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

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

Cluster headache is a clinical entity characterised by strictly unilateral head pain attacks accompanied by ipsilateral autonomic phenomena. We report two patients who had pain episodes mimicking cluster headache attacks, and who experienced a total or partial Horner's syndrome ipsilaterally to pain, persisting for 48 h after the last attack. A dissection of the ipsilateral internal carotid artery at the extra-intracranial passage was present in both cases. These cases highlight the need for extensive neuroradiological investigation in cluster headache patients when atypical features are present.
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PMID:Two symptomatic cases of cluster headache associated with internal carotid artery dissection. 1750 78

A 55-year-old woman developed severe unilateral headaches, periocular numbness, and Horner syndrome after presenting with symptoms consistent with Lyme disease. The combination of Horner syndrome and periocular headache and numbness constituted a diagnosis of Raeder paratrigeminal neuralgia. Although the headaches resolved with antibiotic treatment, the Horner syndrome persisted for at least 1 year. This case expands the spectrum of neurologic manifestations of Lyme disease to include postganglionic Horner syndrome as well as Raeder paratrigeminal neuralgia.
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PMID:Lyme disease associated with postganglionic Horner syndrome and Raeder paratrigeminal neuralgia. 1754 97

Fibromuscular dysplasia (FMD), formerly called fibromuscular fibroplasia, is a group of nonatherosclerotic, noninflammatory arterial diseases that most commonly involve the renal and carotid arteries. The prevalence of symptomatic renal artery FMD is about 4/1000 and the prevalence of cervicocranial FMD is probably half that. Histological classification discriminates three main subtypes, intimal, medial and perimedial, which may be associated in a single patient. Angiographic classification includes the multifocal type, with multiple stenoses and the 'string-of-beads' appearance that is related to medial FMD, and tubular and focal types, which are not clearly related to specific histological lesions. Renovascular hypertension is the most common manifestation of renal artery FMD. Multifocal stenoses with the 'string-of-beads' appearance are observed at angiography in more than 80% of cases, mostly in women aged between 30 and 50 years; they generally involve the middle and distal two-thirds of the main renal artery and in some case also renal artery branches. Cervicocranial FMD can be complicated by dissection with headache, Horner's syndrome or stroke, or can be associated with intracerebral aneurysms with a risk of subarachnoid or intracerebral hemorrhage. The etiology of FMD is unknown, although various hormonal and mechanical factors have been suggested. Subclinical lesions are found at arterial sites distant from the stenotic arteries, and this suggests that FMD is a systemic arterial disease. It appears to be familial in 10% of cases. Noninvasive diagnostic tests include, in increasing order of accuracy, ultrasonography, magnetic resonance angiography and computed tomography angiography. The gold standard for diagnosing FMD is catheter angiography, but this invasive procedure is only used for patients in whom it is clinically pertinent to proceed with revascularization during the same procedure. Differential diagnosis include atherosclerotic stenoses and stenoses associated with vascular Ehlers-Danlos and Williams' syndromes, and type 1 neurofibromatosis. Management of cases with renovascular hypertension includes antihypertensive therapy, percutaneous angioplasty of severe stenoses, and reconstructive surgery in cases with complex FMD that extends to segmental arteries. The therapeutic options for securing ruptured intracerebral aneurysms are microvascular neurosurgical clipping and endovascular coiling. Stenosis progression in renal artery FMD is slow and rarely leads to ischemic renal failure.
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PMID:Fibromuscular dysplasia. 1755 81

Horner's syndrome, or oculosympathetic paresis, results from interruption of the sympathetic trunk innervation to the eye and presents typically with meiosis, ptosis and facial anhydrosis on the affected side.(1) The pathological process ranges from benign, such as cluster headache, or life threatening, such as lung malignancy. Appropriate imaging requires an anatomical appreciation of the complex and circuitous route the neuronal pathway takes as it passes from the central nervous system to the eye.
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PMID:Imaging of Horner's syndrome. 1837 11

Cluster headache (CH) is characterized by a series of sudden attacks of short-lasting severe headache pain with ipsilateral autonomic features, including lacrimation, rhinorrhea, localized sweating, eyelid edema, and partial or complete Horner's syndrome. Just like in migraine, brush allodynia has been described for CH and for short lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) syndrome. Administration of normobaric oxygen is part of the standard therapy for CH attacks. Here, we describe a young male with a first CH attack and the influence of oxygen on pain and concomitant cutaneous allodynia.
Headache 2009 Jan
PMID:Oxygen therapy influences episodic cluster headache and related cutaneous brush and cold allodynia. 1862 8

We present the case of a 40-year-old female patient with sudden onset of anisocoria and unilateral ptosis of the left eye. With the exception of several previous episodes of nausea and vomiting, mild headache and tiredness, combined with the early death of the patient's mother following aortic rupture, patient history and clinical condition showed no pathological findings. Following indicative findings on duplex sonography, a dissection of the left internal carotid artery from its origin to its distal section was detected on CT angiography of the brain vessels and the diagnosis of Horner syndrome due to internal carotid artery dissection was made. Since this condition is associated with serious embolic complications, prompt treatment following diagnosis is of utmost importance. Our patient was treated conservatively using PTT (partial thromboplastin time)-effective heparinisation. Regular checks including kidney ultrasound, blood pressure measurement, imaging and continuous therapy with acetylsalicylic acid are recommended.
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PMID:[Anisocoria and nausea]. 1893 3

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

Dissection of extra- and intradural arteries is a common cause of cerebral insult in younger patients (<45 years). In patients with corresponding craniocervical injury and symptoms (carotidynie, ipsilateral headache, partial Horner syndrome, cranial nerve palsy) arterial dissection is always to be considered. Essential in diagnosing arterial dissection is the verification of the intramural hematoma and morphologic changes in the vessel (stenosis, pseudoaneurysm) by means of CT/CTA (acute phase) or MRI/MRA (subacute phase). These patients need to be monitored in an intensive care unit setting. The acute therapy includes anticoagulation or inhibition of thrombocyte aggregation. We present two cases with delayed cerebral infarction due to traumatic extra- and intradural arterial dissection after a motor vehicle accident. To perform primary diagnostic quickly and adequately may avoid permanent neurological deficit in these patients.
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PMID:[Traumatic dissection of extra- and intradural arteries]. 1973 49

Traumatic internal carotid artery dissection secondary to blunt trauma is a rare event accounting for 0.08 to 0.4% of all traumatic lesions. The spectrum of traumatic lesions that can affect the internal carotid artery includes minor lesions like spasm, intimal tears, or mural contusions and serious lesions like pseudoaneurysms and complete occlusion. Delayed clinical presentation is typical and can include headache, hemiparesis, partial Horner's syndrome, and cranial nerve palsy. Embolization secondary to the dissection can have devastating effects because it may cause ischemic stroke. Traumatic internal carotid artery dissection after safety belt trauma is very rare; it is usually due to direct cervical trauma on the side of the shoulder fixation point, which causes external bruising along the pathway of the safety belt. We present two cases of traumatic internal carotid artery dissection with concomitant cerebral infarcts caused by safety belts; we discuss the clinical, diagnostic, and therapeutic aspects of this lesion.
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PMID:[Traumatic dissection of the internal carotid artery by a safety belt: a report of two cases]. 1982 98


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