Isolated Horner's syndrome and syringomyelia.
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Although syringomyelia has been associated with Horner's syndrome, it is typically associated with other neurological findings such as upper limb weakness or numbness. A patient is described who had an isolated Horner's syndrome as the only manifestation of syringomyelia. A 76 year old woman was discovered to have right upper lid ptosis and right pupillary miosis. Neurological examination was unremarkable, and pharmacological testing was consistent with localisation of the lesion to a first or second order sympathetic neuron. Neuroimaging disclosed a Chiari I malformation with a syrinx extending to the C2 to C4 level. An isolated Horner's syndrome may be the presenting manifestation of syringomyelia. (+info)
Course and distribution of facial corticobulbar tract fibres in the lower brain stem.
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The course and distribution of the facial corticobulbar tract (CBT) was examined by correlating MRI of brain stem lesions with neurological symptoms and signs including central (C-FP) or peripheral facial paresis (P-FP) in 70 patients with localised infarction of the lower brain stem. C-FP occurred more often in patients with lesions of the lower pons or upper medulla of the ventromedial brain stem. Some patients with dorsolateral infarcts of the upper medulla to the lower pons showed C-FP, mostly on the lesion side. P-FP on the side of the lesion was also seen in patients with dorsolateral involvement of the lower pons. Patients with ventromedial infarction of the brain stem showed paresis of extremities contralateral to the lesion. Specific neurological symptoms and signs such as dysphagia, vertigo, nystagmus, Horner's syndrome, ipsilateral cerebellar ataxia, and contralateral superficial sensory impairment were seen in patients with dorsolateral infarcts of the brain stem. It is hypothesised that the facial CBT descends at the ventromedial lower pons, near the corticospinal tract, mainly to the level of the upper medulla, where the fibres then decussate and ascend in the dorsolateral medulla to synapse in the contralateral facial nucleus. (+info)
First rib fracture: a hallmark of severe trauma.
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First rib fractures occurred in 55 patients. This injury is a harbinger of major trauma with 35 patients suffering a major chest injury, and abdominal and cardiac injuries occurring in 18 and eight patients respectively. The mortality associated with this injury was high (36.3%). Neurologic lesions accounted for the majority of deaths, however, unrecognized abdominal injuries and pulmonary complications were significant causes of mortality. Brachial plexus injury (5) and Horner's syndrome (3) occurred in survivors. Three patients had an associated injury of the subclavian artery, and the importance of this association is stressed. One late-developing post-traumatic thoracic outlet syndrome occurred. A fracture of the first rib is a hallmark of severe trauma; its presence should alert the clinician to: 1) generalized massive trauma with abdominal, chest, and cardiac injuries; 2) local injury to the subclavian artery and brachial plexus and; 3) necessity of long-term followup for late-developing sequelae. (+info)
A case of Brown-Sequard syndrome with associated Horner's syndrome after blunt injury to the cervical spine.
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A 26 year old motorcyclist was received by the trauma team in our accident and emergency department after a head on collision with a motor vehicle. He had been correctly immobilised and his primary survey was essentially normal. He was alert and orientated with a Glasgow Coma score of 15 and had no symptoms or signs of spinal injury. His cervical spine radiography was also normal. Neurological examination however, revealed anisocoria, his left pupil being smaller than his right, and a Brown-Sequard syndrome, with a sensory level at C6. Immobilisation was maintained and he was transferred to the regional neurosurgical centre where magnetic resonance imaging revealed a contusion of the left half of the spinal cord adjacent to the 6th cervical vertebrae. Computed tomography revealed no bony injury but spinal column instability was demonstrated after flexion-extension spinal views and he underwent surgery to fuse his spine at the C5-C6 level. This report highlights the necessity to observe strict ATLS guidelines. This must include a thorough examination of the central and peripheral nervous system where spinal injury is suspected, even in the absence of radiographic abnormality and neck pain. This article also presents the unusual phenomena of Brown-Sequard syndrome and unilateral Horner's syndrome after blunt traumatic injury to the cervical spine. (+info)
Isolated abducens nerve paresis associated with incomplete Horner's syndrome caused by petrous apex fracture--case report and anatomical study.
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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. (+info)
Agenesis of the internal carotid artery associated with aortic arch anomaly in a patient with congenital Horner's syndrome.
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We report a rare case of agenesis of the left internal carotid artery (ICA) and an aortic arch anomaly that presented with ipsilateral congenital Horner's syndrome. Digital subtraction angiography revealed left ICA agenesis shortly after its origin and anastomosis between the left maxillary artery and the supraclinoid segment of the left ICA. Aortography of the aortic arch revealed the right subclavian artery arising as the first branch of a left aortic arch, followed by a bicarotid trunk and a left subclavian artery. High resolution CT of the skull base revealed the absence of the left carotid channel, consistent with congenital agenesis of the ICA. (+info)
Trigeminal and polyradiculoneuritis in a dog presenting with masticatory muscle atrophy and Horner's syndrome.
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A 9-year-old, spayed female, Airedale Terrier was euthanatized and necropsied after a progressive clinical course that included Horner's syndrome of the left eye and unilateral atrophy of the masticatory muscles. Although gross lesions were limited, a polyradiculoneuritis and ganglionitis that was most severe in the trigeminal nerves and ganglia were confirmed histologically. The inflammatory infiltrate consisted predominantly of macrophages and B and T lymphocytes that were phenotypically confirmed by immunostaining. Horner's syndrome was the result of damage to postganglionic sympathetic fibers that were incorporated in segments of the inflamed trigeminal nerve and its ophthalmic branch. Histologically, the character and distribution of the inflammation was similar to previously described syndromes of suspected immune-mediated etiology in humans and animals. (+info)
Artemin is a vascular-derived neurotropic factor for developing sympathetic neurons.
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Artemin (ARTN) is a member of the GDNF family of ligands and signals through the Ret/GFRalpha3 receptor complex. Characterization of ARTN- and GFRalpha3-deficient mice revealed similar abnormalities in the migration and axonal projection pattern of the entire sympathetic nervous system. This resulted in abnormal innervation of target tissues and consequent cell death due to deficiencies of target-derived neurotrophic support. ARTN is expressed along blood vessels and in cells nearby to sympathetic axonal projections. In the developing vasculature, ARTN is expressed in smooth muscle cells of the vessels, and it acts as a guidance factor that encourages sympathetic fibers to follow blood vessels as they project toward their final target tissues. The chemoattractive properties of ARTN were confirmed by the demonstration that sympathetic neuroblasts migrate and project axons toward ARTN-soaked beads implanted into mouse embryos. (+info)