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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In younger patients, the clinical symptoms of sudden unilateral headache and facial pain, often combined with Horner syndrome and the cerebrovascular symptoms of TIAs or stroke, should indicate the diagnosis of spontaneous carotid dissection. Angiographic findings can verify this diagnosis, showing various signs of eccentric, narrowing stenosis, false lumen, pseudoaneurysms, or complete occlusion. An addition to noninvasive Doppler ultrasonography, B-mode and Duplex investigations, although more or less nonspecific, give some indications of the diagnosis; modern imaging techniques, especially MRI, can image the intramural hematoma directly. As the hematoma is the source of the intracranial emboli, the therapy of choice in this rarely diagnosed disease should be anticoagulation.
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PMID:[Carotid dissections]. 267 40

Brain infarction caused by arterial occlusion of the internal carotid axis sometimes develops Horner syndrome. The purpose of this study is to clarify the characteristics and mechanism of "Horner type" anisocoria, which is one of the symptoms of Horner syndrome, in patients with brain infarction in regions supplied by the internal carotid artery (ICA). We studied 112 consecutive patients (71 males and 41 females, mean age of 60.8 +/- 12.3 years) with brain infarction with either ICA or the middle cerebral artery (MCA) occlusion, who were admitted to the National Cardiovascular Center within seven days after the onset of stroke. We examined differences in frequency of Horner type anisocoria and its duration after onset by the mechanism (embolic or thrombotic) and site (ICA proximal, ICA distal or MCA) of arterial occlusion. Horner type anisocoria was seen in 26 of 66 cases (39.4%) with embolic occlusion, which was more frequent than in those with thrombotic occlusion (8 of 46 cases, 17.4%) (p < 0.05). In the embolic occlusion group, Horner type anisocoria was seen in 17 of 32 cases (53.1%) with ICA occlusion, which was more frequent than in those with MCA occlusion (9 of 34 cases, 26.5%) (p < 0.05). Horner type anisocoria was more frequently seen in embolic (17 of 32 cases, 53.1%) than in thrombotic ICA occlusion (2 of 21 cases, 9.5%) (p < 0.01). The duration of Horner type anisocoria was shorter in patients with either distal ICA or MCA occlusion than in those with proximal ICA occlusion (p < 0.05). In patients with thrombotic occlusion, there was no distinct characteristics in between those ICA and MCA occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Horner type anisocoria associated with brain infarction of the internal carotid artery axis]. 806 35

From 1990 to 1997, June, 296 patients (156 males and 140 females), aged 16 to 45 years, admitted in the Neurology Department of the University Hospital of Nancy (F) for ischemic stroke, were prospectively evaluated according to a standardized analysis of anamnestic and clinical data, angiography (90 p. 100 of cases), TEE (78 p. 100), hemostasis. Women were younger (mean age = 34.82 y) than men (36.87 y; p = 0.003), with a peak in the 4th decade. Clinical event was a TIA in 14.2 p. 100, a stroke in 51.7 p. 100; it concerned the anterior circulation in 64.5 p. 100, posterior circulation in 25 p. 100, multiple territories in 10.5 p. 100. History of TIA, cervical-cranial pain or Horner syndrome suggestive of dissection, pregnancy or post-partum were found respectively in 60 (20.3 p. 100), 34 (11.1 p. 100) and 13 (9.3 p. 100) cases. Risk factors concerned 87.2 p. 100 of patients, mainly smoking (55.1 p. 100), oral contraceptive (53 p. 100), hyperlipemia (35 p. 100), and were more frequent in case of atheroma and lacunar stroke (p < 0.0000). Etiology, according to TOAST classification, was: atheroma (8.4 p. 100), cardioembolism (8.7 p. 100), small-artery disease (7.1 p. 100), dissection (15.5 p. 100), other determined causes (11.1 p. 100), multiple causes (5.7 p. 100), undetermined cause (34.8 p. 100). Septal pathology was found 34 times. Patients whose stroke remained unexplained were younger (33.7 y vs 37.7, p = 0.002), had less risk factors (p < 0.0000), had more TIA (p = 0.005), more often in the carotid territory (p = 0.008), had a better prognosis (p = 0.01), and showed more often emboli at angiography (p = 0.001). During a mean follow-up of 33 months (median = 19), 21 recurrent strokes occurred and 6 patients died. 134 (46 p. 100) patients had no sequelae, 101 (34.7 p. 100) minor disability, 42 (14.4 p. 100) major sequelae. These results, compared to the main studies of the literature, suggest the interest of common definition criteria and classification of etiologies. In practice, hierarchisation of investigations may be proposed, and vascular risk factors should be tracked in young patients. In patients whose stroke remains unexplained, further studies, as atrial vulnerability, are needed.
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PMID:[Cerebral ischemic accidents in young subjects. A prospective study of 296 patients aged 16 to 45 years]. 1048 47

Horner syndrome is defined as homolateral miosis, ptosis and enophthalmus, and occurs after a lesion of central or peripheral sympathetic pathways. The syndrome is mentioned as side effect for example with dysraphias, the Wallenberg syndrome, ischemic stroke of the middle cerebral artery, mediastinal tumors or iatrogen after pneumothorax interventions. We recently observed a patient with a transient significant miosis, without ptosis and enophthalmus, which we interpreted as an incomplete manifestation of a Horner syndrome occurring with spontaneous pneumothorax.
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PMID:[Horner's syndrome occurring with spontaneous pneumothorax. A case report]. 1175 51

Cervicocephalic arterial dissections (CCAD) are an increasingly recognized cause of ischemic stroke in young adults. Various treatments have been suggested but no controlled trial has ever been performed. Medical treatment has included anticoagulant or platelet antiaggregant therapy. Surgical correction has been proposed for selected patients who have failed medical therapy. Percutaneous balloon angioplasty and stenting have been increasingly used in some patients, although long-term results are unknown. The objective of the study was to review our recent experience with the management and outcome of extracranial CCAD. We identified 27 patients with extracranial CCAD who were evaluated, treated and/or followed by our Stroke Service from September 1995 to August 2001. Clinical presentation, diagnostic evaluation, management, and outcome were reviewed. There were 15 men (56%) and 12 women (44%) with mean ages of 38 and 43 years respectively. Diagnosis was made by cerebral angiography in 15 (56%) patients and by MRI/MRA only in 12 (44%) patients. Twenty-two patients had spontaneous and five had traumatic extracranial CCAD. Most common associated disorders were arterial hypertension (37%) and migraine (26%). One patient presented only with a painful post-ganglionic Horner syndrome, another patient with neck pain and post-ganglionic Horner syndrome, another patient solely with protracted unilateral headaches, three with transient ischemic attacks (TIA), and 21 with ischemic strokes. The internal carotid artery (ICA) was the most frequently involved vessel (63%), followed by the vertebral artery (30%, and multivessel involvement in two patients (7%). Eighteen patients received anticoagulant therapy and nine platelet anti-aggregants. Follow-up extended from 2 to 115 months, with a mean of 58 months. At the end of follow-up, 23 (85%) patients had either no disability or only minor sequelae (modified Rankin score: 0 to 1), and four (15%) patients had moderate limitations (modified Rankin score: 2 to 3). Two patients had a recurrent ischemic stroke, one unrelated to recurrent CCAD, and the other following percutaneous balloon angioplasty/stenting for treatment of a persistent vertebral artery pseudoaneurysm. Most CCAD involved the extracranial ICA. The clinical presentation is variable, most patients having an ischemic stroke or TIAs. The short- and long-term outcome are usually favorable with either anticoagulant or platelet antiaggregant therapy. A medical initial approach to the management of extracranial CCAD is recommended for most patients.
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PMID:Outcome of extracranial cervicocephalic arterial dissections: a follow-up study. 1206 89

A 47-year-old woman presented with headache, acute monocular vision loss, and ipsilateral Horner syndrome. Apart from the optic neuropathy, all cranial nerve function was intact. Magnetic resonance imaging revealed an enlarged pituitary gland with compression of the orbital apex. The surgical specimen was consistent with pituitary apoplexy. The combination of headache, acute visual loss, and ipsilateral Horner syndrome without ophthalmoplegia, which may suggest carotid artery dissection, is evidently an unusual manifestation of pituitary apoplexy.
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PMID:Pituitary apoplexy causing optic neuropathy and horner syndrome without ophthalmoplegia. 1450 93

In young and middle age subjects, spontaneous carotid dissection is an increasingly recognized cause of ischemic stroke. Their usual presentation is facial pain with a Horner syndrome and a contra lateral paresis. Blindness has been reported as a presenting symptom in only a few cases. We report a 50 years old man who presented with amblyopia in the left eye, without periocular pain. Fundoscopy showed papilledema and a peripapillar hemorrhage, compatible with an ischemic optic neuropathy. A magnetic resonance angiography confirmed a left carotid dissection.
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PMID:[Blindness caused by an ischemic optic neuropathy by spontaneous carotid dissection. Report of a case]. 1463 92

Cerebellar and medial medullary infarctions are well-known vertebrobasilar stroke syndromes. However, their development in a patient with distal vertebral artery occlusion has not been previously reported. A 49-year-old man with longstanding hypertension suddenly developed vertigo, right-sided Horner syndrome, and left-sided weakness. An MRI of the brain showed acute infarcts in the right inferior cerebellum (posterior inferior cerebellar artery territory) and the right upper medial medulla (direct penetrating branches of vertebral artery). Magnetic resonance angiogram showed occlusion of the distal vertebral artery on the right side. Atherothrombotic occlusion of the distal vertebral artery may cause this unusual combination of vertebrobasilar stroke.
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PMID:Infarcts presenting with a combination of medial medullary and posterior inferior cerebellar artery syndromes. 1545 Jul 76

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

Traumatic cervical artery dissection (TCAD) is a complication of severe blunt head or neck trauma, the main cause being motor vehicle accidents. TCAD are increasingly recognized, and incidences of up to 0.86% for internal carotid and 0.53% for traumatic vertebral artery dissections (TVAD) among blunt trauma victims are reported. Diagnostic evaluation for TCAD is mandatory in the presence of (1) hemorrhage of potential arterial origin originating from the nose, ears, mouth, or a wound; (2) expanding cervical hematoma; (3) cervical bruit in a patient >50 years of age; (4) evidence of acute infarct at brain imaging; (5) unexplained central or lateralizing neurological deficit or transient ischemic attack, or (6) Horner syndrome, neck or head pain. In addition, a number of centers screen asymptomatic patients with blunt trauma for TCAD. Catheter angiography is the standard of reference for diagnosis of TCAD. Color duplex ultrasound, computed tomographic, and magnetic resonance angiography are noninvasive screening alternatives, but each method has its diagnostic limitations compared to catheter angiography. Anticoagulants and antiplatelet drugs may prevent ischemic stroke, but bleeding from traumatized tissues may offset the benefits of antithrombotic treatment. Endovascular therapy of dissected vessels, thrombarterectomy, direct suture of intimal tears, and extracranial-intracranial bypass should be considered in exceptional cases. Neurological outcome is probably worse in TCAD compared to spontaneous CAD, although it is unclear whether this is due to dissection-induced ischemic stroke or associated traumatic lesions.
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PMID:Traumatic cervical artery dissection. 1729 Jan 11


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