Focal Cerebral Ischemic Symptoms Research Articles

Isolated oculomotor nerve palsy: A rare manifestation of spontaneous internal carotid artery dissection

Introduction: Internal carotid artery (ICA) dissection commonly presents with headache, neck pain, Horner syndrome or with focal cerebral ischemic symptoms. Cranial nerve palsies can also be found, accounting for 12% of spontaneous ICA dissection cases and usually presenting as a syndrome of lower cranial nerve palsies. Therefore, an isolated oculomotor nerve involvement is extremely rare.

2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS Guideline on the Management of Patients With Extracranial Carotid and Vertebral Artery Disease: Executive Summary

Preamble . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e422 1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e424 2. Recommendations for Duplex Ultrasonography to Evaluate Asymptomatic Patients With Known or Suspected Carotid Stenosis . . . . . . . . . . . . . . . . .e425 3. Recommendations for Diagnostic Testing in Patients With Symptoms or Signs of Extracranial Carotid Artery Disease . . . . . . . . . . . . .e426 4. Recommendations for the Treatment of Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e426 5. Recommendation for Cessation of Tobacco Smoking. . . . . . . . . . . . . . . . . . . . . . . . . . .e426 6. Recommendations for Control of Hyperlipidemia. . . . . . . . . . . . . . . . . . . . . . . . . . . . .e427 7. Recommendations for Management of Diabetes Mellitus in Patients With Atherosclerosis of the Extracranial Carotid or Vertebral Arteries. . . . . . . . . . . . …

Stenting for a symptomatic posterior cerebral artery stenosis

Evolvement of endovascular devices and increase of operator expertise have made angioplasty and stenting in intracranial vessels technically possible. Stenting has been reported in treating stenosis in middle and anterior cerebral arteries with favorable outcomes. However, the feasibility of stenting for stenosis in posterior cerebral artery (PCA) has not been established. We report a patient with progressive focal cerebral ischemic symptoms, which were arrested after reconstruction of the associated PCA stenosis with stenting.

Horner Syndrome Due to Carotid Dissection

Internal carotid artery dissection typically presents with a clear history of blunt cranial-cervical trauma. Presenting symptoms include headache, focal cerebral ischemic symptoms, and oculosympathetic paresis (Horner syndrome). It is usually thought that internal carotid dissection is a serious but infrequent cause of Horner syndrome. A review of the literature reveals that carotid dissection is under-recognized as a cause of Horner syndrome, and outcome is thought to be compromised by diagnostic delay. This case report describes a patient who presented to the Emergency Department with a traumatic Horner syndrome caused by internal carotid dissection. The etiology, clinical manifestations, diagnostic evaluation, and treatment options of carotid dissection are discussed.

Prevalence of Platelet Nonresponsiveness to Aspirin in Patients Treated for Secondary Stroke Prophylaxis and in Patients With Recurrent Ischemic Events

To determine the prevalence of platelet nonresponsiveness to aspirin treatment for secondary stroke prophylaxis, the authors studied consecutive patients during a 29-month period. Information regarding their ischemic events, risk factors, and medications was collected. Platelet aggregation in response to collagen and arachidonic acid was used to determine platelet responsiveness to aspirin. A total of 653 patients were evaluated. Of these, 129 patients (20%) were determined to be nonresponsive to aspirin based on continued platelet aggregation in response to collagen, arachidonic acid, or both. A total of 87 (13%) of the 653 patients were clinical aspirin failures (ie, presented with new focal cerebral ischemic symptoms while taking aspirin). Of the patients with new cerebral ischemic symptoms, 57 (66%) were determined to be platelet nonresponsive to aspirin. The odds ratio for platelet nonresponsiveness to aspirin in patients who suffered a recurrent ischemic event while taking aspirin was 14.25 (95% confidence interval: 8.5-23.7; P < .5). Continued platelet aggregation despite aspirin treatment occurred in 20% of ambulatory patients treated for secondary stroke prophylaxis. The prevalence of nonresponsiveness to aspirin was statistically higher in those patients who suffered recurrent cerebral ischemia while taking aspirin (P < .5) compared with patients who remained without new ischemic symptoms.

Bilateral internal carotid artery dissection due to trivial trauma

Internal carotid artery dissection (ICAD) is a known cause of unilateral headache and focal cerebral ischemic symptoms. Other symptoms include oculosympathetic paresis, facial pain, neck pain, subjective carotid bruits, and cranial nerve deficits. Traumatic dissection has an obvious precipitating incident preceding the neurologic or visual symptoms. An ICAD that occurs spontaneously or from trivial trauma usually lacks an obvious incident and thus requires awareness of its possibility for accurate detection and treatment. Dissections arise from a defect in the internal elastic lamina allowing penetration of blood into the arterial wall. Despite its low incidence, ICAD must be considered in young to middle-aged patients who present with headache and transient cerebral or retinal ischemic symptoms. This report describes a patient who had bilateral internal carotid artery dissections following trivial trauma. The etiologies, clinical manifestations, diagnostic modalities, treatment options, and outcomes of ICAD are discussed.

Traumatic dissections of the extracranial internal carotid artery.

Traumatic dissections of the extracranial internal carotid artery (ICA) in 18 patients aged 19 to 55 years were studied. All had suffered blunt head or neck injury of marked or moderate severity; motor-vehicle accidents were the leading cause of the injury. Delayed focal cerebral ischemic symptoms were the most common presenting symptoms. Less commonly noted was focal unilateral headache associated with oculosympathetic paresis or bruit. Following a head injury, the abrupt onset of focal cerebral symptoms after a lucid interval should raise the suspicion of arterial injury, particularly when computerized tomography fails to show abnormalities that would explain the evolving neurological deficits on the basis of direct trauma to the brain. Unilateral headaches, oculosympathetic palsy, and bruits also help in establishing the diagnosis. Focal cerebral ischemic symptoms may develop months or years after the initial trauma. These delayed symptoms are caused by embolization from a thrombus within a residual dissecting aneurysm. Common angiographic findings, in decreasing order of frequency, are: aneurysm, stenosis of the lumen, occlusion, intimal flap, distal branch occlusion (embolization), and slow ICA-to-middle cerebral artery flow. Although two patients died as the result of massive cerebral infarction and edema and some were left with severe neurological deficits, most made a good recovery. Residual dissecting aneurysms and occlusion seem to occur more frequently with traumatic dissections than with spontaneous dissections of the extracranial ICA.

Spontaneous dissection of the cervical internal carotid artery.

We studied 36 patients (21 women and 15 men) with spontaneous dissection of the internal carotid arteries. The ages of these patients ranged from 21 to 63 years. Focal unilateral headache was the most common symptom. Other common clinical manifestations (in decreasing order of frequency) included focal cerebral ischemic symptoms, oculosympathetic paresis, bruits, light-headedness, and neck pain. Less common symptoms were syncope, amaurosis fugax, scalp tenderness, swelling in the neck, and dysgeusia. Common angiographic manifestations (in decreasing order of frequency) were elongated, irregular, and frequently tapered narrowing of the lumen; abrupt luminal reconstitution (often at the carotid canal); aneurysms; intimal flaps; slow internal carotid artery--middle cerebral artery flow; tapered occlusion; and distal branch occlusions. The incidence of hypertension in these patients was considerably higher than that in the general population. Angiographic evidence of fibromuscular dysplasia was found in 14% of the patients, but atherosclerotic changes were uncommon. Follow-up ranged from 14 to 140 months (mean, 58.5 months). Twenty-three patients with 29 dissected internal carotid arteries were also restudied angiographically. The stenosis of the internal carotid artery either completely resolved or substantially improved in more than 85% of the dissected vessels. About two-thirds of the dissecting aneurysms either resolved or decreased in size. Clinically more than 85% of the patients had an excellent or complete recovery. Recurrence of the dissection or rupture of a dissecting aneurysm was not noted. Despite their disconcerting appearance on angiography, spontaneous dissections of the internal carotid arteries are often associated with a good prognosis.