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

Thirty-two cluster headache patients and healthy controls (n = 16-20 for the various tests) were examined by means of a Whitaker pupillometer during pain-free intervals. Eye drops of the sympathomimetic agents tyramine, hydroxyamphetamine, and phenylephrine were instilled into the conjunctival sacs on separate occasions, and pupillary diameters recorded at standard time intervals. The mydriatic responses of the two pupils were compared. A moderate, but statistically significant, basal relative miosis was found on the pain side in cluster headache. The symptomatic-side pupils were less responsive than their counterparts when stimulated with tyramine and hydroxyamphetamine, the difference being statistically significant for the OH-amphetamine test. With the phenylephrine test, however, the mydriasis on the symptomatic side significantly exceeded that of the contralateral pupil. This pattern of reactions does not quite correspond to those of "ordinary" Horner's syndrome (1st, 2nd, and 3rd neuron lesion). There are, however, gross similarities with the recently reported pattern in central sympathetic neuron dysfunction. In cluster headache there is probably a "Horner-like picture" rather than a proper Horner's syndrome.
Cephalalgia 1987 Dec
PMID:Cluster headache pathogenesis: a pupillometric study. 342 28

Spontaneous dissection of the internal carotid artery as a cause of Horner's syndrome has only been recognized in recent years. The authors describe three patients with this condition. Associated symptoms included ipsilateral orbital and frontal headache (3 patients), neck and facial pain (2), amaurosis fugax (1), and dysgeusia (1). The symptoms resolved in all patients within three months, yet oculosympathetic paralysis has persisted. Diagnosis of carotid dissection required cerebral arteriography, and the angiographic features are presented. Patients were treated with platelet antiaggregants, and they have remained neurologically stable during follow-up (mean, 12 months; range, 10-14 months).
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PMID:Painful Horner's syndrome due to spontaneous carotid artery dissection. 358 97

Eight patients with Horner's syndrome (five with a 1st neuron lesion and three with a 2nd neuron lesion) were examined for their pupillary responses to pharmacologic stimulation with tyramine (2%) and with phenylephrine (1%) eye drops. The same patients were also evaluated for their forehead sweating pattern on stimulation with body heating and pilocarpine injection, using the Evaporimeter. Five patients had a brain stem (1st sympathetic neuron) lesion, while three patients had had a traumatic C8-Th1 root avulsion and hence had a preganglionic neuron lesion. The average response with the phenylephrine eye test and the pilocarpine sweat test differed markedly between the two groups; only the central neuron lesion group had a supersensitivity reaction to both drugs. These procedures may be of diagnostic value in localizing the lesion in patients with a Horner's syndrome of unknown etiology. Patients with 3rd neuron lesion have not been examined with this combination of techniques.
Cephalalgia 1987 Jun
PMID:Sweat gland and pupillary responsiveness in Horner's syndrome. 360 67

The term "Raeder's syndrome," which now seems to mean any painful postganglionic Horner's syndrome, has been used in the past to describe patients with a wide variety of underlying pathology, including such serious lesions as middle cranial fossa neoplasms and such benign conditions as unilateral vascular headache syndromes. The purpose of this review which is based on the literature and some recent experience with 41 cases of Raeder's syndrome, is to help clarify this syndrome and to aid the clinician in its evaluation and treatment. Patients with Raeder's syndrome have been divided into three major groups. In the first group, the painful postganglionic Horner's syndrome is associated with multiple parasellar cranial nerve involvement and these patients require full neuroradiological investigation to uncover such lesions as local or metastatic tumors within the middle cranial fossa. The second and third groups do not have the multiple cranial nerve damage and their prognoses are benign. The characteristics, clinical investigation and medical therapy of each of these two benign groups are outlined and discussed. Extensive neuroradiological investigation is not recommended for patients in the second or third groups. Common to all three groups of Raeder's syndrome is the association of unilateral headache with the interruption of the postganglionic oculosympathetic fibers along the course of the internal carotid artery.
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PMID:Raeder's syndrome. A clinical review. 624 81

We studied 12 patients with intracerebral hemorrhage in the head of the caudate nucleus. These cases accounted for 7% of a consecutive series of intracerebral hemorrhage. The clinical findings differed from more common varieties of supratentorial hemorrhage. All patients had acute onset of vomiting, headache, stiff neck, decreased level of consciousness, and behavioral changes in a pattern that simulated subarachnoid hemorrhage. Seven patients had gaze paresis and hemiparesis, with or without sensory loss. Two of these seven patients had, in addition, elements of Horner's syndrome. The prognosis for recovery was good. No patient had recurrent hemorrhage or persistent hydrocephalus.
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PMID:Caudate hemorrhage. 650 25

A 35-year-old woman had partial, right-sided Horner's syndrome seven years prior to admission. Facial sweating was normal. Ipsilateral headache and facial pain followed a year later. Three months before admission a left-sided carotid body tumor was resected successfully. Soon thereafter, a mass was noted below the right mandibular angle and carotid angiography showed features typical of a carotid body tumor at the carotid bifurcation. To our knowledge this is the first report of such a lesion causing Raeder's syndrome. Review of other reported cases of this usually benign syndrome shows that some may be associated with serious but treatable diseases of the internal carotid artery.
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PMID:Carotid body tumor associated with partial Horner's syndrome and facial pain ('Raeder's syndrome'). 661 87

The angiographic, clinical, and genetic characteristics of fibromuscular dysplasia (FMD) are reviewed in 37 patients (mean age 48 years) selected from a pool of 4000 angiograms of carotid or vertebral arteries. FMD was a neglected pathogenic factor in 28 patients with hemorrhagic or ischemic cerebral lesions. The aneurysms found in 19 patients had conventional appearance and were mainly located in the internal carotid or middle cerebral arteries and on the same side as the most affected cervical artery, which suggests that aneurysms and FMD are pathogenically related. A clinical syndrome is presented where headache, ECG-abnormalities, hypertension, mental distress, tinnitus, vertigo, arrhythmia, TIA, and syncope are frequent components. Hemicrania, sometimes combined with ipsilateral Horner's Syndrome, was found in patients with advanced lesions in the carotid artery of the same side. An associated occurrence of stroke in pedigrees, especially among young and middle aged females, indicates that FMD in the majority of cases in inherited as an autosomal dominant trait with reduced penetrance in males.
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PMID:Fibromuscular dysplasia and the brain. I. Observations on angiographic, clinical and genetic characteristics. 706 80

The differential diagnosis of chronic facial pain is facilitated by a knowledge of anatomy. Nasal and dental conditions are prevalent causes of facial pain. Orbital discomfort with ophthalmoplegia or Horner's syndrome generally has a vascular etiology. The lower-half headache or atypical facial neuralgia also is vascular in origin and should be referred to as facial migraine. Previously, chronic iatrogenic trigeminal neuralgia has been erroneously included in the category of lower-half headaches. This disabling condition is due to repeated trauma to the trigeminal nerve.
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PMID:Differential diagnosis of chronic facial pain. 723 31

The clinical and therapeutic aspects in 26 patients with cluster headache are reported. The patient's age ranged between 14 and 60 years old (average 31.5 years); 22 were male and 4 female. The patients constituted a consecutive series of typical cases (only one was a chronic cluster) with regular headache attacks; in 69.2 per cent of the cases there were associated symptoms and signs (ipsilateral lacrimation, stuffiness of the ipsilateral nostril and Horner's syndrome). In seven patients the cluster was induced by alcohol ingestion (during an active cluster period) and a cluster attack was reproduced by isosorbitol dinitrate (vasodilator drug) in one patient. All patients received orally either methysergide maleate, prednisone or both. The first drug used, in 20 patients, was methysergide maleate in a dosage of 3--6 mg daily over a four weeks period. Eight patients received prednisone only, which presented side-effects or no improvement with methysergide, in a dosage of 40--60 mg daily and tapered off over a period of four weeks. Methysergide maleate and prednisone were given to 11 patients in association, because of moderate effect of the first drug. The clinical effect of the treatment was judged according to the following three categories: freedom from the attacks; slight improvement of the attacks; no improvement of the attacks. In 57.6 per cent of the cases (15 patients) there was freedom of the attacks, in 30.7 per cent of the cases (8 patients) there was a slight improvement and in 3 patients there was no improvement.
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PMID:[Cluster headache: clinical and therapeutic aspects in 26 cases]. 746 27

A 52-year-old man presented with unilateral left periorbital and frontotemporal pain associated with a partial ipsilateral Horner's syndrome of the postganglionic type and representing a pericarotid syndrome. MRI demonstrated a perivascular subacute hematoma at the level of the cervical portion of the left internal carotid artery with a markedly reduced flow-void signal. MR angiography confirmed the narrowed lumen of the dissected cervical internal carotid artery. There was also a right-sided precavernous carotid aneurysm. Three months later the left-sided pain had subsided, with complete resolution of the hematoma and incomplete restoration of the left carotid lumen seen on MR angiography. Dissection of the carotid wall may cause the oculosympathetic paralysis by producing a lesion of the superior cervical ganglion, the internal carotid nerve, or the perivascular sympathetic plexus. Whereas in pericarotid syndrome the most common cause is cervical carotid dissection, Raeder's syndrome additionally involving parasellar cranial nerves, may be caused by any paracavernous/cavernous lesion, including neoplasms and intracranial carotid aneurysms. The clinical distinction is useful to determine the appropriate diagnostic investigation, in view of the different pathoanatomical localization and different disease spectrum. As demonstrated in the present case, the combination of MRI and MR angiography is a reliable noninvasive tool to investigate the differential diagnosis of pericarotid syndrome, accurately depicting occlusive, stenotic or aneurysmal lesions of the carotid artery. We suggest that intraarterial angiography is no longer necessary.
Headache 1995 Mar
PMID:Noninvasive investigation of pericarotid syndrome: role of MR angiography in the diagnosis of internal carotid dissection. 772 79


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