Cases reported "Horner Syndrome"

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1/8. Pitfalls in the interpretation of MIBG scans in cervical neuroblastoma.

    Cervical neuroblastoma (CNB) is relatively rare, accounting for less than 5% of these tumors. Because it arises from the cervical sympathetic chain, complete resection will leave the child with Horner's syndrome in a high proportion of cases. Advances in technology have allowed for the development of diagnostic and imaging modalities more specific to the disease. One of these has been the advent of radiolabeled meta-iodobenzylguanidine (MIBG) to assess the primary tumor and focal metastatic involvement. This nuclide is also taken up by normal salivary-gland tissue; this may be altered, however, in the presence of sympathetic denervation. We present a case of a primary CNB associated with Horner's syndrome, which led to confusion in interpretation of the subsequent MIBG scan. We alert the reader to potential pitfalls in the use of this examination in this disease entity.
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2/8. Acquired Horner's syndrome: clinical review.

    BACKGROUND: Horner's syndrome results from disruption of the sympathetic innervation to the eye anywhere along its three-neuron circuit. It is essential to be familiar with the oculosympathetic pathway, the structures that are in close proximity to it, and the disease processes that may interrupt it when an evaluation is made of an acquired Horner's syndrome, since it may be a manifestation of a life-threatening condition. case reports AND DISCUSSION: Four patients with acquired Horner's syndrome resulting from various etiologies are presented. The first case is that of a 41-year-old man with a history of central retinal artery occlusion and Horner's syndrome caused by an internal carotid dissection. The second patient, a 51-year-old man with a Pancoast tumor, initially went to his chiropractor with sympyoms of weakness and pain in the upper extremity. The third case involves a 49-year-old woman with an enlarged thyroid gland. The fourth patient is a 70-year-old man with a history of a stellate ganglionectomy. The sympathetic pathway to the eye, its anatomical correlates, pharmacologic testing, and the systemic diseases that may cause Horner's syndrome are reviewed. CONCLUSION: Familiarity with the sympathetic pathway to the eye and its anatomical relationships enables one to understand the mechanism by which a Horner's syndrome has developed.
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3/8. pituitary apoplexy causing optic neuropathy and horner syndrome without ophthalmoplegia.

    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.
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4/8. Reversible Horner's syndrome and dysthyroid ocular myopathy associated with Hashimoto's disease.

    BACKGROUND: Although it has been frequently stated that thyroid disease induces Horner's syndrome, there have been few reports describing the anatomical relation of goiter to the cervical preganglionic sympathetic nerve fibers in acquired Horner's syndrome, which is identified by the eye-drop test for adrenergic sensitivity. CASE: A 40-year-old woman with Hashimoto's disease presented with vertical diplopia, and blepharoptosis and miosis on the left side. OBSERVATIONS: Computed tomography scan showed hypertrophy of the right inferior rectus muscle, which resulted from a dysthyroid process, causing the limitation of upward movement of the right eye. The eye-drop test for adrenergic sensitivity revealed that only the left pupil dilated significantly after administration of 5% tyramine, and the Mueller's muscle on the left side did not respond. These results suggest that Horner's syndrome was due to a preganglionic sympathetic lesion. magnetic resonance imaging (MRI) of the neck showed chronic inflammatory lesions in both lobes of the thyroid gland identified by a high-intensity signal. CONCLUSION: The reconstruction technique of MRI demonstrated that the swollen left lobe of the thyroid gland was compressing the pathway of the cervical preganglionic sympathetic nerve fibers.
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5/8. Asymmetry of salivary gland I123 metaiodobenzylguanidine (MIBG) uptake in a patient with cervical neuroblastoma and Horner's syndrome--possible etiologic mechanisms.

    Horner's syndrome may be due to a variety of serious underlying disorders including cervical neuroblastoma. Horner's syndrome results from a unilateral disruption of the sympathetic innervation to the head and neck. We report a patient with cervical neuroblastoma in whom post operative metaiodobenzylguanidine (MIBG) scans showed a striking decrease in uptake in the ipsilateral salivary glands. Since the bio-distribution of I123 metaiodobenzylguanidine in the salivary glands in also dependent on sympathetic innervation, the presence of Horner's syndrome can be reflected in the MIBG scan.
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6/8. Patterns of salivary gland uptake in I-131 MIBG scintigraphy.

    I-131 MIBG scintigraphy is routinely used in the diagnosis of neuroendocrine tumours with high specificity. The radiopharmaceutical is taken up via uptake mechanism and actively transported into storage vesicules. The organs with dense sympathetic innervation such as salivary glands, heart, lachrymal glands, spleen and rarely adrenal medulla are normally visualized with I-131 MIBG. Asymetrical salivary gland uptake is important in a patient with suspected neuroendocrine tumours. Absence of radioactivity may be a result of sympathic denervation or tumor. Bilateral radioactivity absence is observed usually due to drugs or radiopharmaceutical storage conditions. Detailed examination of cervical region is crucial for localisation of neuroendocrine tumours. Therefore, possible false positives should be kept in mind.
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7/8. Horner's syndrome. Sweat gland and pupillary responsiveness in two cases with a probable 3rd neurone dysfunction.

    Two patients with a Horner's syndrome due to a probable 3rd neurone lesion were examined with regard to the pupillometric and evaporimetric patterns. The results are compared with those found in patients with a Horner's syndrome due to a 1st or 2nd neurone lesion, previously described by our group. Concurring with observations by others, the pupil on the symptomatic side did not dilate at all when stimulated with hydroxy-amphetamine eye drops. Postganglionic dysfunction may thus be distinguished from 1st and 2nd neurone dysfunction. Supersensitivity was present on the side of the Horner's syndrome, both on pupillometry (phenylephrine stimulation) and in the medial part of the forehead at evaporimetry (pilocarpine stimulation). The lateral part of the forehead, however, did not demonstrate deficient evaporation in these postganglionic sympathetic lesions.
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8/8. Raeder's syndrome. A case with an unusual localization.

    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.
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