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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine patients with dissections of the cervical arteries are presented. Dissections cause approximately three per cent of non-haemorrhagic stroke and are usually observed in young and middle-aged patients. Dissections very often give rise to head or neck pain. Carotid artery dissection may lead to lower cranial nerve dysfunction and an incomplete Horner's syndrome in case of subadventitial dissection, and to cerebral ischaemia in case of subintimal spread. Vertebral artery dissection may cause brain stem ischaemia (subintimal dissection) or in rare cases a subarachnoid haemorrhage (subadventitial spread). The history frequently reveals a (trivial) traumatic event. Diagnosis is usually established by angiography or MRI. The prognosis is good and recurrences are rare. Treatment with anticoagulants or acetylsalicylic acid seems recommendable, though scientifically unproven.
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PMID:[Dissection of cervical arteries as a cause of cerebral ischemia or cranial nerve dysfunction]. 221 57

The pathophysiology and treatment of acute subarachnoid hemorrhage (SAH) are reviewed. SAH occurs when blood is released into the subarachnoid space, which surrounds the brain and spinal cord. Symptoms of SAH include severe headache, nausea, vomiting, neck pain, nuchal rigidity, and photophobia. The initial hemorrhage is fatal in 20-30% of patients. Complications of SAH include rebleeding, hydrocephalus, delayed cerebral ischemia associated with cerebral vasospasm, and seizures. The likelihood of rebleeding is increased by measures that rapidly lower intracranial pressure. The risk of developing hydrocephalus is associated with the volume of blood within the subarachnoid space and ventricular system. Cerebral vasospasm develops in 20-40% of patients, and up to 50% of affected patients die or suffer permanent neurological damage. Seizures occur in 5-15% of patients with SAH. Radiologic procedures form the foundation for the diagnosis of SAH. The most commonly used rating scale classifies the severity of SAH based on the clinical presentation of the patient. Surgery is the definitive treatment for the prevention of rebleeding. Hydrocephalus can only be treated surgically, most commonly by insertion of a drain. The only measures proved to be effective for treatment of delayed cerebral ischemia are volume expansion and the induction of hypertension. The calcium-channel blocker nimodipine was recently approved for treatment of arterial spasm in SAH. Intravenous nicardipine is also being studied for the same indication. These agents may improve clinical outcome substantially by limiting fixed neurological deficits. To prevent seizures, prophylactic antiepileptic therapy with phenytoin sodium is generally accepted. The SAH complications of rebleeding, hydrocephalus, delayed cerebral ischemia, and seizures are managed by surgical, drug, and fluid therapy.
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PMID:Pathophysiology and treatment of subarachnoid hemorrhage. 240 1

First symptoms and initial clinical, ultrasonographic and neuroradiological findings ascertained a mean of 5.6 days (SD = 5.6 days), 7.7 days (7.0), and 11.2 days (8.0) after symptom onset were analysed in 44 patients who suffered a spontaneous internal carotid artery dissection (ICD) verified by magnetic resonance imaging, angiography, or both. Common symptoms signalling dissection were unilateral headache in 68%, transient ischaemic attack in 20%, and cerebral infarction in 9%. Severe pain preceded cerebral ischaemia by more than 3 days in 60% of those patients who eventually suffered a stroke. However, only 2 were admitted because of pain alone and 33 for evolving neurological deficits. During the first month, ipsilateral severe headache occurred in 89%, neck pain in 36%, ipsilateral cerebral ischaemia in 82%, ocular ischaemia in 16%, oculosympathetic palsy in 48%, and cranial nerve palsy in 5%. Recent "trivial" head or neck trauma was elicited in 41%. Doppler and duplex sonography confirmed the clinical suspicion of ICD in 91.5% and in 96% of those with a significant stenosis or occlusion. MRI demonstrated a thickened vessel wall in all 33 imaged carotid dissections and a mural haematoma in 30. None of the 32 patients who received anticoagulant treatment subsequently deteriorated. Monitoring anticoagulant treatment with ultrasonographic follow-up studies demonstrated recanalization in 70% and persistent occlusion in 30%. The results demonstrate that familiarity with the initial symptoms, especially headache, and performance of an ultrasonographic study without delay are the cornerstones of an early diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spontaneous internal carotid artery dissection: early diagnosis and management in 44 patients. 779 22

Arterial dissection results from bleeding into the vessel wall. Some cases are associated with cervical trauma or have evidence of an underlying vascular disease; many occur without any history of injury or detectable arterial disease. Among the cervical cephalic arteries, the extracranial segment of the internal carotid artery is the vessel most commonly involved; intracranial carotid dissections are much rare. Carotid dissection occurs predominantly in young or middle-aged adults and shows no sex predominance. Although clinical manifestations can be extremely diverse (from isolated headache to rapidly lethal stroke), the most common and suggestive syndrome associates "local" symptoms (such as head or neck pain, Horner's syndrome, pulsatile tinnitus or lower cranial nerves palsy) and delayed (up to several weeks) symptoms of cerebral ischaemia in the territory of the internal carotid artery territory. Dissection can be bilateral or associated with dissection of the vertebral artery. Angiography has long been considered the gold standard for the diagnosis. As this procedure carries a risk of cerebral complications, noninvasive diagnostic approaches such as magnetic resonance imaging and ultrasound have been developed and are increasingly used. The prognosis of carotid dissections depends on the presence and severity of ischaemic brain damage. Recurrent dissections seem extremely rare. Normalization or improvement of the vascular abnormalities during the subsequent weeks is frequent and is an excellent argument in favour of the diagnosis. Although no controlled trial has ever been performed, anticoagulant treatment is often used for a few months when the dissection involves the extracranial segment of the carotid artery. No standard treatment of intracranial carotid dissection has emerged.
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PMID:[Internal carotid artery dissection]. 815 34

Aneurysms of the vertebral artery (VA) are relatively uncommon, accounting for less than 0.5-3.0% of all aneurysms and 20% of aneurysms originating in the posterior fossa. There are three distinct forms of aneurysms: saccular, fusiform and dissecting. The diagnosis of dissecting aneurysm is based on the findings of angiography, surgery and autopsy. Irregular fusiform appearance, intramural retention of contrast medium in the venous phase and alternating irregular stenotic and dilated segment (string and pearl sign) are the basal angiographic findings. Patients with dissection of VA often develop subarachnoid hemorrhages (SAHs), with the typical neck pain or suffer cerebral ischemia. Because of the high risk of rebleeding of dissecting aneurysms, they should be treated as soon as possible, with occlusion of the VA. Nowadays, both surgical and endovascular procedures allow the treatment of dissecting vertebral aneurysms. Anyway, one should be aware that vertebral occlusion performed proximal to PICA origin may be followed by ischemic complications. In this paper, we discuss the diagnostic and therapeutic difficulties associated with dissecting vertebral aneurysms on the basis of personal observation and a review of the literature.
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PMID:Dissecting vertebral aneurysm. Report of a case. 980 Jun 12

Cranial nerve palsy in internal carotid artery (ICA) dissection occurs in 3--12% of all patients, but in 3% of these a syndrome of hemicranias and ipsilateral cranial nerve palsy is the sole manifestation of ICA dissection, and in 0.5% of cases there is only cranial nerve palsy without headache. We present two cases of lower cranial nerve palsy. The first patient, a 49-year-old woman, developed left eleventh and twelfth cranial nerve palsies and ipsilateral neck pain. The angio-RM showed an ICA dissection with stenosis of 50%, beginning about 2 cm before the carotid channel. The patient was treated with oral anticoagulant therapy and gradually improved, until complete clinical recovery. The second patient, a 38-year-old woman, presented right hemiparesis and neck pain. The left ICA dissection, beginning 2 cm distal to the bulb, was shown by ultrasound scanning of the carotid and confirmed by MR angiogram and angiography with lumen stenosis of 90%. Following hospitalisation, 20 days from the onset of symptoms, paresis of the left trapezius and sternocleidomastoideus muscles became evident. The patient was treated with oral anticoagulant therapy and only a slight right arm paresis was present at 10 months follow-up. Cranial nerve palsy is not rare in ICA dissection, and the lower cranial nerve palsies in various combinations constitute the main syndrome, but in most cases these are present with the motor or sensory deficit due to cerebral ischemia, along with headache or Horner's syndrome. In the diagnosis of the first case, there was further difficulty because the cranial nerve palsy was isolated without hemiparesis, and the second case presented a rare association of hemiparesis and palsy of the eleventh cranial nerve alone. Compression or stretching of the nerve by the expanded artery may explain the palsies, but an alternative cause is also possible, namely the interruption of the nutrient vessels supplying the nerve, which in our patients is more likely.
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PMID:Spontaneous carotid dissection presenting lower cranial nerve palsies. 1123 57

We studied the clinical and neuroradiological features of 41 cases with spontaneous bilateral internal carotid artery dissection (ICAD), including 3 cases in our hospital and 38 retrieved from the English literature. Bilateral ICAD accounts for 15.8% of young stroke patients with ICAD in our hospital. The most common presentations are head and/or neck pain, cerebral ischemia, carotid bruit and Horner's syndrome. The cerebral ischemic symptoms are extremely variable in bilateral ICAD, including unilateral hemisphere, bilateral hemisphere or brainstem-like symptoms. Although the underlying pathogenesis remains uncertain, good vascular and clinical outcomes are achieved for spontaneous bilateral ICAD.
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PMID:Spontaneous bilateral internal carotid artery dissection with acute stroke in young patients. 1705 83

Internal carotid artery dissection (ICAD) is a condition involving separation of the artery's intimal lining from its medial division, with subsequent extension of the dissection along varying distances of the artery, usually in the direction of blood flow. ICAD may produce cerebral ischemia due to occlusion of the involved artery. This occlusion may occur at or near the site of the dissection, or "downstream" as a result of embolization from a dislodged thrombus fragment. The problem any chiropractic physician faces in identifying ICAD patients is that the condition may present without any symptoms or the symptoms may appear benign (e.g., headache, neck pain or cervicogenic dizziness). Consequently, it may be impossible to identify some ICAD patients, especially in the early stages of the pathology. As the ICAD progresses and neural blood flow is compromised, the symptom picture typically manifests more completely. The chiropractic physician must be alert to characteristic findings of a progressing ICAD, since an immediate referral to a medical specialist may be required.
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PMID:Identification of internal carotid artery dissection in chiropractic practice. 1754 19

Cervical-artery dissection (CAD) is a major cause of cerebral ischaemia in young adults and can lead to various clinical symptoms, some of which are benign (eg, headache, neck pain, Horner's syndrome, and cranial-nerve palsy), but most patients have a stroke or transient ischaemic attack. In addition to trauma to the neck, other risk factors have been suggested, such as infection, migraine, hyperhomocysteinaemia, and the 677TT genotype of the 5,10-methylenetetrahydrofolate reductase gene (MTHFR 677TT), although evidence is sparse. An underlying arteriopathy, which could in part be genetically determined, is believed to have a role in the development of CAD. Importantly, both research on and optimum management of CAD strongly rely on diagnostic accuracy. Although the functional outcome of CAD is good in most patients, socioprofessional effects can be important. Incidence of the disorder in the general population is underestimated. Mortality and short-term recurrence rates are low but possibly also underestimated. Further research is warranted to improve our understanding of the underlying pathophysiology, to assess the long-term outcome, and ultimately to provide treatment and prevention strategies.
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PMID:Cervical-artery dissections: predisposing factors, diagnosis, and outcome. 1953 38

Internal carotid artery dissection (ICAD) is a rare entity that either results from traumatic injury or can be spontaneously preceded or not by a minor trauma such as sporting activities. It represents a major cause of stroke in young patients. The diagnosis should be suspected with the combination of Horner's syndrome, headache or neck pain, and retinal or cerebral ischaemia. The confirmation is frequently made with a magnetic resonance angiography (MRA). Although anticoagulation with heparin followed by vitamin-K-antagonists is the most common treatment, there is no difference in efficacy of antiplatelet and anticoagulant drugs at preventing stroke and death in patients with symptomatic carotid dissection. We describe a patient with ICAD following deep sea scuba diving, who presented with Horner's syndrome and neck pain and was successfully treated with anticoagulants.
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PMID:Horner's Syndrome due to a Spontaneous Internal Carotid Artery Dissection after Deep Sea Scuba Diving. 2752 39


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