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At least 19 recordsLinked to original sources
PubMed2003

Horner syndrome.

Horner syndrome refers to the constellation of signs resulting from the interruption of sympathetic innervation to the eye and ocular adnexae. Classically, the clinical findings include a triad of ipsilateral blepharoptosis, pupillary miosis, and facial anhidrosis. The history, additional clinical examination features, and pharmacologic testing may help localize the lesion and suggest an etiology. An appropriate evaluation of Horner syndrome and a timely elucidation of the etiology may allow for a potentially life-saving intervention.

Adrenergic Uptake Inhibitors↗
PubMed1989

[Benign superior vena cava syndrome associated with Horner syndrome--report of a case].

Superior vena cava syndrome is commonly caused by malignant diseases such as lung cancer, malignant lymphoma and so forth. It is uncommon that benign diseases obstruct the superior vena cava or its major tributaries. But there are some documented cases of benign superior vena cava syndrome induced by mediastinitis, benign mediastinal tumors, and uncommon lesions having their primary origin in the mediastinum. A 41-year-old male patient had recognized his ptotic palpebra two years ago and chest roentgenographic examination disclosed a tumor shadow occupying the apex of the right thorax but he was almost asymptomatic except venous dilatation of the anterior chest wall. Venography revealed obstruction of the brachiocephalic vein and superior vena cava. At thoracotomy the tumor was found to be impacted at the apex of the thoracic fornix and to be cystic. Primary site of the tumor was at the chest wall and its histological finding was compatible with that of neurilemmoma. Postoperative venography confirmed complete patency of the brachiocephalic vein and superior vena cava.

Adult↗
PubMed2004

SUNCT syndrome in association with persistent Horner syndrome in a Chinese patient.

This is the first case report of a chinese patient with SUNCT (shortlasting, unilateral, neuralgiform headache attacks with conjunctival injection and tearing) presenting with persistent Horner's syndrome. She had episodic, brief, right periorbital pain in association with ipsilateral eye injection, lacrimation and rhinorrhea as well as persistent ipsilateral miosis and ptosis. She had partial response to a combination of indomethacin and carbamazepine therapy.

China↗
PubMed2006

Horner syndrome after sympathectomy in the thoracoscopic era.

OBJECTIVE: Horner syndrome after sympathectomy has significantly decreased in current surgical practice. This is predominantly due to refinements in operative techniques, and an improved understanding of the patterns of sympathetic outflow pathways. We present a review of our experience with this disconcerting complication of sympathectomy when undertaken for palmar hyperhidrosis. METHODS AND TECHNIQUE: Over a 12-year period (1992 to 2004), patients undergoing sympathectomy for palmar hyperhidrosis were prospectively evaluated. In all patients the thoracoscopic approach was attempted bilaterally. The technique entailed the accurate identification of the second thoracic ganglion, followed by its dissection and resection. Excessive manipulation and cautery on the sympathetic chain was avoided. RESULTS: A total of 1137 procedures were undertaken in 567 patients. In 1 patient (during the early part of the technical experience) a unilateral Horner syndrome was noted on the first postoperative day; this effect was noted to have resolved spontaneously within 6 months. Review at 3 months was possible in 382 patients, either directly or telephonically. In these patients no further case of Horner syndrome was documented. CONCLUSIONS: The key to avoiding the development of a Horner syndrome after sympathectomy entails a thorough appreciation of the appropriate surgical anatomy, avoidance of violent manipulation and traction of the sympathetic chain, and the avoidance of diathermy on the sympathetic chain. The adherence to these principles has consigned Horner syndrome after sympathectomy as an entity of historical interest.

Horner Syndrome↗
PubMed1998

Pediatric Horner syndrome.

INTRODUCTION: The purpose of this study was to define the etiologies of Horner syndrome in the pediatric population. METHODS: A retrospective review was performed of the medical records of all pediatric Horner syndrome patients (< 18 years old) examined by the pediatric ophthalmology services at two large referral centers. RESULTS: Seventy-three pediatric Horner syndrome patients were identified. Of these, 31 (42%) were congenital, 11 (15%) were acquired without surgical intervention, and 31 (42%) were acquired after a surgical procedure of the thorax, neck, or central nervous system. Of the congenital Horner syndrome patients, a history of delivery with the use of forceps, vacuum extraction, shoulder dystocia, fetal rotation, or postterm delivery was elicited in 16 patients (53%). Concomitant brachial plexus injury was identified in only 3 patients. Two patients had congenital varicella syndrome and 1 patient was diagnosed with neuroblastoma. This patient had a palpable supraclavicular mass and stridor. Diagnosis of the patients with acquired Horner syndrome included neuroblastoma (2), trauma (1), rhabdomyosarcoma (1), brainstem vascular malformation (1), disseminated sclerosis (1), and not determined (5). CONCLUSION: In children with congenital Horner syndrome, a history of forceful manipulation of the infant during birth may reduce the need for extensive systemic evaluation. Without such history, a decision to proceed with further evaluation is made with consideration of the relative incidence of neuroblastoma by age and the physical findings. All acquired pediatric Horner syndrome patients without a known etiology require thorough evaluation because of the frequent association of serious underlying disease.

Birth Injuries↗
PubMedDate not supplied

[Deferred Horner syndrome following thoracoplasty].

INTRODUCTION: Horner syndrome (HS) involves an injury affecting the ocular sympathetic nerve, which gives rise to myosis, palpebral ptosis and enophthalmos, and is accompanied by hemifacial anhidrosis in its complete forms. Its extension means that its involvement can occur in different structures and as a result of different medical and surgical processes. CASE REPORT: We describe the case of two patients who developed a subacute form of HS without involvement of the sweating process and which was not accompanied by any other clinical features affecting the orbit, neck, brain, spinal cord or of a radicular nature. Both of them had been submitted to thoracoplasty as therapy for tuberculosis over 30 years earlier. The complementary studies that were conducted did not reveal involvement of the ocular sympathetic nerve anywhere other than in the pleura. CONCLUSIONS: The lesion would have been produced in the endothoracic fascia, where the cervical sympathetic chain is closely related to the apical pleura, and the physiopathological mechanism would be fibrosis of the aforementioned structures. Many reports have been published that describe the onset of HS as an acute complication following thoracic surgery, but its late development is infrequent.

Aged↗
PubMed2005

Horner syndrome after unintended subdural block. A report of 2 cases.

Horner syndrome is considered a common finding after epidural analgesia or anesthesia in obstetric patients. Conversely, Horner syndrome is very uncommon in nonobstetric patients. We report 2 cases of Horner syndrome after attempted epidural lumbar anesthesia in 2 patients undergoing peripheral vascular surgery. Spinal fluoroscopy with contrast medium showed subdural catheterization in both cases. Horner syndrome after lumbar epidural anesthesia can be an indicator of inadvertent subdural catheter placement.

Aged↗
PubMedDate not supplied

Effect of 0.5% apraclonidine on ptosis in Horner syndrome.

To demonstrate the effect of apraclonidine on anisocoria and ptosis in Horner syndrome, one drop of 0.5% apraclonidine was instilled in both eyes of 3 patients who presented with acute Horner syndrome, and the effect on ptosis and anisocoria was documented. As reported in the literature, one drop of 0.5% apraclonidine reverses the anisocoria of Horner syndrome. In addition, 0.5% apraclonidine leads to a complete resolution of the ptosis associated with Horner syndrome, a finding reported once in the literature. Apraclonidine is a safe and readily available alternative to cocaine for the diagnosis of Horner syndrome.

Adrenergic alpha-Agonists↗
PubMed2005

Horner syndrome due to first rib fracture after major thoracic trauma.

A case of Horner syndrome diagnosed during the follow-up after major thoracic trauma is presented in this report. A 10-year-old boy was admitted to the emergency service with severe thoracic trauma with left clavicular and first rib fracture after a traffic accident. During the follow-up, myosis and ptosis were recognized in his left eye. Cranial tomography and neurological examination were all normal. The symptoms were thought to be caused by compression of the local hematoma to the cervical ganglia. After 30 days of conservative treatment with tube thoracostomies, he was discharged with his Horner syndrome. After 6 months of follow-up, the findings of Horner syndrome were found to be partially resolved. First rib fracture associated with Horner syndrome is very rarely seen in children, and only 2 cases were found in English-language literature. Our case seems to be the third reported case. Horner syndrome should be kept in mind in cases of first rib fractures. When head trauma is considered, as it can be mistaken with anisocoria, this knowledge may help the surgeon in differential diagnosis.

Child↗
PubMed2003

Horner syndrome related to ipsilateral carotid wall hematoma after stent placement for the treatment of carotid stenoses.

BACKGROUND AND PURPOSE: We prospectively studied the incidence and natural history of Horner syndrome following stent-supported percutaneous angioplasty of the carotid artery (SPAC). We assessed the hypothesis that postinterventional Horner syndrome is related to ipsilateral carotid wall hematoma. METHODS: We performed duplex sonography of the carotid arteries and clinical examination in 28 consecutive patients before and 4 hours +/- 2, 24 hours +/- 2, and 7 days +/- 1 after SPAC. RESULTS: Within 24 hours +/- 2 after SPAC, 11 of the 28 patients developed ipsilateral Horner syndrome. Ten of these 11 patients had a postinterventional sonographic appearance of a carotid wall hematoma, whereas only two of the 17 patients without Horner syndrome had this finding (P <.001). In all patients, both Horner syndrome and carotid wall hematoma had resolved 7 days +/- 1 after SPAC. CONCLUSION: Horner syndrome appears to be a common yet transient event after SPAC. Although postinterventional Horner syndrome is significantly related to ipsilateral carotid wall hematoma, causality of the procedure-related formation of a carotid wall hematoma and oculosympathetic disturbance remains unproven.

Adult↗
PubMed1992

Congenital Horner syndrome associated with non-cervical neuroblastoma.

Horner syndrome may be caused by a neuroblastoma involving the cervical sympathetic nervous system. A two-year-old girl presented with Horner syndrome and a discrete, distant neuroblastoma, suggesting that these two conditions represent a more widespread dysgenesis of the sympathetic nervous system.

Child, Preschool↗
PubMed1982

Horner syndrome during lumbar epidural analgesia for obstetrics.

Horner syndrome (ptosis, miosis, anhidrosis, and facial and conjunctival vasodilation) is a recognized complication of lumbar epidural analgesia for labor and delivery. Alone, it presents no significant risk to mother or fetus, as resolution is spontaneous and complete. Horner syndrome may, however, be associated with significant maternal hypotension and therefore should be an indication for close maternal and fetal monitoring to provide reassurance.

Adult↗
PubMed2006

Efficacy of apraclonidine 0.5% in the diagnosis of Horner syndrome in pediatric patients under low or high illumination.

PURPOSE: To evaluate the efficacy and safety of apraclonidine 0.5% in the diagnosis of Horner syndrome in pediatric patients. DESIGN: Prospective, interventional case series. METHODS: Ten pediatric patients with a diagnosis of Horner syndrome and 10 age-matched controls with physiologic anisocoria underwent pharmacological testing with apraclonidine. The difference between the pupil diameters of both eyes under low (room light off) and high (room light on) ambient illumination before and one hour after apraclonidine was instilled was recorded. Any adverse effects during the examination or reported by the patient's parents were recorded. RESULTS: The mean differences in pupil diameters before and after apraclonidine testing in the Horner syndrome group were -2.05 mm and 0.97 mm, respectively, under low illumination (P = .0049) and -1.48 mm and 1.1 mm, respectively, under high illumination (P = .0051). Three patients with Horner syndrome showed positive values (reversal of anisocoria) only under high ambient illumination, but not under low illumination. There was no statistical difference in the mean differences in pupil diameter before and after apraclonidine testing in the control group. Conjunctival hyperemia was noted in two patients with Horner syndrome and in three patients in the control group. No systemic adverse effects were noted during the examination or were reported by patients' parents. CONCLUSIONS: The application of apraclonidine in pediatric patients is safe and effective in the diagnosis of Horner syndrome. The reversal of anisocoria was more obvious under high (room light on) ambient illumination.

Adolescent↗
PubMedDate not supplied

Harlequin sign (hemifacial flushing and contralateral hypohidrosis) in a 4-year-old girl with Horner syndrome.

We report a Japanese infant with Horner syndrome whose clinical examination and testing suggested the location of the causative lesion. A 4-year-old Japanese girl had an acquired right ocular ptosis and unequal pupils presenting shortly after birth. She also exhibited left hemifacial flushing and loss of sweating on the contralateral side (harlequin sign). Physical examination demonstrated 2.0 mm of ptosis of the right upper lid with normal elevator function. The diameters of the pupils were 4 mm on the left and 2.5 mm on the right. No sweating was induced in the right frontal region at 40 degrees C for 15 minutes of sweat challenge test. Otherwise, no abnormalities were found by the neurophysiologic examinations or magnetic resonance imaging of the brain. Based on the clinical examination, we speculated that the responsible lesion might be in the preganglionic areas. Harlequin sign was informative for making the diagnosis of Horner syndrome.

Child, Preschool↗
PubMed2006

Pediatric horner syndrome: etiologies and roles of imaging and urine studies to detect neuroblastoma and other responsible mass lesions.

PURPOSE: To evaluate the frequency of etiologies of Horner syndrome in children and suggest an imaging and laboratory diagnostic protocol to evaluate for neuroblastoma and other lesions in a child presenting with Horner syndrome and no known cause. DESIGN: Retrospective chart and data review. METHODS: A retrospective review of all children seen at a large pediatric neuro-ophthalmology referral center with a diagnosis of Horner syndrome between 1993 and 2005 with particular attention to underlying etiologies and the results of imaging and urine catecholamine studies. RESULTS: Fifty-six children met criteria for Horner syndrome and further review. Twenty-eight children (50%) had no previously identified cause for Horner syndrome. Of these children, 24 (85.7%) had urine catecholamine metabolite studies, and all had negative results. Twenty (71.4%) had complete modern imaging of the brain, neck, and chest. Of the 18 children who had complete imaging and urine studies, responsible mass lesions were found in six (33%). Four had neuroblastoma, one had Ewing sarcoma, and the other had juvenile xanthogranuloma. Of all patients (diagnosis known and unknown), neoplasm was the etiology in 13 of 56 (23%) of patients. CONCLUSIONS: We confirm that Horner syndrome in a child of any age without a surgical history requires a complete examination to exclude a mass lesion. In such patients, we recommend brain, neck, and chest magnetic resonance imaging (MRI) with and without contrast as well as urinary catecholamine metabolite testing. However, imaging is more sensitive than urine testing in this setting.

Abdominal Neoplasms↗
PubMed2000

Idiopathic horner syndrome in the golden retriever.

OBJECTIVES: Various reports have noted a high incidence of idiopathic Horner syndrome in golden retriever dogs. The author seeks to document this condition in the breed. MATERIALS AND METHODS: A prospective study was made of cases of Horner syndrome in dogs referred to the author throughout a 10-year period. As part of the general clinical, ophthalmic, and neurologic examination, denervation hypersensitivity testing was performed to localize the responsible lesion. Follow-up results were obtained in all cases by repeat examination or telephone contact. RESULTS: Of 155 dogs in the study, 110 were golden retrievers, 100 of which were diagnosed as having idiopathic second order Horner syndrome. Ninety-five of the golden retrievers were male, some neutered. Signs resolved spontaneously in all cases within 6 months. CONCLUSIONS: There is a high incidence of idiopathic second order Horner syndrome in the male golden retriever.

Animals↗
PubMed2003

False negative hydroxyamphetamine test in horner syndrome caused by acute internal carotid artery dissection.

A patient with Horner syndrome from internal carotid artery dissection initially had a false negative hydroxyamphetamine test. Two months later, the ophthalmic signs had disappeared but the hydroxyamphetamine test was positive. This case illustrates that hydroxyamphetamine testing may be falsely negative in acute Horner syndrome because norepinephrine stores in oculosympathetic postganglionic terminals have not yet been depleted. However, the hydroxyamphetamine test may be positive even after the ophthalmic signs of Horner syndrome have disappeared.

Adult↗