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

Thunderclap headache is a sudden, high-intensity headache often associated with subarachnoid hemorrhage secondary to a ruptured intracerebral aneurysm. A variety of less common causes have now been described. This report presents the cases of 2 patients who experienced thunderclap headache after regrowth of an aneurysm, without hemorrhage of previously coiled aneurysms. Thunderclap headache after endovascular occlusion of a ruptured intracranial aneurysm may be a symptom of aneurysm regrowth and may warrant angiographic investigation.
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PMID:Thunderclap headache without subarachnoid hemorrhage associated with regrowth of previously coil-occluded aneurysms. 1903 39

Although endovascular intervention is the first-line treatment of intracranial aneurysm, intraprocedural rupture or extravasation is still an endangering event. We describe two interesting cases of extravasation during embolotherapy for ruptured peripheral cerebral pseudoaneurysms. Two male patients were admitted after development of sudden headache with presentation of intracerebral and subarachnoid hemorrhage, respectively. Initial angiographic assessment failed to uncover any aneurysmal dilatation in both patients. Two weeks afterwards, catheter angiography revealed aneurysms each in the peripheral middle cerebral artery and anterior inferior cerebellar artery. Under a general anesthesia, endovascular embolization was attempted without systemic heparinization. In each case, sudden extravasation was noted around the aneurysm during manual injection of contrast after microcatheter navigation. Immediate computed tomographic scan showed a large amount of contrast collection within the brain, but they tolerated and made an unremarkable recovery thereafter. Intraprocedural extravasation is an endangering event and needs prompt management, however proximal plugging with coil deployment can be sufficient alternative, if one confronts with peripheral pseudoaneurysm. Peculiar angiographic features are deemed attributable to extremely fragile, porous vascular wall of the pseudoaneurysm. Accordingly, it should be noted that extreme caution being needed to handle such a friable vascular lesion.
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PMID:Extravasation during Aneurysm Embolization without Neurologic Consequences. Lessons learned from Complications of Pseudoaneurysm Coiling. Report of 2 Cases. 1909 73

A case of acute subdural haematoma from an intracranial aneurysm is presented. Although the patient presented with isolated subdural haematoma, the clinical signs were consistent with the classical signs of subarachnoid haemorrhage including thunderclap headache. An aneurysm of the anterior cerebral artery was the origin of the bleeding, and no subarachnoid blood was identified during operation. Rupture of a sacculate aneurysm should be suspected in patients with non-traumatic acute subdural haematoma.
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PMID:[Subdural haematoma from aneurysm without concurrent subarachnoid haemorrhage]. 1912 72

Spontaneous thrombosis of an intracranial aneurysm is a rare event. It is predominantly observed with aneurysms that are large and have relatively narrow necks. We report here a case of a 48-year-old woman presenting with subarachnoid hemorrhage (SAH) due to rupture of a 2-mm aneurysm of the anterior cerebral artery treated by microsurgical clipping. Six months after treatment of the aneurysm, the patient presented with severe headache. SAH was excluded, but computed tomographic angiography (CTA) revealed the recurrence of a large aneurysm (7 mm) that was confirmed by cerebral angiography (DSA). Endovascular treatment was scheduled for several days later, but DSA also revealed spontaneous occlusion of the recurrent aneurysm. On the control CTA performed one week later, the recurrent aneurysm had again reappeared, again confirmed by DSA, and was subsequently treated by coil embolization.
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PMID:Spontaneous thrombosis of a recurrent clipped intracranial aneurysm. 1914 9

Seckel syndrome is an autosomal recessive disorder characterized by intrauterine and postnatal growth delay, microcephaly with mental retardation, and facial dysmorphisms including micrognathia, a recessed forehead, and a large beaked nose. Occurring in 1 in 10,000 children without sex preference, it is the most common primordial microcephalic osteodysplastic dwarfism and has been associated with a variety of congenital brain malformations and intracranial aneurysms. Moyamoya syndrome is an idiopathic, chronic, progressive cerebrovascular disorder marked by stenosis of the intracranial internal carotid arteries and concurrent development of hypertrophied collateral vessels. These tortuous arterial collaterals appear radiographically as "puffs of smoke," giving the syndrome its name. In this report, the authors describe the case of a 16-year-old girl with coincident Seckel and moyamoya syndromes. To their knowledge, this is the first reported case of such an association being treated with surgical revascularization. The patient presented with persistent headaches and a 2-year history of progressive hand, arm, and face numbness. Imaging studies revealed multiple completed cerebral infarcts, global ischemic changes, and vascular anatomy consistent with moyamoya syndrome. Bilateral pial synangioses successfully revascularized each hemisphere with resolution of the patient's symptoms. The patient died 1 year later of complications related to treatment of a rapidly progressing intracranial aneurysm. This report documents the first case associating moyamoya and Seckel syndromes. In addition, the report reveals the rapid development of an intracranial aneurysm in a patient with this syndrome. When coupled with previous reports of other types of cerebrovascular disease in patients with Seckel syndrome or other primordial dwarfisms, the authors' findings are important because they suggest that physicians treating patients with dwarfism should consider the diagnosis of moyamoya syndrome when symptoms suggestive of cerebral ischemia are present. Prompt diagnosis and treatment of moyamoya syndrome, including the use of proven surgical revascularization procedures such as pial synangiosis, may significantly improve the long-term outcomes of these patients.
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PMID:Seckel syndrome and moyamoya. 1933 12

Intracranial aneurysm rupture continues to cause high mortality and morbidity. Determining the aetiology, identifying the risk factors and improving diagnostic accuracy are ongoing challenges. We retrospectively reviewed consecutive autopsies over 30 years (1977-2006) in Auckland, New Zealand, and identified 403 cases of subarachnoid haemorrhage to examine these challenges within a fatal case population. Females (67%) outnumbered males. Ruptured posterior circulation aneurysms were frequent (25%). Left ventricular hypertrophy was documented in 45% of cases, with fatty metamorphosis of the liver also prominent (16%). About 6.5% had additional unruptured aneurysm/s. Most patients were sedentary at onset (39% being asleep); 6% were involved in significant physical exertion; 69% were found dead or collapsed; the remaining patients reported headache (27%) or atypical primary symptoms (4%). Warning headache over recent days to months occurred in 38%, among whom misdiagnosis was notable. Our findings regarding warning headache patterns and the range of atypical presentations are aimed at improving clinician discernment in managing this condition.
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PMID:Clinical lessons and risk factors from 403 fatal cases of subarachnoid haemorrhage. 1937 7

An aim of the study was to compare frequencies of vascular diseases in first-degree relatives (FDR) of patients with intracranial aneurysms (IA) and FDR of controls. Pedigrees have been selected through interviews in 194 patients with IA (96 men and 98 women) and in 193 age- and sex-matched controls. Only FDR with complete information about their disorders have been included in the study: 1011 FDR of patients with IA and 812 controls. The frequency of strokes was 2.5 times and hemorrhages --3.7 times higher in FDR of patients with IA compared to controls. Only 0.9% of FDR of patients with IA had the rupture of intracranial aneurysm. The frequency of headaches was 2.8 times, ischemic heart disease--2.7 times and arterial hypertension --2 times greater in FDR of patients with IA compared to controls. Moreover, sudden death occurred 5.8 times more often in FDR of patients with IA. The data obtained suggest that vascular defects leading to the development of IA may be, in part, genetically determined. Prevention of stroke and cardiovascular disease is necessary for FDR of patients with IA.
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PMID:[Vascular diseases in first-degree relatives of patients with intracranial aneurysms]. 1989 96

A case of arterial stenosis after coil migration in intracranial aneurysm embolization is presented. A 51-year-old woman suffered sudden onset of headache and unconsciousness. Computed tomography demonstrated diffuse subarachnoid hemorrhage and cerebral angiography disclosed a right internal carotid artery (ICA) bifurcation aneurysm and a right ICA-anterior choroidal artery aneurysm. The aneurysms were treated by endovascular embolization with Guglielmi detachable coils. During the embolization procedure of the ICA bifurcation aneurysm, a coil strand detached in the sac had migrated into the ICA. We did not retrieve the migrated coil, because the free coil strand was stable in the ICA and did not cause distal flow reduction. The patient suffered vasospasm of the right ICA and underwent intra-arterial infusion of fasudil hydrochloride and percutaneous transluminal angioplasty of the ICA on day 9. The patient experienced infarction in the territory of the right anterior cerebral artery area and needed a ventriculo-peritoneal shunt for hydrocephalus. The patient was discharged with mild right hemiparesis. Follow-up angiography after six months revealed right ICA and middle cerebral artery stenosis, but the free strand of the migrated coil had not moved in the right ICA. We suspect that the coil strand might have induced thrombosis or intimal hyperplasia of the proximal M1 segment and right ICA. Although late stenosis of the parent artery might be rare, it should be recognized as a long term complication of a migrated free coil strand in the endovascular treatment of intracranial aneurysms.
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PMID:[Arterial stenosis after coil migration in embolization of an aneurysm]. 2008 1

Thunderclap headache, a severe headache which is maximal in intensity at onset, is associated with numerous underlying disorders, including subarachnoid hemorrhage, unruptured intracranial aneurysm, cervical artery dissection, cerebral venous sinus thrombosis, stroke, intracranial hemorrhage, reversible cerebral vasoconstriction syndrome, and reversible posterior leukoencephalopathy. After exclusion of all possible causes, thunderclap headache may be considered a primary headache. This review summarizes the diagnostic considerations and clinical approach to thunderclap headache, with particular emphasis on the reversible cerebral vasoconstriction syndromes.
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PMID:Abrupt-onset severe headaches. 2035 89

A 61-year-old woman suffered cisternal coil migration in the follow-up period after endovascular coil embolization for a ruptured cerebral aneurysm. She presented with sudden onset of headache. Computed tomography demonstrated diffuse subarachnoid hemorrhage, and cerebral angiography disclosed a left anterior choroidal artery aneurysm. The aneurysm was treated by endovascular embolization with Guglielmi detachable coils. During the embolization procedure, the microcatheter perforated the aneurysm. For direct closure of the perforation site with coils, the microcatheter was withdrawn and coils were deployed partially in the subarachnoid space and partially in the aneurysm sac. The coil mass was spread in the subarachnoid space around the aneurysm immediately after embolization. The patient was discharged with no neurological deficit. Three months later, follow-up radiography demonstrated obvious reduction in the size and compaction of the coil mass. Magnetic resonance angiography and digital subtraction angiography demonstrated stable occlusion of the aneurysm. The coil mass probably spread in the cistern around the aneurysm and was compacted by the shape memory of the coils and pulsation of the brain and vessels, as the subarachnoid clots around the aneurysm had disappeared. This case suggests that cisternal coil migration should be considered in the follow up of intracranial aneurysm treated with detachable coils.
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PMID:Unusual cisternal coil migration in the follow-up period after aneurysm perforation during endovascular coiling. 2161 62


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