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

The authors present three cases of dissecting aneurysms of the posterior inferior cerebellar artery (PICA). A literature search revealed only three previous cases. Analysis of these six cases showed a unique clinical picture. Three patients developed subarachnoid hemorrhage, and the other three had ischemia. All patients complained of occipital headache or neck pain, regardless of the initial symptoms. Heralding episodes were recorded in four cases. Angiography showed a characteristic fusiform dilatation of the PICA and a narrowing proximal to and distal to the lesion. Various surgical treatments were performed in five cases. Intraoperative observation showed a sausage-like swelling of the PICA or one of its branches with various discoloration depending on the age of the intramural clot. The outcomes were favorable.
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PMID:Dissecting aneurysms of the posterior inferior cerebellar artery. 206 17

The CBF studies performed so far during attacks of migraine, may be interpreted as favouring "the vascular theory." This applies to migraine with aura as well as to migraine without aura. Migraine without aura may be due to mild focal CBF reduction--too mild to be detected by the available CBF techniques (i.e. 20% or less) and too mild to produce ischemia and aura phenomena. Migraine with aura may be due to focal CBF reduction severe enough to produce ischemia (i.e. 50% or more) and therefore also aura phenomena. The phenomenon termed "spreading oligemia" typically seen in CBF studies during migraine with aura, may be an artifact reflecting a gradual decrease of CBF in an area of constant size. The typical "march" of the aura symptoms may reflect differences in the ischemic threshold of various neurones leading to dysfunction of more and more neurones as the blood flow gradually decreases. It is concluded that migraine with and without aura may be due to the same disease process--the only difference being the intensity of vasospasm and CBF reduction.
Headache 1990 Apr
PMID:Migraine with and without aura: the same disease due to cerebral vasospasm of different intensity. A hypothesis based on CBF studies during migraine. 209 26

To better understand and treat painful conditions, one needs to identify the cause, discover the source, and develop knowledge of peripheral and central pain transmission; headaches are no exception. The development of appropriate animal models is important. Accordingly, we have reviewed the anatomy, neurochemistry, electrophysiology, and pharmacology of the trigeminovascular system in experimental animals and emphasized whenever possible the relevance of this final common pathway to migraine, cluster, and other headache syndromes in humans. For example, based on recent anatomic dissections, the pericarotid cavernous sinus plexus was suggested as an important focus to investigate cluster headache pathophysiology. This plexus is an anatomic point of convergence for the nerves giving rise to the signs of sympathetic and parasympathetic activity and sensory symptoms that develop in cluster patients. As in other nociceptive systems, trigeminovascular axons assume at least two important roles. One concerns the transmission of nociceptive information. Electrophysiologic evidence supports the trigeminal nucleus caudalis as an important site for the convergence of visceral (vessel) and somatic (forehead) inputs to mediate the referral of vascular pain to superficial tissues. A second important role concerns the initiation of local increases in blood flow and enhanced protein permeability (sterile inflammation) via the axonal release of vasoactive neuropeptides. Plasma extravasation develops within the dura mater following trigeminal stimulation. Extravasation can be blocked by the administration of ergot alkaloids or sumatriptan, a new serotonin-like agonist, and a prejunctional (neuronal) mechanism of action for these drugs (such as blockade of release) was suggested based on experimental evidence. Whether vasoconstriction also relates to the therapeutic efficacy remains to be determined. As in other organ systems, real or threatened tissue injury provides an important stimulus for depolarizing sensory fibers. The stimulus may come from external conditions such as reduced blood flow or hypoglycemia. The brain may also possess intrinsic neuronal mechanisms by which nociceptors may be synthesized (e.g., glutamate-induced neurotoxicity, seizures). Molecules of relevance include bradykinin, prostaglandins, leukotrienes, and potassium. Experimental evidence was presented demonstrating that the trigeminal nerve mediates hyperemia within cortical gray matter by axon-reflex like mechanisms. An important role for this nerve was established during the hyperemic period of recirculation after ischemia or during severe hypertension above the limits of autoregulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Basic mechanisms in vascular headache. 217 82

Three cases of chronic subdural hematoma (CSDH) revealed by transient neurological accidents are reported. Although well-known this condition is rare: 1 to 9 p. 100 of CSDHs. Questioning may bring out a history of cranial injury and headache, even minor ones, which are unusual in transient ischemic accidents (TIA). Transient phenomena, such as motor aphasia or speech interruption, point to the diagnosis, especially in male patients over 60 years of age. The finding at electroencephalography of a delta activity more than 48 hours after a TND should exclude the diagnosis of TIA until a CT scan is performed. Since the causes of neurological deficits regressing within less than 24 hours may be ischemia as well a hemorrhage or tumour, the term of transient neurological accident (TNA) should preferably be used, and an emergency CT scan should be performed for diagnostic and therapeutic purposes. Owing to the possibility of another concomitant cause of TNA, the finding of a subdural haematoma should not deter from pursuing cardiovascular examinations. The mechanism of TNA probably involves a vascular factor, as suggested by I-123 IMP cerebral SPECT which shows an intercritical decrease in cerebral blood flow and/or an epileptic factor.
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PMID:[Chronic subdural hematoma and transient neurologic deficits]. 219 36

Three women with well-documented migraine associated with intracerebral hemorrhage are described. In each case, migraine headaches began during adulthood. Unusually severe and protracted headache heralded the onset of fixed neurological deficits associated with lobar intracerebral hemorrhage. Striking carotid artery tenderness was characteristic. Except for a history of migraine, no cause for intracerebral hemorrhage could be established. In each case arteriography showed extensive spasm of the appropriate extracranial or intracranial artery. Surgical pathology following evacuation of two hematomata demonstrated signs of vessel wall necrosis associated with subacute inflammatory changes. Vasospasm associated with severe migraine attacks may result in ischemia of intracranial vessel walls, leading to necrosis and subsequent vessel rupture when perfusion pressure is restored.
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PMID:Migraine with vasospasm and delayed intracerebral hemorrhage. 198 18

Temporal muscle blood flow was measured with the xenon 133 clearance technique in 40 patients with chronic tension-type headache and in 13 control subjects. Pressure-pain threshold in the temporal region was determined with an algometer. Patients and control subjects did not differ in any of the blood flow parameters. Resting blood flow at the two sides was highly correlated (Spearman coefficient, r = .61) and no right/left differences could be demonstrated. In both patients and control subjects, blood flow increased approximately fivefold during isometric work (1/3 of a maximum surface electromyogram). Reactive hyperperfusion after isometric work was found in 8 patients and in 1 control subject. There was no definite correlation between the pressure-pain threshold and the corresponding blood flow. It is not likely that temporal muscle ischemia is the cause of muscle tenderness and pain in patients with chronic tension-type headache.
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PMID:Temporal muscle blood flow in chronic tension-type headache. 234 94

This study was designed to investigate the hemodynamic characteristics of cavernous angiomas of the brain. Five adult patients with a cavernous angioma underwent local cortical blood flow studies and vascular pressure measurements during surgery for the excision of the cavernous angioma. Clinical presentation included headache in four patients, seizures in four patients, and recurring diplopia in one patient. Magnetic resonance imaging demonstrated the cavernous angiomas in all patients and revealed an associated small hematoma in two. Four patients with a cerebral cavernous angioma were operated on in the supine position and the remaining patient, whose lesion involved the brain stem, was operated on in the sitting position. Mean local cortical blood flow (+/- standard error of the mean) in the cerebral cortex adjacent to the lesion was 60.5 +/- 8.3 ml/100 gm/min at a mean PaCO2 of 35.0 +/- 0.6 torr. Mean CO2 reactivity was 1.1 +/- 0.2 ml/100 gm/min/torr. The local cortical blood flow results were similar to established normal control findings. Mean pressure within the lesion in the patients undergoing surgery while supine was 38.2 +/- 0.5 mm Hg; a slight decline in cavernous angioma pressure occurred with a drop in mean systemic arterial blood pressure and PaCO2. Mean pressure in the cavernous angioma in the patient operated on in the sitting position was 7 mm Hg. Jugular compression resulted in a 9-mm Hg rise in cavernous angioma pressure in one supine patient but no change in the patient in the sitting position. Direct microscopic observation revealed slow circulation within the lesions. The hemodynamic features demonstrated in this study indicate that cavernous angiomas are relatively passive vascular anomalies that are unlikely to produce ischemia in adjacent brain. Frank hemorrhage would be expected to be self-limiting because of relatively low driving pressures.
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PMID:Vascular pressures and cortical blood flow in cavernous angioma of the brain. 239 87

Among 86 patients with aneurysms arising from the vertebral artery or its branches, 24 had dissecting aneurysms. The patients with dissecting aneurysms were characteristically relatively young males. Twenty-one patients presented with subarachnoid hemorrhage (SAH) and three with ischemia. Severe headache or neck pain occurred in all three patients with ischemia. Five of the 21 patients with SAH and all three patients with ischemia experienced recurrent episodes. Angiography typically showed fusiform dilatation and proximal and/or distal narrowing of the affected artery. The difficulty of diagnosing this disorder is pointed out. Surgery was performed in 19 patients, the most common technique being clip-occlusion of the proximal vertebral artery. There were no postoperative deaths or rebleeding; a lateral medullary syndrome developed in three patients. The observation at surgery of intramural clot with characteristic discoloration was limited to the cases operated on within 36 days after the ictus. After this period, the aneurysm was whitish gray in color and had become firm. Of 36 other cases of vertebral dissecting aneurysm reported in the literature, 20 were operated on. The indications for surgery are discussed.
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PMID:Dissecting aneurysms of the intracranial vertebral artery. 240 89

Vasodilators of resistive vessels may induce ischemia in patients with coronary artery disease. To evaluate this possibility during prostacyclin (PGI2; scalar doses up to 10 ng/kg/min) and prostacyclin analog (iloprost; scalar doses up to 6 ng/kg/min) infusions, we studied 33 patients with angina pectoris and proved coronary artery disease. Patients were also submitted to dipyridamole (0.15 mg/kg/min for 4 minutes) and exercise stress testing (starting at 25 W and increasing 25 W every 2 minutes). In a preliminary study the hemodynamic and side effects of iloprost were studied in seven healthy subjects. At an iloprost dose of 4 to 6 ng/kg/min, these subjects had a significant decrease in mean arterial pressure and total peripheral and pulmonary vascular resistances. Side effects were limited to facial flushing and slight headache and were readily reversible. PGI2 induced typical chest pain and significant ST segment depression in six patients with severe coronary artery disease (three with left main and three with triple vessel disease) and poor exercise tolerance (means +/- SD = 362 +/- 99 seconds). All six patients had had angina during the dipyridamole infusion. Similar findings were observed after iloprost infusion in four of these. Aminophylline (125 mg iv) completely relieved chest pain. Although the rate-pressure products occasionally rose during PGI2 and iloprost infusions, there were no significant changes between ischemic (11.3 +/- 2.3 and 10.6 +/- 1.4 X 10(-3) U) and preischemic (10.8 +/- 1.5 and 10.7 +/- 1.4 X 10(-3) U) rates of infusion. Our data indicate that PGI2 and iloprost may induce ischemia independently of changes in oxygen demand, and suggest that these drugs dilate small coronary vessels. This may result in decreased subendocardial perfusion pressure and/or "coronary steal."
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PMID:Myocardial ischemia induced by prostacyclin and iloprost. 240 9

A 49-year-old female with no history of hearing disturbance developed sudden onset of headache and was admitted with no neurological deficits other than mild nuchal rigidity. Computed tomography (CT) showed subarachnoid hemorrhage. Four-vessel cerebral angiography disclosed no aneurysm. A second angiogram obtained on the 14th day showed vasospasm of the bilateral posterior cerebral arteries and right anterior inferior cerebellar artery, but still failed to demonstrate an aneurysm. Following the second angiography, she developed mild disturbance of consciousness and cerebellar ataxia of the right limbs, and repeat CT showed an infarct in the right cerebellar hemisphere. When she regained consciousness a few days later, she was completely deaf on the right side. The third angiography revealed a right vertebral artery dissecting aneurysm. Following clipping of the proximal portion of the right vertebral artery, she did well and was discharged, although right cerebellar ataxia and deafness persisted. Neuro-otological evaluation, including pure-tone audiography, auditory brainstem responses, electrocochleography, and caloric testing, indicated that her deafness resulted from ischemia in the territory of the right internal auditory artery due to vasospasm.
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PMID:[Unilateral nerve deafness due to rupture of a right vertebral artery aneurysm. Case report]. 247 75


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