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)

A 57-year-old man experienced daily episodes of unilateral headache accompanied by homolateral partial Horner syndrome and rhinorrhea for more than 40 years. Treatment with indomethacin eliminated these headaches. The patient's illness is best classified as "chronic paroxysmal hemicrania" as described by Sjaastad and Dale.
 ...
PMID:Chronic paroxysmal hemicrania: a disabling headache syndrome responding to indomethacin. 65 67

Since 1978, the authors have observed 7 cases of dissecting aneurysm in the internal carotid artery. Symptoms were severe headache and subsequent neurologic deficit in young persons (3 women, 4 men; mean age 35 years). The underlying pathology was spontaneous dissection of the cervical internal carotid artery, with surgical confirmation in 3 cases and typical angiographic patterns in all cases. Spontaneous dissection of the cervical internal carotid artery is being increasingly recognized as a cause of cerebral ischemia in young adults. Moreover this clinicopathologic event is more common than had previously been supposed. The etiology remains unclear, except in 15% of cases in which dystrophy of the media (Marfan's syndrome) is in cause. No history of cervical trauma can be found. Typical clinical features consist in ipsilateral headache preceding an abrupt neurologic deficit in a 40-year-old person. An incomplete Horner syndrome (oculosympathetic paresis without facial anhidrosis) associated with facial pain and numbness is pathognomonic, but the majority of dissections are less typical. The typical angiographic pattern is an elongated regular stenosis of the high cervical internal carotid artery, 2 cm above the non-involved bulbus ("string sign"). The dissection may modify to a tapered occlusion above the point of origin of the internal carotid artery. The natural course is spontaneous resolution of the stricture, without relapse. Optimal management is non-operative since medical treatment has proved to be efficient. These cases confirm the benign course and overall good prognosis of spontaneous dissections of the internal carotid artery which are not as rare as the scarcity of reports might indicate.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Spontaneous dissection of the internal carotid artery. Apropos of 7 cases and a review of the literature]. 217 45

Blood plasma beta-endorphin concentrations were measured in 87 patients with various facial and head pain syndromes: trigeminal neuralgia or neuropathy Horner syndrome and migraine, facial autonomic pains. beta-endorphin concentrations were measured before and after treatment. In the groups under investigation, the neuropeptide showed opposite changes in plasma levels after the therapy depending on the type of the syndrome.
 ...
PMID:[Beta-endorphin levels in patients with pain syndromes in the areas of the face and head]. 253 37

In younger patients, the clinical symptoms of sudden unilateral headache and facial pain, often combined with Horner syndrome and the cerebrovascular symptoms of TIAs or stroke, should indicate the diagnosis of spontaneous carotid dissection. Angiographic findings can verify this diagnosis, showing various signs of eccentric, narrowing stenosis, false lumen, pseudoaneurysms, or complete occlusion. An addition to noninvasive Doppler ultrasonography, B-mode and Duplex investigations, although more or less nonspecific, give some indications of the diagnosis; modern imaging techniques, especially MRI, can image the intramural hematoma directly. As the hematoma is the source of the intracranial emboli, the therapy of choice in this rarely diagnosed disease should be anticoagulation.
 ...
PMID:[Carotid dissections]. 267 40

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

This report concerns a 88-year-old diabetic and hypertensive woman with pontine hemorrhage who presented with Foville syndrome and contralateral hyperhidrosis. She was admitted to our hospital for sudden onset of headaches and disturbed consciousness. Neurologic examination revealed bilateral miosis, Foville syndrome and superficial hemianesthesia on the right side of the face and body. No associated Horner syndrome and other autonomic dysfunction were observed. Laboratory data were normal except for diabetic findings. Brain CT and MRI revealed a hematoma in the left side at the lower pons. One month after the onset, hemihyperhidrosis on the face, arm and upper trunk contralateral side of the lesion appeared abruptly, and gradually disappeared a week later. Sweating on the ipsilateral side was normal and no new lesion was seen on the brain CT then. Only a few cases of contralateral hyperhidrosis due to pontine lesion have been reported. We suggest that the contralateral inhibitory sweating pathway was disrupted though the ipsilateral excitatory one was intact. Contralateral hyperhidrosis attributed to imbalance of the perspiratory control can be observed in the subacute or late phase after pontine hemorrhage.
 ...
PMID:[Pontine hemorrhage presenting with Foville syndrome and transient contralateral hyperhidrosis]. 1088 41

A 50-year-old man complained of headache around his left orbit, left frontal pain and paresthesia associated with left incomplete Horner syndrome. MRI demonstrated a mass at the level of medulla oblongata. Left vertebral angiogram revealed an aneurysm of left vertebral artery. Following the removal of the aneurysm, these Raeder's syndrome-like symptoms improved. Therefore, they were probably caused by a compression of the spinal tract of the trigeminal nerve and the central sympathetic tract by the aneurysm. This is the first report of Reader's syndrome-like symptoms caused by vertebral artery aneurysm, thus indicating that MRI and cerebral angiogram are necessary for differential diagnosis of this syndrome.
 ...
PMID:[A case presenting with Raeder's syndrome-like symptoms due to vertebral artery aneurysm]. 1199 93

Cervicocephalic arterial dissections (CCAD) are an increasingly recognized cause of ischemic stroke in young adults. Various treatments have been suggested but no controlled trial has ever been performed. Medical treatment has included anticoagulant or platelet antiaggregant therapy. Surgical correction has been proposed for selected patients who have failed medical therapy. Percutaneous balloon angioplasty and stenting have been increasingly used in some patients, although long-term results are unknown. The objective of the study was to review our recent experience with the management and outcome of extracranial CCAD. We identified 27 patients with extracranial CCAD who were evaluated, treated and/or followed by our Stroke Service from September 1995 to August 2001. Clinical presentation, diagnostic evaluation, management, and outcome were reviewed. There were 15 men (56%) and 12 women (44%) with mean ages of 38 and 43 years respectively. Diagnosis was made by cerebral angiography in 15 (56%) patients and by MRI/MRA only in 12 (44%) patients. Twenty-two patients had spontaneous and five had traumatic extracranial CCAD. Most common associated disorders were arterial hypertension (37%) and migraine (26%). One patient presented only with a painful post-ganglionic Horner syndrome, another patient with neck pain and post-ganglionic Horner syndrome, another patient solely with protracted unilateral headaches, three with transient ischemic attacks (TIA), and 21 with ischemic strokes. The internal carotid artery (ICA) was the most frequently involved vessel (63%), followed by the vertebral artery (30%, and multivessel involvement in two patients (7%). Eighteen patients received anticoagulant therapy and nine platelet anti-aggregants. Follow-up extended from 2 to 115 months, with a mean of 58 months. At the end of follow-up, 23 (85%) patients had either no disability or only minor sequelae (modified Rankin score: 0 to 1), and four (15%) patients had moderate limitations (modified Rankin score: 2 to 3). Two patients had a recurrent ischemic stroke, one unrelated to recurrent CCAD, and the other following percutaneous balloon angioplasty/stenting for treatment of a persistent vertebral artery pseudoaneurysm. Most CCAD involved the extracranial ICA. The clinical presentation is variable, most patients having an ischemic stroke or TIAs. The short- and long-term outcome are usually favorable with either anticoagulant or platelet antiaggregant therapy. A medical initial approach to the management of extracranial CCAD is recommended for most patients.
 ...
PMID:Outcome of extracranial cervicocephalic arterial dissections: a follow-up study. 1206 89

A 47-year-old woman presented with headache, acute monocular vision loss, and ipsilateral Horner syndrome. Apart from the optic neuropathy, all cranial nerve function was intact. Magnetic resonance imaging revealed an enlarged pituitary gland with compression of the orbital apex. The surgical specimen was consistent with pituitary apoplexy. The combination of headache, acute visual loss, and ipsilateral Horner syndrome without ophthalmoplegia, which may suggest carotid artery dissection, is evidently an unusual manifestation of pituitary apoplexy.
 ...
PMID:Pituitary apoplexy causing optic neuropathy and horner syndrome without ophthalmoplegia. 1450 93

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


1 2 3 4 Next >>