as to ischemia through compression of the nerve supplying vessels. The 3 cases presented here emphasize once again the important fact that meningeal carcinomatosis remains a cytological diagnosis, several lumbar punctures being sometimes necessary, and that cerebrospinal fluid studies cannot yet be supplanted by other diagnostic techniques like contrast-enhanced CT or MRI with gadolinium.
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PMID:[Bilateral deafness, an initial manifestation of meningeal carcinomatosis]. 160 23

In 1983, a previously healthy 21-year old mother came to University Hospital in Dijon, France feeling weak and had a severe frontal headache with vomiting. Clinical and biochemical tests were normal. She smoked 20 cigarettes/day and used a high dosed combined oral contraceptive (OC) (ethinyl estradiol and cyproterone acetate). 15 days later, the headache returned and she could not understand spoken words and the bilateral section of the brain had slowed. Yet her mental status was normal as were cerebrospinal fluid and cerebral computerized tomography tests. The antiherpes virus drug, vidabarine, did not alleviate symptoms. At least 1 month later, a severe left pulmonary embolism caused acute right heart failure. She also had a prethrombotic left iliac vein, so physicians began heparin therapy, adding nifedipine and buflomedil to control the spasms in the right internal iliac artery and both external iliac arteries. Acute ischemia of the lower limbs eased within a week but sensory disorders remained for 2 months. Satisfactory collaterality transpired due to a blocked left external iliac artery and left iliac vein. The following signs and symptoms indicated her condition to be homocystinuria: blond hair with deep blue eyes, macrocytic anemia, factor VII deficit (51%), strong positive Brandt's reaction, cystine homocystine in the plasma, and presence of homocystine, cystathionine, and methionine in the urine. Physicians took her off the OC and discharged her on vitamin B6/day, folic acid/day, betaine citrate/day, and the anticoagulant Coumadin. A subsequent check of her 19-year old sister found she had it too. They assessed the patient's condition yearly. In 1988, her left leg developed edema and she limped when not using elastic stockings. Effects of iliac vein phlebitis were evident. She no longer suffered from headaches. Since plasma methionine was within the normal range and homocystine no longer was present in plasma and urine, the physicians halted the anticoagulant therapy. In conclusion, the OC precipitated this partial form of homocystinuria.
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PMID:Vascular manifestations in homocystinuria. 161 Jun 63


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