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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The origin of the vertebral artery is a frequent site for the development of stenosing lesions. The flow deficit caused by the stenosis of one vertebral artery is normally compensated for by intracranial anastomosis between the carotid and basilar arteries or by the opposite vertebral artery. A number of patients, however, have inadequate intracranial anastomosis and hypoplasia or stenosis of the opposite vertebral artery, and symptoms of brain ischemia develop. We describe here four cases in which a new technique, a subclavian vertebral artery autogenous vein bypass graft, was used to deal with the diseased segment of the vertebral artery. Transient postoperative problems included lymphocele and Horner syndrome. All four bypasses were patent at the time of angiography one week postoperatively. All four patients were relieved of symptoms of vertebrobasilar insufficiency.
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PMID:Vertebral artery bypass. 94 61

A new cerebral syndrome is described which occurs rather frequently with ischemia affecting the common pathway of the internal carotid and middle cerebral arteries. The syndrome consists of contralateral brachiofacial hemiparesis, possibly with hemianopia and/or aphasia, and ipsilateral thermoregulatory hemihypohidrosis with an ipsilateral central Horner syndrome. It is caused by an ischemic lesion of the crossed pathways descending from the cerebrum and the uncrossed hypothalamo-spinal sympathetic pathways descending through the subthalamic region. It is suggested to name the syndrome "telodiencephalic ischemic syndrome".
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PMID:The telodiencephalic ischemic syndrome. 615 86

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

Spontaneous dissection of the cervical internal carotid artery (sICAD) causes, in more than 90% of patients, carotid territory ischemia, local signs and symptoms on the side of dissection, or both, whereas the remaining sICAD remain clinically asymptomatic. Local signs and symptoms include head, facial, or neck pain, Horner syndrome, pulsatile tinnitus, and cranial nerve palsy. Head, facial, or neck pain occurs in 64-74% and is the presenting symptom in up to 58.5%, and the only manifestation in 2.2-4.5%. Headache is observed in 65-68%, facial pain in 34-53%, and neck pain in 9-26%. Horner syndrome consisting essentially of miosis and ptosis is detected in 28-41%. Cranial nerve palsy is reported in 8-16%; the lower cranial nerves IX-XII are most commonly affected, in particular the hypoglossal nerve. The facial nerve may also be involved; dysgeusia results mainly from involvement of the chorda tympani (0.5-7.0%) or the glossopharyngeal nerve. Transient pareses of the ocular motor (III, IV and VI) and trigeminal nerves have been observed. Pulsatile tinnitus is reported in 16-27%. About three quarters of sICAD cause ischemic events, which include ischemic stroke in 80-84%, transient ischemic attack in 15-16%, amaurosis fugax in 3%, ischemic optic neuropathy in 4%, and retinal infarct in 1%. Patients with sICAD causing ischemia show a lower prevalence of Horner syndrome and palsy of the caudal cranial nerves than patients with sICAD causing no ischemic events, whereas headache, neck pain, and pulsatile tinnitus are equally frequent in both groups. After an ischemic stroke, independency defined by a moderate Rankin scale score of 0-2 occurs in 63-90%, whereas the outcome of retinal infarct and ischemic optic neuropathy are not well known.
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PMID:Clinical manifestations of carotid dissection. 1729 Jan 13

Ultrasound allows the reliable exclusion of spontaneous dissection of the cervical internal carotid artery (sICAD) in patients with carotid territory ischemia. The possibility of falsely positive ultrasound findings indicates that cervical magnetic resonance imaging (MRI) and angiography must confirm ultrasonic suspicion of sICAD. The sensitivity of ultrasound for assessing sICAD which causes no carotid territory ischemia, but headache, neck pain, Horner syndrome, or palsy of the cranial nerves on the side of dissection is about 70%, and for identifying spontaneous dissection of the vertebral artery (sVAD) the sensitivity is 75-86%. The negative predictive value and specificity for ultrasound diagnosis of the latter two types of cervical artery dissection is unknown. Consequently, all patients with clinical suspicion of sICAD causing no ischemic event or sVAD should undergo cervical MRI and angiography. Ultrasound is useful for noninvasive monitoring of vessel recanalization and for determining the duration of antithrombotic therapy.
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PMID:Ultrasound diagnosis of cervical artery dissection. 1729 Jan 27

A 52-year-old man developed sudden occipital headache followed by vomiting and vertigo. On admission, he displayed right Horner syndrome with ipsilateral reduced facial sensation to pain and temperature that crossed in the body, affecting the left limbs. In addition, he had right hemiparesis. Diffusion weighted magnetic resonance images showed a high intensity lesion localized in the lower and right lateral medulla oblongata. Magnetic resonance angiography showed severe luminal stenosis in the right vertebral artery and T2-weighted sampling perfection with application optimized contrasts using different flip angle evolution (SPACE) showed arterial wall expansion. T1-weighted SPACE showed subacute intramural hematoma at that point, suggesting arterial dissection. First described in 1946, Opalski syndrome is considered a variant of Wallenberg syndrome with ipsilateral hemiparesis. This motor impairment is considered as a result of extension of the ischemia from the lateral medulla to the upper cervical cord involving corticospinal fibers caudal to pyramidal decussation. This case adds information regarding the anatomy of the pyramidal decussation.
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PMID:[Opalski syndrome caused by vertebral artery dissection]. 2600 59

Internal carotid artery dissection (ICAD) results from disruption of the intima of the arterial wall, and can lead to intrusion of blood into the arterial wall and form an intramural hematoma. The hematoma can compress the true lumen of the vessel, causing functional stenosis or occlusion. The classic triad signs of ICAD include pain in the ipsilateral neck, head and orbital regions; a (partial) Horner syndrome; and cerebral or retinal ischemia. However, not all ICAD patients present with this classic signs. In some cases, ocular manifestations are the initial (and sometimes the only) findings. We summarize the ocular manifestations associated with ICAD in 3 categories: visual symptoms, oculosympathetic palsy, and ocular motor nerve palsy.
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PMID:Ocular manifestations of internal carotid artery dissection. 3113 Dec 45