Cases reported "Abducens Nerve Injury"

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1/25. Cranial nerve palsy as a complication of operative traction.

    STUDY DESIGN: Case report. OBJECTIVE: This report documents one case of diplopia from abducens (sixth cranial) nerve palsy after spinal surgery using a Jackson table and cranial traction. SUMMARY OF BACKGROUND DATA: Cranial nerve deficits have frequently been described in the orthopedic literature after trauma, halo pelvic traction, and halo skeletal fixation. The theorized mechanism of injury to the abducens nerve involves stretch or traction force, which causes localized ischemia or a change in nerve position. An extensive literature search failed to show this type of injury using Gardner-Wells tongs in conjunction with the Jackson table. methods: This is a case report that included a chart review, examination of the patient, and a literature search. RESULTS: The patient had complete spontaneous resolution of abducens nerve dysfunction within 6 months. CONCLUSIONS: It is important for the surgeon to be aware of this potential complication and to inform patients who have diplopia that develops from abducens nerve palsy that most of these cranial nerve deficits spontaneously improve.
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2/25. Cyclic esotropia after a traumatic sixth nerve palsy in a child.

    Cyclic esotropia is a rare phenomenon in which esotropia and orthophoria alternate over a period of 48 to 96 hours. The mechanism that underlies the phenomenon is unknown. Cyclic esotropia often occurs after a fusion-disrupting event. We report an unusual case of cycling esotropia with onset after a traumatic sixth nerve palsy. The cyclic phase persisted for 2 years, following a 48-hour alternate-day pattern. After strabismus surgery for the esotropic angle, the deviation disappeared and the patient remained orthotropic, with 1 year of follow-up to date.
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3/25. Abducens palsy after lumbar puncture.

    OBJECTIVE: We report the case of a 43-year-old patient with neuralgic shoulder amyotrophy who developed abducens palsy on the left 4 days after diagnostic lumbar puncture (LP), which recovered completely within 4 months. RESULTS: Side effects after spinal tap are due to prolonged spinal fluid leakage and delayed closure of a dural defect causing intracranial hypotension. Downward 'sagging' of the brain and traction on cranial nerves may lead to abducens palsy. This case and a review of the literature illustrate the higher risk with the use of large-size traumatic needles in LP for cranial sixth nerve palsies. CONCLUSION: The presented case emphasizes the use of atraumatic small-size needles for lumbar puncture.
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4/25. Bilateral sixth nerve palsy after head trauma.

    Gaze deficits are not uncommon after head trauma and might be caused by injury to the central nervous system, the peripheral nerve, or the motor unit. Traumatic bilateral sixth cranial nerve palsies are a rare condition and are typically associated with additional intracranial, skull, and cervical spine injuries. We describe a case of a complete bilateral sixth nerve palsy in a 44-year-old male patient with trauma with no intracranial lesion, no associated skull or cervical spine fracture, and no altered level of consciousness. The emergency physician should be aware of the differential diagnosis, initial workup, and injuries associated with a traumatic gaze deficit.
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5/25. esotropia following posterior superior alveolar nerve block.

    Adequate use of local anesthetics is an important phase of modern dentistry. Regardless of the care used in administration of local anesthetics, unusual reactions can occur. A case is presented in which posterior superior alveolar administration of two percent lidocaine 1/100,000 epinephrine resulted in medial rotation of the orbit (esotropia).
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6/25. Bilateral chronic subdural hematomas with neurologic symptoms complicating spinal anesthesia.

    BACKGROUND AND OBJECTIVES: Intracranial subdural hematoma is a rare but potentially fatal complication of spinal anesthesia (SA). This case is intended to highlight the importance of careful follow-up of patients with a chronic headache that develops after SA. CASE REPORT: A 38-year-old woman underwent saphenous vein ligation for varices under SA. On the first postoperative day, she complained of severe postural headache that was controllable with oral analgesics. Two weeks later, bilateral abducens nerve palsy with diplopia developed. brain magnetic resonance imaging (MRI) showed small bilateral subdural hygromas. diplopia and headache (no longer postural) were relieved after administration of dexamethasone, but reappeared 6 wks later. This time, MRI showed large subdural hematomas. The patient was treated with burr-hole decompression. CONCLUSIONS: Persistent headache after SA requires careful neurologic and radiologic follow-up for exclusion of chronic intracranial bleeding. Pharmacologic treatment may mask some neurologic symptoms and delay diagnosis of intracranial complications related to SA.
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7/25. Ocular palsy following Le Fort 1 osteotomy: a case report.

    A 33-year-old female patient developed an ipsilateral sixth nerve palsy and partial third nerve palsy following a Le Fort 1 osteotomy. Complete resolution occurred at 10 weeks.The likely mechanism of injury secondary to pterygo-maxillary dysjunction is highlighted, with description of the relevant anatomy.Previous cases of ocular motility complications following Le Fort 1 osteotomy are discussed.We recommend that significant care be taken in osteotome placement in the pterygo-maxillary fissure, particularly in those prone to unpredicted fractures such as older patients, or where the anatomy is congenitally abnormal or altered by previous surgery.
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8/25. Bitemporal head crush injuries: clinical and radiological features of a distinctive type of head injury.

    OBJECT: Most craniocerebral injuries are caused by mechanisms of acceleration and/or deceleration. Traumatic injuries following progressive compression to the head are certainly unusual. The authors reviewed clinical and radiological features in a series of patients who had sustained a special type of cranial crush injury produced by the bilateral application of rather static forces to the temporal region. Their aim was to define the characteristic clinical features in this group of patients and to assess the mechanisms involved in the production of the cranial injuries and those of the associated cerebral and endocrine lesions found in this peculiar type of head injury. methods: Clinical records of 11 patients were analyzed with regard to the state of consciousness, cranial nerve involvement, findings on neuroimaging studies, endocrine symptoms, and outcome. Furthermore, an experimental model of bitemporal crush injury was developed by compressing a dried skull with a carpenter's vice. Seven of the 11 patients were 16 years old or younger. All patients presented with a characteristic clinical picture consisting of no loss of consciousness (six patients), epistaxis (nine patients), otorrhagia (11 patients), peripheral paralysis of the sixth and/or seventh cranial nerves (10 patients), hearing loss (five patients), skull base fractures (11 patients), pneumocephalus (11 patients), and diabetes insipidus (seven patients). Ten patients survived the injury and most recovered neurological function. CONCLUSIONS: Static forces applied to the head in a transverse axis produce fractures in the skull base that cross the midline structures without producing significant cerebral damage. Stretching of cranial nerves at the skull base explains the nearly universal finding of paralysis of these structures, whereas an increase in the vertical diameter of the skull accounts for the occurrence of diabetes insipidus in the presence of an intact function of the anterior pituitary lobe. The association of clinical, endocrine, and neuroimaging findings encountered in this peculiar type of head injury supports the idea that this subset of injured patients has a distinctive clinical condition, namely the syndrome of bitemporal crush injury to the head.
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9/25. Fourth and sixth cranial nerve injury after halo traction in children: a report of two cases.

    BACKGROUND: Spinal traction is the application of a longitudinal force to the spinal column as a means of stabilizing a damaged or abnormal spine. Although not well documented in the ophthalmic literature, complications include cranial nerve palsies, with the sixth nerve being most commonly affected. Fourth nerve palsies have not previously been reported to our knowledge. We present 2 cases of combined fourth and sixth palsies after cervical traction. methods: Retrospectively, we reviewed the ophthalmic findings in 2 children with diplopia after spinal traction. RESULTS: Case 1 suffered a traumatic rotatory atlantoaxial subluxation and underwent halo traction. Case 2 required traction to correct a scoliosis secondary to osteogenesis imperfecta. In both cases, sixth nerve palsies were apparent soon after traction. Careful orthoptic examination revealed additional fourth nerve involvement. After 3 months, both cases showed partial resolution of the cranial nerve injuries. CONCLUSIONS: Cranial nerve injury may occur with spinal traction. Fourth nerve palsy may be underreported because of masking by a coinciding sixth nerve palsy.
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10/25. Posttraumatic abducens to oculomotor nerve misdirection.

    INTRODUCTION: Paradoxical patterns of extraocular muscle, eyelid, or pupillary movements can occur following injury between divisions of the oculomotor nerve, trigeminal and abducens nerves, and trigeminal and oculomotor nerves. We report three cases of unusual ocular motility and eyelid movements that are a result of aberrant connections between the abducens and oculomotor nerves. methods: Three patients with unusual eye movement abnormalities after trauma were studied. A complete ophthalmic examination plus neuroradiologic evaluation were performed. RESULTS: Each patient manifested an aberrant connection between the 6th and 3rd cranial nerves resulting in third nerve function during sixth nerve stimulation. Two patients demonstrated complete third nerve palsies except for adduction on attempted abduction. The third showed improved bilateral ptosis on abduction. CONCLUSIONS: The neuroanatomical abnormalities involve intraorbital structures in one patient and central nervous system pathways in the others. Explanations such as retrograde regeneration, ephaptic transmission, or denervation supersensitivity do not appear to explain these unusual eye movements. The most likely mechanism involves some form of peripheral neuronal misdirection. These rare sixth to third nerve misdirection cases add support to the "neuronal misdirection hypothesis" of aberrant eye movements after trauma.
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