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

Focal cerebral ischemic symptoms, Horner's syndrome and mostly ipsilateral headache are the characteristic clinical triad of extracranial carotid artery dissection. Lower cranial nerve palsies seem to be uncommon and rare. By means of two cases with identical clinical symptoms and of a literature review we make clear, that ipsilateral lower cranial nerve palsies, especially a hypoglossal nerve palsy, are not uncommon. Without focal cerebral ischemic symptoms they can be the only sign of extracranial carotid artery dissection. Computed tomography of the skull base with regard to the high cervical internal carotid artery is as an usually quickly available examination an alternative to magnetic resonance imaging.
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PMID:[Unilateral caudal cranial nerve paralysis in extracranial carotid dissection]. 815 Apr 8

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

In order to assess the prevalence and characteristics of cephalic pain in internal carotid artery (ICA) dissection, and to compare clinical and angiographic features of patients with painful and non-painful dissections, we observed 65 patients with angiographically diagnosed extracranial ICA dissection from 1972 to 1990. Forty-eight patients (74%) complained of a cephalic pain which was inaugural in 38 (58.5%). It was homolateral to the dissection in 79% of cases and lasted from 1 h to 30 days, with a median of 5 days. Signs of cerebral or retinal ischemia were observed in 79% of patients, often delayed and occurring up to 29 days after the onset of pain. A painful Horner's syndrome was present in 31% of patients, and was the only manifestation of dissection in 16%. The clinical presentation of the dissections and angiographic findings were similar in patients with and without pain except for a past history of migraine which was more frequent in patients with painful dissections. Cephalic pain is frequent and often inaugural in carotid dissection. Its recognition is important for early diagnosis and treatment.
Cephalalgia 1994 Feb
PMID:Head pain in non-traumatic carotid artery dissection: a series of 65 patients. 820 21

We describe a patient with a Raeder's paratrigeminal neuralgia consisting of left-sided frontal and orbital pain, Horner syndrome (including anhydrosis of the forehead), and sensory loss in the territory of the first division of the trigeminal nerve. The involvement of the ophthalmic nerve is not consistent with the usual localization of this syndrome to the pericarotid sympathetic plexus. Oculosympathetic and sympathetic fibers supplying the sweat glands of the forehead join the ophthalmic nerve in the cavernous plexus localized in the cavernous sinus. Therefore, this seems to be the most likely site of the lesion when the ophthalmic nerve is involved.
Cephalalgia 1993 Apr
PMID:Raeder's syndrome. A case with an unusual localization. 849 57

The spontaneous cervical artery dissection (SCAD) is one of the main causes of cerebro-vascular accident in the young adult. It may results from minor cervical trauma. The pathophysiological basis of the neurological complications remain unclear. For that reason, the treatment of SCAD is often empirical. In a retrospective study (1984-1994), we have reviewed 20 cases admitted to Notre-Dame Hospital for a SCAD confirmed by angiography. The initial clinical diagnosis was missed in 65% of the cases despite a suggestive symptomatology (headache 80%, hemiparesis 65% and Horner 45%). We have studied the clinical evolution as related to blood pressure, volemia, haematocrit and the administered treatment (aspirin, Coumadin). 60% of the patients (mean age 39) deteriorated in the hours following their admission. Their was one death (5%) and 85% had neurological sequelae. This study suggest that SCAD is a potentially serious disease. A delayed diagnosis may lead to a poor prognosis. Early aggressive treatment aiming at an optimal cerebral perfusion could improve the patients outcome.
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PMID:[Spontaneous dissection of the cervical arteries]. 856 30

The main symptom of arterial dissection is intense acute unilateral headache. The pain is commonly located around the eye, in the temple or the front with a carotid artery dissection [CAD] and in the posterior neck and occiput with a vertebral artery dissection [VAD]. Transient or persistent cerebral ischemic symptoms are similarly frequent but usually occur later in the time course. Horner's syndrome indicating a lesion of perivascular sympathetic fibres represents the third leading symptom and occurs in more than one third of the patients. Compression of local structures such as lower nerve or radicular palsies is rare. This constellation of symptoms in a young patient without vascular risk factors should rise suspicion of a dissection, in particular, if there is a preceding 'trivial' trauma. Characteristic features on Doppler/duplex sonography provide the diagnosis of dissection in almost all CAD and the majority of VAD. MRI demonstrating the mural hematoma allows reliable confirmation of the suspected diagnosis. Angiography is necessary only in selected cases, more often in VAD than in CAD. Brain infarction may be prevented, if premonitory symptoms, which occur in 60 to 80% of the patients, are recognized as such. Therefore, if there is clinical and sonographic suspicion of CAD or VAD, anticoagulation therapy with heparin should should be started before other imaging procedures finally prove the diagnosis. Because immediate anticoagulation may prevent cerebral embolism, this treatment strategy seems appropriate, although its efficacy has not been established by a controlled study. Anticoagulation should be continued until resolution of the dissection.
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PMID:[Cerebral artery dissection]. 871 29

The ciliospinal reflex response is mainly mediated by second- and third-order sympathetic nerves to the dilatator muscle of the iris. As the pupillary response to various pharmacological agents indicates a sympathetic dysfunction in patients with cluster headache, the ciliospinal reflex was studied in 25 patients. Five of these patients with cluster headache exhibited a Horner-like syndrome (miosis, ptosis) on the symptomatic side. The pupillary responses to phenylephrine and tyramine showed that the Horner-like syndrome was due to postganglionic sympathetic nerve dysfunction. Their ciliospinal reflex response on the symptomatic side was significantly less than in controls and in other patients with cluster headache, lacking a Horner-like syndrome. This also applied to the nonsymptomatic side compared to the majority of cluster headache patients without any clinical evidence of sympathetic nerve dysfunction. These findings seem to delineate those patients with a Horner-like syndrome as a subgroup, distinctly separated from the majority of cluster headache patients. Furthermore, the findings indicate that the Horner-like syndrome is not a consequence of repeated attacks of headache over many years, but is a manifestation of bilateral cephalic sympathetic dysfunction being more marked on the symptomatic side. In 18 (72%) of our 25 patients, an asymmetric and lower ciliospinal reflex response on the symptomatic side was seen. In 3 (12%) patients, there was no difference in the response. In 4 patients (16%), the incorrect side was indicated by an asymmetric reflex response. Two of these patients (8%) had suffered from cluster headache on alternating sides. In summary, the findings support the concept that dysfunction of the sympathetic nervous system, whether peripheral or central is involved in the pathophysiology of cluster headache.
Headache 1996 Oct
PMID:Ciliospinal reflex response in cluster headache. 891 67

A 55-years-old woman had left neck pain and headache, dizziness, left Horner's sign, left abducens palsy, diplopia, left peripheral facial palsy, left loss of hearing, left tinnitus, left paralysis of vocal cord and soft palate, dysphagia, left limb ataxia, truncal ataxia, disturbance of temperature and pain sensation over Th10 on the right involving the right face. Left vertebral angiography revealed tapering occlusion of the left vertebral artery. Right vertebral angiography showed normal angiogram of the basilar artery and bilateral anterior inferior cerebellar arteries. MRI disclosed infarcts in the left lateral inferior pons, left lateral medulla, and cerebellum of territories in the anterior inferior cerebellar artery and posterior inferior cerebellar artery. T2 weighted image showed septum (intimal flap) in the left vertebral artery. This is the very rare case of lateral inferior pontine syndrome and lateral medullary syndrome due to the vertebral artery dissection.
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PMID:[A case of vertebral artery dissection with lateral inferior pontine syndrome and lateral medullary syndrome]. 921 27

A 31-year-old woman had left-sided miosis, ptosis, and hypopigmented iris probably since birth. At 22, she developed intermittent headaches, always in the left frontotemporal region. These headaches lasted from 1 to 2 days and recurred every 1-2 months. Pain attacks were pressing-pulsatile in character, moderate in intensity, and frequently accompanied by nausea, vomiting, and moderate phono- and photophobia. Various treatment alternatives, such as conventional analgesics and ergotamine failed to improve the attacks. Pizotifen was partially effective. The results of pupillometry and evaporimetry studies were consistent with a 3rd neuron sympathetic hypofunction on the symptomatic side. Autonomic studies and clinical features were consistent with a congenital Horner's syndrome. Conceivably, a sympathetic hypofunction may play a role in the pathogenesis of such headache or in its lateralization. Indomethacin and sumatriptan both seemed to provide absolute pain relief. Some clinical features, the fact that the IHS criteria for migraine are fulfilled and that sumatriptan is efficient, demonstrate the similarity to migraine. The coexistence of strict unilaterality of pain and the probable, complete response to indomethacin indicate a similarity to hemicrania continua in its remitting form. Further information on the effect of sumatriptan in hemicrania continua will help clarify the position of this case vs. hemicrania continua. At this stage, it is probably not possible to classify this case properly.
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PMID:Congenital (?) Horners syndrome and ipsilateral headache. 921 66

Dissections of the carotid and vertebral arteries are a common cause of stroke in young adults. The diagnosis may be missed because the typical signs and symptoms are often delayed in onset, or easily confused with other more commonly encountered entities. Dissections of the carotid and vertebral arteries may occur spontaneously or may accompany mild to severe trauma. They present with a variety of findings including headache, neck and face pain, Horner's syndrome, or stroke.
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PMID:Carotid and vertebral artery dissections. 925 40


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