Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Congenital Horner's syndrome is an infrequent illness caused by a lesion of the cervical sympathetic nerve fiber. It's clinical features are facial anhidrosis, ptosis, miosis, and hypochromia iridis of the affected side. The subject of this report, a full-term male newborn, had had a smooth birth process but was found on the second day of life to have narrowing of the palpebral fissure and absence of facial flushing on the right side when he cried. Ophthalmologic examination revealed a smaller right pupil. The above abnormalities proved to result from a post-ganglionic lesion, after pharmacologic test. Roentgenograms of the skull, chest and cervical spine were normal, and a computed tomography scan of the cervical spine showed no abnormalities. The diagnosis was of congenital Horner's syndrome. Since no congenital Horner's syndrome to the newborn period could be found in previous literature, this report is presented.
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PMID:Congenital Horner's syndrome: report of one case. 151 4

Two patients with congenital Horner's syndrome had unilateral facial flushing. Both showed pupillary supersensitivity to epinephrine as well as anhidrosis on the affected side of the face and neck. Facial skin temperature after exercise increased on the intact side, but decreased on the affected side. Thermal vasodilation in the major portions of the face is regulated by sympathetic vasodilator fibres, and less predominantly by adrenergic vasoconstrictor fibres. The asymmetry of facial flushing may have been caused by impaired sympathetic vasodilation and further intensified by active vasoconstriction due to supersensitivity to circulating catecholamine on the affected side.
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PMID:Congenital Horner's syndrome with unilateral facial flushing. 230 38

A 54-year-old man was admitted to our hospital because of a persistent pain of the left cervix and scapular region of three-month duration and an abnormal shadow in the chest roentgenograms. Neurological examinations, chest roentgenograms, chest CT scanning, vertebral tomograms and myelogram revealed Pancoast's syndrome concomitant with Horner's syndrome. Four months later, the patient complained of a sudden onset of unilateral flushing and sweating appearing on the right face, cervix and upper chest. Eye drop tests with cocaine, epinephrine and tyramine indicated the lesion of ciliospinal centers between the 8th cervical and 2nd thoracic spines. The unilateral flushing and sweating attack appearing on the intact side without Horner's syndrome seemed to be an excessive response by an intact sympathetic pathway, the other side failing to respond because of a sympathetic deficit.
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PMID:[Harlequin syndrome (unilateral flushing and sweating attack) due to a spinal invasion of the left apical lung cancer]. 233 28

Facial flushing and sweating were investigated in five patients who complained of the sudden onset of unilateral facial flushing in hot weather or when exercising vigorously. One patient probably suffered a brainstem infarct at the time that the unilateral flush was first noticed, and was left with a subtle Horner's syndrome on the side opposite to the flush. The other four had no other neurological symptoms and no ocular signs of Horner's syndrome. Thermal and emotional flushing and sweating were found to be impaired on the non-flushing side of the forehead in all five patients whereas gustatory sweating and flushing were increased on that side in four of the five patients, a combination of signs indicating a deficit of the second sympathetic neuron at the level of the third thoracic segment. CT and MRI of this area failed to disclose a structural lesion but latency from stimulation of the motor cortex and thoracic spinal cord to the third intercostal muscle was delayed on the non-flushing side in one patient. The complaint of unilateral flushing and sweating was abolished in one patient by ipsilateral stellate ganglionectomy. The unilateral facial flushing and sweating induced by heat in all five patients was thus a normal or excessive response by an intact sympathetic pathway, the other side failing to respond because of a sympathetic deficit. The onset in the four cases of peripheral origin followed strenuous exertion, which suggested that an anterior radicular artery may have become occluded at the third thoracic segment during torsion of the thoracic spine.
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PMID:Harlequin syndrome: the sudden onset of unilateral flushing and sweating. 180 67

Sweating and flushing of the forehead and cheeks in response to body heating, embarrassment and strong gustatory stimulation were investigated in 23 patients with a unilateral lesion in the sympathetic pathway to the face. A lesion anywhere along this pathway impaired thermoregulatory sweating and flushing on the denervated side of the forehead in most patients and also of the cheek in some cases. Emotional sweating was also diminished on the denervated side of the forehead irrespective of the site of lesion, but impairment of emotional vasodilatation was noted only with peripheral (second or third neuron) lesions. These findings suggest that sympathetic vasodilator fibres accompany vasoconstrictor and sudomotor fibres through conventional sympathetic pathways to the face. Gustatory sweating and flushing were symmetrical in most patients but flushing was more marked on the denervated side in three cases. Gustatory sweating was accompanied by flushing on the denervated side of the forehead in one patient following section of the T2 and T3 roots. It is concluded that the cervical sympathetic outflow is the main pathway for thermoregulatory flushing and emotional blushing and that diminution or absence of such vasodilator reactions is a usual component of Horner's syndrome unless the responsible lesion is confined to the first thoracic root. Gustatory vasodilatation and sweating is preserved and becomes exaggerated in some instances.
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PMID:Facial flushing and sweating mediated by the sympathetic nervous system. 358 Aug 35

When trying to establish the likely anatomical site (preganglionic or postganglionic) of a lesion causing congenital Horner's syndrome, the distribution of facial flushing (the "harlequin" sign), may be seen. In babies and young children, facial flushing is a relatively simple clinical sign to demonstrate, compared with facial sweating. In unilateral facial flushing the areas that do not flush are almost always identical to the anhidrotic areas. However, neither facial flushing nor testing the pupil reactions with pholedrine or hydroxyamphetamine can be relied on to predict the probable site of any lesion causing congenital Horner's syndrome. Two patients with congenital Horner's syndrome are presented which demonstrated the "harlequin" sign and in whom clinical examination and pharmacological testing gave conflicting evidence for localisation of the site of the causative lesion. The presentation of congenital Horner's syndrome should be investigated and include MRI or CT to exclude a serious underlying cause.
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PMID:The "harlequin" sign and congenital Horner's syndrome. 921 51

A 37-year-old woman with a 5-year history of multiple sclerosis is reported. She began having recurrent syncope even in the sitting position; other neurological features included hiccup, faciooro-lingual flushing and clumsiness of the hands. She had alternating Horner's syndrome, mild hypoalgesia of the right face, exaggerated deep tendon reflexes of the upper extremities, decreased deep sensation and ataxia of the upper extremities, and incomplete transverse myelopathy with a T4 sensory level. Head-up tilt testing confirmed orthostatic hypotension with relative preservation of the heart rate increase. Magnetic resonance imaging indicated abnormal intensities in the paramedian tegmentum and base of the medulla, which may have been additionally responsible for orthostatic hypotension. Steroid pulse therapy and L-threo-3,4-dihydroxyphenylserine caused regression of brainstem signs and reduced syncopal attacks.
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PMID:Orthostatic hypotension in a case with multiple sclerosis. 923 62

Harlequin syndrome is an autonomic syndrome of heat, emotion and exercise induced flushing and sweating limited to one side of the face in combination with impairment of sweating and flushing on the contralateral side, Two women aged 32 and 39 years displayed this syndrome. In one patient no other neurological symptoms were found; MRI of cervicothoracic spine failed to disclose a structural lesion. The second patient had four years before presented with a Horner's syndrome on the contralateral side, where MRI now disclosed a tumour located in the paravertebral thoracic region at the apex of the lung.
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PMID:[Harlequin syndrome]. 955 41

Asymmetrical facial sweating and flushing has been named the "Harlequin Sign". This is a rare feature, as evident from only 12 cases described up to date. The "Harlequin Sign" represents a local autonomic dysfunction due to a cervical sympathetic deficit located at the pre or postganglionic level on the non-flushing side. We observed slow onset and progression of the "Harlequin Sign" in a 19-year-old man, with preexisting slight miosis on the non-flushing side. The differential diagnosis included other forms of dysautonomia and a secondary origin of this partial Horner's syndrome. Both pupils normally reacted to light, convergence, and pilocarpine eye-drop instillation, but the affected side showed supersensitivity to phenylephrine. Deep tendon reflexes were normal, thus excluding Adie's syndrome. The absence of cholinergic supersensitivity in the iris muscles indicated normal function of the ciliary ganglion and excluded the ocular parasympathetic deficit, also evident for the coexisting Horner's syndrome. The clinical features could be explained by assuming that the lesion was located at the level of postganglionic sympathetic fibers, probably due to trans-synaptic postganglionic neuronal degeneration at the level of the stellate ganglion, thus determining the onset of the hemifacial symptoms.
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PMID:The "Harlequin Sign". Case description and review of the literature. 985 75

Ear cleaning helps maintain the normal otic environment and is important in the treatment of otitis. Over cleaning, however, may trigger otitis through maceration of the epidermal lining. Simple manual cleaning is useful for routine cleansing but doesn't remove tightly adherent debris. Bulb syringes are more vigorous but may damage the ear in inexperienced hands. Devices using mains water pressure or dental machines are also available. Thorough cleaning of the ear canals and middle ear cavity can only be achieved by retrograde flushing using specially adapted catheters, feeding tubes or video otoscopes under anaesthesia. Myringotomy, inspection and cleaning of the middle should be performed if the tympanic membrane appears abnormal. There are a wide variety of cleaning fluids available. Ceruminolytics soften and dissolve cerumen to facilitate cleaning. Surfactants emulsify debris, breaking it up and keeping it in solution. Astringents dry the ear canal surface, preventing maceration. Maintaining a low pH and incorporating antimicrobial agents can inhibit microbial proliferation and glucocorticoids can be used to reduce inflammation. Adverse effects and contraindications following ear cleaning can include maceration, contact reactions, otitis media, ear canal avulsion, vestibular syndrome, Horner's syndrome, facial nerve paralysis and deafness. Care should be exercised in selecting cleaning fluids if the tympanic membranes are ruptured.
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PMID:Ear cleaning: the UK and US perspective. 1503 May 61


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