1/59. Schwannoma of the cervical sympathetic chain. The virginia experience.We present 4 cases of schwannomas arising from the cervical sympathetic chain. These lesions are uncommon and most often present as an asymptomatic solitary neck mass. Preoperative diagnosis can be difficult, even with the aid of computed tomography, magnetic resonance imaging, ultrasound, and angiography. While a paraganglioma can often be ruled out, exact determination of the nerve of origin is frequently elusive until the time of surgery. Operative excision remains the treatment of choice, often requiring sacrifice of a portion of the sympathetic chain. Postoperative Horner's syndrome is common, but does not appear to have an adverse effect on the patient.- - - - - - - - - - ranking = 1keywords = nerve (Clic here for more details about this article) |
2/59. brown-sequard syndrome associated with Horner's syndrome after a penetrating trauma at the cervicomedullary junction.STUDY DESIGN: Case report of a 21-year-old man that had concurrence of brown-sequard syndrome and Horner's syndrome after a penetrating trauma in the neck. OBJECTIVES: This report analyzes the location of lesions that cause a combination of Horner's and brown-sequard syndrome. It is important to know the anatomic structure of spinal cord and the sympathetic nerve chain. SETTING: spinal cord Unit, Department of Physical medicine and rehabilitation, Hospital La Fe, Valencia, Instituto Oftalmologico de Alicante, Alicante, spain. methods: Description of a single patient case report. RESULTS: The clinical findings and MRI showed a good correlation. The Horner's syndrome was confirmed with a 4% cocaine test. The patient received a conservative treatment with high-dose steroid therapy (NASCIS-3). CONCLUSION: The patient presented with Brown-Sequard syndrome and Horner's syndrome. Clinical examination and MRI made a quick and correct diagnosis. The patient recovered completely after the conservative treatment.- - - - - - - - - - ranking = 1keywords = nerve (Clic here for more details about this article) |
3/59. horner syndrome associated with implantation of a vagus nerve stimulator.PURPOSE: To report a case of horner syndrome that occurred after implantation of a vagus nerve stimulator. methods: Case report. RESULTS: A 6-year-old female with cerebral dysgenesis and intractable partial seizures presented with horner syndrome after vagus nerve stimulator implantation. CONCLUSION: horner syndrome can occur as a result of the vagus nerve stimulator implant procedure and should be included as one of its possible surgical complications.- - - - - - - - - - ranking = 7keywords = nerve (Clic here for more details about this article) |
4/59. Sympathetic paraganglioma as an unusual cause of Horner's syndrome.BACKGROUND: Paragangliomas are rare tumors arising from paraganglionic tissue of neural crest origin. They are present in any location where autonomic ganglia are found. The most common location in the head and neck is the carotid body, followed by the jugular bulb and vagus nerve. methods: A 30-year-old woman with a slowly growing left neck mass, aniscoria, and left eyelid ptosis was found to have a vascular tumor consistent with a paraganglioma arising near the left carotid bifurcation. After preoperative embolization, the patient underwent resection of the tumor. RESULTS: The tumor was found to be arising from the left sympathetic trunk and did not involve any other surrounding structures. Histopathologic analysis revealed the typical findings of a paraganglioma. CONCLUSIONS: Sympathetic paragangliomas are exceedingly rare tumors in the head and neck and should be considered in the differential diagnosis when clinical and radiographic evidence suggest a paraganglioma. The presentation is typically a slow-growing neck mass with the presence of an ipsilateral Horner's syndrome.- - - - - - - - - - ranking = 1keywords = nerve (Clic here for more details about this article) |
5/59. Spontaneous internal carotid artery dissection with lower cranial nerve palsy.BACKGROUND: Typical presentation of spontaneous internal carotid artery (ICA) dissection is an ipsilateral pain in neck and face with Horner's syndrome and contralateral deficits. Although rare, lower cranial nerve palsy have been reported in association with an ipsilateral spontaneous ICA dissection. CASE STUDIES: We report three new cases of ICA dissection with lower cranial nerve palsies. RESULTS: The first symtom to appear was headache in all three patients. Examination disclosed a Horner's syndrome in two cases (1 and 2), an isolated XIIth nerve palsy in two patients (case 1 and 3) and IX, X, and XIIth nerve palsies (case 2) revealing an ipsilateral carotid dissection, confirmed by MRI and angiography. In all cases, prognosis was good after a few weeks. CONCLUSIONS: These cases, analysed with those in the literature, led us to discuss two possible mechanisms: direct compression of cranial nerves by a subadventitial haematoma in the parapharyngeal space or ischemic palsy by compression of the ascending pharyngeal artery.- - - - - - - - - - ranking = 9keywords = nerve (Clic here for more details about this article) |
6/59. Horner's syndrome after carotid endarterectomy--a case report.Horner's syndrome is described in a patient with anisocoria and unilateral lid ptosis 48 hours after an ipsilateral carotid endarterectomy. This case illustrates a rare iatrogenic complication of sympathetic nerve dysfunction following elective surgery.- - - - - - - - - - ranking = 1keywords = nerve (Clic here for more details about this article) |
7/59. Isolated abducens nerve paresis associated with incomplete Horner's syndrome caused by petrous apex fracture--case report and anatomical study.A 17-year-old male presented with a wound on the right temporal region, oozing hemorrhagic necrotic brain tissue and cerebrospinal fluid, following a fall. Computed tomography showed temporoparietal and petrous apex fractures on the right. Neurological examination revealed abducens nerve paresis, ptosis, and myosis on the right side. The patient was treated surgically for the removal of the free bony fragments at the fracture site and to close the dural tear. The abducens nerve paresis, ptosis, and myosis persisted at the 3rd monthly postoperative follow-up examination. The anatomy of the abducens nerve at the petroclival region was studied in four cadaveric heads. Two silicone-injected heads were used for microsurgical dissections and two for histological sections. The abducens nerve has three different angulations in the petroclival region, located at the dural entrance porus, the petrous apex, and the lateral wall of the cavernous segment of the internal carotid artery. The abducens nerve had fine anastomoses with the trigeminal nerve and the periarterial sympathetic plexus. There were fibrous connections extending inside the venous space of the petroclival area. The abducens nerve seems to be vulnerable to damage in the petroclival region, either directly by trauma to its dural porus and petrous apex or indirectly by stretching of the nerve through the nervous and/or fibrous connections. Concurrent functional loss of the abducens nerve and the periarterial sympathetic plexus clinically manifested as incomplete Horner's syndrome in our patient.- - - - - - - - - - ranking = 13keywords = nerve (Clic here for more details about this article) |
8/59. Raeder's syndrome.Raeder's paratrigeminal syndrome is a disorder manifested by unilateral ptosis, miosis, intact facial sweating, and severe pain in the distribution of the ophthalmic division of the fifth nerve. It is a clinical pattern where, usually, a middle-aged male gets a severe throbbing supraorbital headache accompanied by ptosis and miosis. The headache is intermittently present for several weeks or months. Facial sweating may or may not be affected. This report describes a female with Raeder's syndrome who had unilateral facial anhibrosis.- - - - - - - - - - ranking = 1keywords = nerve (Clic here for more details about this article) |
9/59. Clinical case seminar: Riedel's thyroiditis: report of a case complicated by spontaneous hypoparathyroidism, recurrent laryngeal nerve injury, and Horner's syndrome.A 42-yr-old woman presented with hyperthyroidism and a large, firm, irregular goiter. Within a few weeks she became hypothyroid. Five months later she developed increasingly severe neck pain and compressive symptoms. The goiter had become rock hard. A fine needle aspiration biopsy showed features of chronic thyroiditis and fibrosis. She partially responded to a course of glucocorticoids. tamoxifen was added, with marked improvement in goiter size and pain. Both medications were tapered off. Two months later the patient experienced paresthesias of the fingertips, perioral numbness, and a seizure. She was found to have spontaneous primary hypoparathyroidism. Three months later the patient became hoarse and experienced difficulty in breathing. She was found to have a massively enlarged thyroid with compression of the right internal jugular vein and encasement of the right carotid artery as well as tracheal narrowing. She also had right vocal cord paralysis due to recurrent laryngeal nerve involvement. Because of airway compromise, an emergency isthmusectomy was performed, and the patient was given a postoperative course of glucocorticoids with gradual improvement. Postoperative diagnosis was Riedel's thyroiditis. Two months later she presented with near-syncope and was found to have bradycardia, hypotension, and right Horner's syndrome, presumably due to compression of the right carotid sheath. She was given i.v. glucocorticoids and tamoxifen. Six months later and 18 months after her initial presentation, the patient is doing remarkably well. Her goiter has regressed by more than 50%, and she no longer has any pain or difficulty breathing. She remains a little hoarse and has persistent hypothyroidism and hypoparathyroidism. She is taking prednisone (5 mg, this is being tapered very slowly) and tamoxifen (20 mg) daily. This case illustrates the protean manifestations of Riedel's thyroiditis, a rare but fascinating disease. The epidemiology of this disease, its pathophysiology and complications, and the roles of surgery and medical therapy are reviewed.- - - - - - - - - - ranking = 5keywords = nerve (Clic here for more details about this article) |
10/59. Early detection of severe cholestatic hepatopathy in COACH syndrome.COACH syndrome is a disorder with cerebellar vermis hypoplasia, oligophrenia, ataxia, coloboma, and hepatic fibrosis. Sixteen cases with certain COACH diagnosis have been reported so far. Neurologic abnormalities are the first symptoms in most cases. The majority of cases were diagnosed late in childhood or adolescence. Complications of the hepatopathy contribute extensively to the morbidity and lethality in the course of the disease. Major complications are portal hypertension, esophageal varices, and gastrointestinal bleeding. We report of a child with only mild neurologic symptoms, but severe hepatic fibrosis with cholangiopathy, and review the literature. This is the first description of profound cholestatic hepatopathy in a very young child with COACH syndrome. The patient was found to have cerebellar vermis hypoplasia, unilateral optical nerve coloboma, mild dysmorphic signs, and a ventricular septum defect. Routine laboratory investigations eventually revealed elevated liver enzymes. prothrombin time was abnormal. Ultrasound scan of the liver was normal. Hepatotropic viral infections were excluded. We performed a liver biopsy at the age of 16 months, confirming an early stage of cirrhosis with septal fibrosis and pseudolobules, inflammatory infiltrates, signs of cholestasis, and reduced numbers of intrahepatic bile ducts. Early detection and differentiation of liver pathology are important in COACH syndrome. Progressive destructive cholangiopathy may contribute to hepatic fibrosis in COACH syndrome. liver disease can be severe even in cases with mild neurologic deficits.- - - - - - - - - - ranking = 1keywords = nerve (Clic here for more details about this article) |
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