Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study considers diagnostic problems in the case of a 52 year old patient presenting with left sided headache and Horner's syndrome. Color Doppler sonography of the internal carotid artery with transcranial duplex sonography showed decreased blood flow velocity and increased impedance of flow in the left internal carotid artery. Flow velocity in the left middle cerebral artery was moderately decreased whereas flow in the proximal segment of the anterior cerebral artery and in the posterior communicans artery was re-directed towards the left internal carotid artery. These findings indicated the need for cerebral angiography which revealed that a vast section of the distal segment of the left internal carotid artery was dissected. Pharmacological treatment with low molecule heparine brought prompt resolution of the signs and symptoms as well as normalization of the blood flow parameters, as examined with Doppler ultrasonography Color Doppler ultrasonography would appear to have high utility in the initial diagnosis of internal carotid artery dissection and the usefulness of this method in the monitoring of treatment.
 ...
PMID:[Doppler ultrasonography in diagnosis of internal carotid artery dissection--case report]. 1652 25

For decades, glucocorticoid therapy has been a well-recognized abortive treatment for cluster headaches. However, the role of steroid hormones, including both glucocorticoids and sex steroids, in the pathophysiology and therapy of cluster headaches has been a topic of much debate and speculation. Current research now points to the importance of cortisol and testosterone in the pathogenesis of cluster headaches, and they appear to be linked mechanistically to another hormone, melatonin. Melatonin, unlike cortisol or testosterone, is not a product of the hypothalamic pituitary axis but of the retinohypothalamic pineal axis, and is the major biomarker of circadian rhythms. The regulation of steroids and melatonin in the pathogenesis of cluster headaches in turn depends on the sympathetic nervous system. Accumulated evidence suggests sympathetic dysfunction--embodied in the Horner sign so commonly seen in the cluster headache--as a necessary ingredient in the inception of the cluster headache. Sympathetic dysfunction now is thought to be associated with the hypercortisolism, hypotestosteronism, and lower-than-normal melatonin levels in the active cluster patient. Future research may hold the key to a fuller explanation of the complex interaction of hormonal systems in the cluster headache.
Curr Pain Headache Rep 2006 Apr
PMID:Steroid hormones in cluster headaches. 1653 69

Paragangliomas of the head and neck arise from collections of cells from the neural crest associated with cranial or sympathetic nerves. Such lesions are rare in children. The majority of paragangliomas in the paediatric age groups have been familial, occurring in association with an adrenal pheochromocytoma. Children typically present with a neck mass and systemic evidence of catecholamine hypersecretion. We present the case of a 12-year-old boy with a history of increasing headache, drowsiness and Horner's syndrome for 8 months. The patient underwent exploration of the neck mass under general anaesthesia. The lesion was found to be in continuity with the left sympathetic chain. It was highly vascular but was removed en mass and sent for histological analysis. The histology showed that the mass was a well-circumscribed encapsulated tumour and that complete excision was achieved. The post-operative period was uneventful and the patient recovered well after the operation. On review at 6 months following surgery, his scars were maturing satisfactorily but the Horner's syndrome was persistent. Sympathetic chain paragangliomas are very rare tumours in the head and neck but should be considered in the differential diagnosis when clinical and radiographic evidence suggest a paraganglioma. The presentation is typically of a slow-growing neck mass with the presence of an ipsilateral Horner's syndrome. To our knowledge, this is the first reported case of a sympathetic chain paraganglioma in a child.
 ...
PMID:Sympathetic paraganglioma presenting with Horner's syndrome in a child. 1678 77

The first patient with chronic paroxysmal hemicrania (CPH), a 41-year-old woman, first seen in 1961, was followed until an adequate treatment was found, 12 years later. Clinically, attack frequency and duration differed widely from the general pattern of cluster headache. Ocular variables, such as intraocular pressure and corneal indentation pulse amplitudes, also differed in our case (clear symptomatic side increment during attacks) and cluster headache. Pupil reactions to directly and indirectly acting sympathicomimetic drugs were also vastly different in our case and cluster headache: no signs of Horner s syndrome in our patient, while cluster headache exhibits a "Horner-like pattern." In cluster headache, there is a relative hypohidrosis in the forehead on the symptomatic side if body temperature is increased, and a clear hyperhidrosis on direct parasympathomimetic stimulation. This was not so in our case. Indomethacin was highly effective in our case, while "cluster headache drugs," such as ergotamine/sumatriptan, were ineffective. Indomethacin was inactive in cluster headache. Accordingly, our case seemed to differ decisively from cluster headache: CPH had been discovered.
Curr Pain Headache Rep 2006 Aug
PMID:Chronic paroxysmal hemicrania: from the index patient to the disease. 1683 45

Dissection of a cervicocerebral artery (CAD) is the second leading cause of stroke at younger ages. The pathogenesis of spontaneous CAD is not fully clarified. Defective connective tissue components may cause an arteriopathy predisposing to CAD in combination with certain trigger and risk factors. The clinical spectrum includes local pain in the neck, headaches, Horner's syndrome, isolated cranial nerve deficits, and hemispheric or brainstem infarction. Noninvasively, CAD is confirmed by Duplex sonography, MRI, and MRA. There is no controlled study for best treatment or management. Rational initial empiric treatment in acute CAD to prevent secondary embolism is partial thromboplastin time-guided anticoagulation by intravenous heparin followed by anticoagulation with warfarin. Carotid surgery for treating CAD is not recommended. The duration of anticoagulation is best guided by Doppler sonography follow-up and should extend until normalization of blood flow or at least 6 months after the vessel was occluded. Caution should be recommended for exercises that involve excessive head movements. The recurrence rate for CAD is low at <1%/year except for patients with known hereditary connective tissue disorders or in cases with familial dissections.
 ...
PMID:[Clinical treatment and therapy for dissected cervicocerebral artery]. 1689 46

A 59-year-old man presented with acute onset of visual loss in his right eye. He was treated under a diagnosis of retinal artery thrombosis. Ultrasonography revealed obstruction of the ipsilateral internal carotid artery (ICA). He had no risk factor for stroke and he denied any history of trauma. Follow-up ultrasonography obtained 6 months later showed spontaneous ICA recanalization. Cerebral angiography demonstrated an arterial wall flap suggesting ICA dissection at the craniocervical junction. He then remembered suffering hemicranial headache and Horner's sign of several days' duration after jumping off a stepladder 1 year earlier. The present case is quite unusual in that persistent carotid arterial wall dissection was thought to proceed to ICA obstruction and manifested as retinal ischemia after a long asymptomatic period.
 ...
PMID:Internal carotid artery obstruction derived from persistent arterial wall dissection associated with old trivial trauma. 1693 60

A cluster headache is an attack of half-sided very strong pain in or behind an eye, lasting for up to a few hours with tearing and rhinorrhea and sometimes Horner's syndrome. The attacks occur in clusters of weeks' to some months' duration. A cluster headache is a neurovascular primary headache which seems to involve the hypothalamus. The clinical picture, diagnosis and investigations are reviewed. The attack can be treated with oxygen or subcutaneous sumatriptan, and verapamil, ergotamine and prednisolone can be successfully used for prophylaxis. Early diagnosis and specific treatment are emphazised.
 ...
PMID:[Cluster headache (Horton's headache)]. 1721 69

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.
 ...
PMID:Cervicocranial arterial dissection. 1728 90

Traumatic cervical artery dissection (TCAD) is a complication of severe blunt head or neck trauma, the main cause being motor vehicle accidents. TCAD are increasingly recognized, and incidences of up to 0.86% for internal carotid and 0.53% for traumatic vertebral artery dissections (TVAD) among blunt trauma victims are reported. Diagnostic evaluation for TCAD is mandatory in the presence of (1) hemorrhage of potential arterial origin originating from the nose, ears, mouth, or a wound; (2) expanding cervical hematoma; (3) cervical bruit in a patient >50 years of age; (4) evidence of acute infarct at brain imaging; (5) unexplained central or lateralizing neurological deficit or transient ischemic attack, or (6) Horner syndrome, neck or head pain. In addition, a number of centers screen asymptomatic patients with blunt trauma for TCAD. Catheter angiography is the standard of reference for diagnosis of TCAD. Color duplex ultrasound, computed tomographic, and magnetic resonance angiography are noninvasive screening alternatives, but each method has its diagnostic limitations compared to catheter angiography. Anticoagulants and antiplatelet drugs may prevent ischemic stroke, but bleeding from traumatized tissues may offset the benefits of antithrombotic treatment. Endovascular therapy of dissected vessels, thrombarterectomy, direct suture of intimal tears, and extracranial-intracranial bypass should be considered in exceptional cases. Neurological outcome is probably worse in TCAD compared to spontaneous CAD, although it is unclear whether this is due to dissection-induced ischemic stroke or associated traumatic lesions.
 ...
PMID:Traumatic cervical artery dissection. 1729 Jan 11

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.
 ...
PMID:Clinical manifestations of carotid dissection. 1729 Jan 13


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>