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Results for “HORNER SYNDROME”

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PubMed2007

Neuroimaging strategies for three types of Horner syndrome with emphasis on anatomic location.

OBJECTIVE: The purposes of this study were to review the anatomy of the oculosympathetic pathway, to describe the clinical characteristics of the three types of Horner syndrome, and to illustrate underlying pathologic features with an emphasis on neuroimaging strategies based on three symptom complexes. CONCLUSION: Horner syndrome results from interruption of the oculosympathetic pathway and is usually associated with unique clinical features classified into central, preganglionic, and postganglionic types according to the anatomic location of the underlying pathologic process.

Adult↗
PubMed1987

Shot in the neck in Spain (a rare cause of an isolated Horner's syndrome).

Horner's syndrome is rare. A bullet wound in the neck is a rare cause of the syndrome, and it is exceedingly uncommon for a Horner's syndrome to be the sole noteworthy clinical result of a gunshot wound of this part of the anatomy. Two cases of bullet injury of the neck are described wherein a permanent Horner's syndrome was the only important sequel.

Adult↗
PubMedDate not supplied

A case of Horner syndrome with intermittent mydriasis in a patient with hypoplasia of the internal carotid artery.

We report a rare case of hypoplasia of the right internal carotid artery (ICA) with ipsilateral congenital Horner syndrome. The etiology and pathogenesis of hypoplasia of the ICA is not well understood. Multiple types of collateral flow have been reported to develop to maintain blood supply to the ipsilateral cerebral hemisphere. Although collateral flow may allow these patients to remain asymptomatic, we postulate that the enlarged posterior communicating artery (PcomA) in our patient caused mass effect on the cisternal segment of cranial nerve III causing intermittent mydriasis apart from Horner syndrome.

Adolescent↗
PubMed1986

Topographic analysis of Horner's syndrome.

Horner's syndrome or oculosympathetic paralysis is not an uncommon finding in patients with head and neck neoplasms. While in most cases the syndrome is easily established at the bedside, it can be confirmed and topographically defined as a central, preganglionic, or postganglionic lesion through sequential pharmacologic testing. The importance of such localization lies in differentiating neoplasia vs. a benign condition as the cause of the syndrome. Such variants as congenital Horner's, an alternating Horner's, and a pseudo-Horner's syndrome are discussed in regard to their differential features.

Cocaine↗
PubMed2000

Ocular effects of apraclonidine in Horner syndrome.

OBJECTIVE: To determine the location of action of apraclonidine, an alpha-adrenergic receptor agonist that reduces aqueous production and lowers intraocular pressure (IOP). METHODS: The study cohort consisted of 6 patients with Horner syndrome (decreased or absent sympathetic innervation of 1 eye). We instilled 1% apraclonidine into the affected eye, and the changes in IOP and pupil diameter (PD) of both eyes were measured over 4 hours. In a separate session, apraclonidine was instilled into the normal eye and the measurements were repeated. RESULTS: The average baseline IOP was 16.3 mm Hg for affected eyes and 16.7 mm Hg for normal eyes. The average maximum ipsilateral reduction in IOP was 5.8 mm Hg in affected eyes and 5.2 mm Hg in normal eyes; this difference was not statistically significant. The average baseline PDs for affected and normal eyes were 3.2 mm and 4.2 mm, respectively. Instillation of apraclonidine into affected eyes produced mydriasis of 1.0 to 4.5 mm; baseline anisocoria reversed in all patients. There was no significant change in the PD of normal eyes after ipsilateral instillation of apraclonidine. CONCLUSIONS: Apraclonidine's major site of pharmacologic action for reduction of aqueous production is on postjunctional alpha(2) receptors in the ciliary body. The up-regulation of alpha receptors that occurs with sympathetic denervation unmasks apraclonidine's alpha(1) effect, which clinically causes pupil dilation. Apraclonidine may be a useful medication for the diagnosis of Horner syndrome. Arch Ophthalmol. 2000;118:951-954

Adrenergic alpha-Agonists↗
PubMed2001

Duration of positive urine for cocaine metabolite after ophthalmic administration: implications for testing patients with suspected Horner syndrome using ophthalmic cocaine.

PURPOSE: To determine the duration of positive urine for benzoylecgonine, the major metabolite excreted in the urine, after topical ophthalmic administration of cocaine as one would perform for testing the presence of Horner syndrome. METHODS: Two drops of cocaine 10% were applied to each eye of 50 normal subjects. Urine samples were collected 4 to 6, 24, 48, 72, and 96 hours later. Each sample was assayed for benzoylecgonine using a screening competitive enzyme donor immunoassay followed by a highly specific and sensitive confirmatory gas chromatography-mass spectrometry assay. We employed assays and cutoff levels that fulfilled guidelines required by the Substance Abuse and Mental Health Services of the United States Department of Health and Human Services to mimic measures that exist for federal workplace drug testing. RESULTS: Of the 50 subjects, there were 25 women and 25 men, ranging in age from 19 to 59 years (median age, 40 years). Positive screening samples were obtained in 47 of 50 subjects (94%) 4 to 6 hours, 35 of 50 (70%) 24 hours, and 1 of 50 (2%) 48 hours after topical application of cocaine. None of the samples tested positive at 72 hours or beyond. Using the confirmatory assay's cutoff as the gold standard for a positive test, the sensitivity of the screening assay was 96% 4 to 6 hours, 90% 24 hours, and 14% 48 hours after topical application. Urine benzoylecgonine concentration was negatively correlated with body mass index and positively correlated with urine creatinine concentration. CONCLUSIONS: Patients should be informed that their urine may test positive for cocaine, if assayed according to US federal guidelines and using the protocol employed in this study, up to 2 days after undergoing testing for Horner syndrome.

Adult↗
PubMed2005

Abducens nerve palsy and Horner syndrome due to metastatic tumor in the cavernous sinus.

A 41-year-old man was diagnosed as having primary parotid carcinoma on the right side. After radical parotidectomy, radiation therapy and systemic chemotherapy, the primary parotid carcinoma was completely remitted. Two years later, right abducens nerve palsy and Horner syndrome appeared. Neuroimaging demonstrated a gadolinium-enhanced lesion in the posterior portion of the right cavernous sinus, and metastasis of parotid carcinoma was suspected. After radiosurgery and systemic chemotherapy, the intracavernous lesion disappeared. This is the first case of combination of abducens nerve palsy and ipsilateral Horner syndrome due to metastasis from parotid carcinoma to the cavernous sinus.

Abducens Nerve Diseases↗
PubMedDate not supplied

[Horner syndrome as the first symptom of nasopharyngeal cancer. Two case reports].

INTRODUCTION: Horner syndrome (HS) is produced by damage to the oculosympathetic pathway and gives rise to palpebral ptosis, enophthalmos and myosis. Anhidrosis also occurs in cases in which the lesion is located before the separation of the vasomotor and sudomotor fibres at the start of the internal carotid artery. Nasopharyngeal cancer may damage the cranial nerves, mainly in the cavernous sinus, and very few cases of HS due to infiltration of the tumour into the parapharyngeal space have been reported. CASE REPORTS: Case 1: a 67-year-old male with a 10-day history of HS on the left side without anhidrosis. The aetiological study revealed a nasopharyngeal lymphoepithelioma; the tumour became smaller and HS disappeared following treatment with chemotherapy. Case 2: a 48-year-old male with a 1-week history of HS without anhidrosis, and a 2-month history of deafness and pain in the right ear. The aetiological study showed a nasopharyngeal lymphoepithelioma and serous otitis. The tumour became smaller and HS disappeared following treatment with chemotherapy. CONCLUSIONS: It is important to carry out studies of the nasopharynx in patients with this syndrome to allow early diagnosis and treatment of a region that is not readily available for direct examination. The existence of an associated pathology in the ear or the paranasal sinuses strongly suggests that its origins lie in the nasopharynx.

Aged↗
PubMed1995

[Horner syndrome following insertion of a chest tube].

We describe a case of Horner syndrome following insertion of a chest tube in a 27 year old male. The syndrome was discovered the day after insertion of the tube and persisted for at least three months. By the time of a control examination six months after insertion the symptoms had disappeared. Caution must be taken when inserting a chest tube. Pressure of the tip of the tube against the thoracic aperture should be avoided.

Adult↗
PubMed2007

[Dysgenesis of the carotid artery associated with congenital ipsilateral Horner syndrome].

We report a case with dysgenesis of the carotid artery associated with congenital Homer syndrome. A 6-year-old boy, who had undergone surgical repair for pulmonary atresia, ventricular septal defect, and patent ductus arteriosus at 20 months of age, presented with miosis of the left eye, and anhidrosis of the left face, neck, and shoulder girdle. Since the anhidrosis was obvious in early childhood, he was suspected as having congenital Horner syndrome. Cranial and cervical CT showed unpredicted abnormalities of the left carotid arteries, including the absence of an internal carotid artery (ICA), and hypoplasia of the common carotid and external carotid arteries. The anterior and middle cerebral arterial flow was supplied through the communicating arteries. Congenital agenesis of the ICA was highly suspected, because the left carotid canal could not be discerned at all. The concurrence of agenesis of ICA with ipsilateral Horner syndrome is accounted for by simultaneous organogenesis of the carotid artery and cervical sympathetic nerve, both of which are derived from neural crest cells. Developmental anomalies of the cervical neural crest, though rare, should be included in the differential diagnosis of congenital Homer syndrome.

Carotid Artery, Internal↗
PubMed2003

Restoration of involuntary tonic contraction of the levator muscle in patients with aponeurotic blepharoptosis or Horner syndrome by aponeurotic advancement using the orbital septum.

Müller's muscle can be thought of as a large serial type of muscle spindle of the levator muscle. Effective stretching of the mechanoreceptor in the proximal part of Müller's muscle by voluntary phasic contraction of the levator muscle for initial opening of the eye induces involuntary tonic contraction of the levator muscle as a stretch reflex via the mesencephalic trigeminal nucleus, to maintain an adequate visual field. After disinsertion of the levator aponeurosis from the tarsus by habitual rubbing, elongation of Müller's muscle secondary to thinning (aponeurotic blepharoptosis) or paralysis (Horner syndrome) desensitises the mechanoreceptor of Müller's muscle, resulting in blepharoptosis. Shortening of the elongated and thinned Müller's muscle by instillation of phenylephrine, and surgical shortening, and fixation of the disinserted, elongated, and thinned aponeurosis using the orbital septum, restored involuntary tonic contraction of the levator muscle in nearly all of 2000 patients with aponeurotic blepharoptosis and in 11 patients with Horner syndrome.

Adolescent↗
PubMed1983

[Congenital Horner syndrome].

The authors report a case of congenital Horner's syndrome. Through ophthalmological tests, it is realized a comparative study between a patient with congenital Horner's syndrome and a patient who is a carrier of this syndrome acquired by a cervical sympathectomy. We have come to the conclusion that possibly there is a congenital lesion ea the third sympathetic neuron.

Child↗
PubMed2000

Recognizing Horner's syndrome.

Horner's syndrome is a dramatic finding identified by perianesthesia nurses after regional anesthesia. This article describes the relationship between Horner's syndrome and regional anesthesia while explaining the signs and symptoms as they relate to blockade of the sympathetic nervous system.

Adult↗
PubMedDate not supplied

Congenital horner syndrome and hemiplegia secondary to carotid dissection.

A 5-month-old infant had right Horner syndrome and left hemiplegia. Magnetic resonance imaging confirmed smaller cerebral hemisphere and magnetic resonance angiography showed reduced blood flow in the internal carotid artery on the right. A diagnosis of congenital hemiplegia and carotid occlusion secondary to maternal trauma during pregnancy was made.

Accidents, Traffic↗