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Nicholas Theodore - One of the best experts on this subject based on the ideXlab platform.
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basilar artery thrombosis after reduction of cervical spondyloptosis a cautionary report
Journal of Neurosurgery, 2012Co-Authors: Luis M Tumialan, Nicholas TheodoreAbstract:Traumatic cervical spondyloptosis is a rare clinical entity typically associated with complete neurological deficit. The inherent mechanics of this fracture-dislocation pattern contorts the vertebral arteries in such a way that it may result in dissection or compromised flow through those vessels. Thus, intimal injury or thrombus from stasis of flow may result. Reduction of the spondyloptosis restores flow to the vertebral arteries, but it also may mobilize thrombus or propagate an intimal dissection within the previously contorted vessel. The authors review their experience in the care of a 43-year-old man who sustained C4–5 spondyloptosis while riding an all-terrain vehicle. On arrival, the patient demonstrated no motor function below C-4 but had sensation to the nipple line (American Spinal Injury Association Spinal Cord Injury Classification B). The patient's Cranial Nerve Examination was unremarkable. Computed tomography of the cervical spine demonstrated complete spondyloptosis at C4–5. The patient ...
Luis M Tumialan - One of the best experts on this subject based on the ideXlab platform.
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basilar artery thrombosis after reduction of cervical spondyloptosis a cautionary report
Journal of Neurosurgery, 2012Co-Authors: Luis M Tumialan, Nicholas TheodoreAbstract:Traumatic cervical spondyloptosis is a rare clinical entity typically associated with complete neurological deficit. The inherent mechanics of this fracture-dislocation pattern contorts the vertebral arteries in such a way that it may result in dissection or compromised flow through those vessels. Thus, intimal injury or thrombus from stasis of flow may result. Reduction of the spondyloptosis restores flow to the vertebral arteries, but it also may mobilize thrombus or propagate an intimal dissection within the previously contorted vessel. The authors review their experience in the care of a 43-year-old man who sustained C4–5 spondyloptosis while riding an all-terrain vehicle. On arrival, the patient demonstrated no motor function below C-4 but had sensation to the nipple line (American Spinal Injury Association Spinal Cord Injury Classification B). The patient's Cranial Nerve Examination was unremarkable. Computed tomography of the cervical spine demonstrated complete spondyloptosis at C4–5. The patient ...
Rajani Jagana - One of the best experts on this subject based on the ideXlab platform.
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Acute Thyrotoxic Bulbar Myopathy with Encephalopathic Behaviour: An Uncommon Complication of Hyperthyroidism
Case reports in endocrinology, 2013Co-Authors: Neeraja Boddu, Sridhar Badireddi, Karl David Straub, John Schwankhaus, Rajani JaganaAbstract:Objective. Acute thyrotoxic bulbar palsy is rare, severe, and rapidly progressive. We describe a case of thyrotoxicosis with bulbar palsy, encephalopathy, and pyramidal tract dysfunction. Case Report. 64-year-old white male with toxic multinodular goiter presented with rapid atrial fibrillation. He had mild tremor, normal Cranial Nerve Examination, 4/5 strength in all extremities, normal reflexes, and down going plantars. TSH was low at 0.09 (normal: 0.34–5.6 uIU/mL), and free T4 was high at 5.22 (normal: 0.47–1.41 ng/dL). Despite optimal AV nodal blockade, he had persistent rapid atrial fibrillation. He later developed cervical dystonia, rigidity, clonus, dysarthria, dysphagia, vocal cord palsy, and absent gag reflex. Thyroid storm was suspected. Neuroimaging and cerebrospinal fluid cultures were nondiagnostic. Acetylcholine receptor antibodies were negative. Swallow ability was impaired with heavy secretions. Remarkable improvement in symptoms was noted after initiation of treatment for thyroid storm. Conclusion. Pyramidal tract symptoms and bulbar palsy may occur with thyrotoxicosis. Cranial Nerve involvement and encephalopathy raise a question of primary brain mechanism causing bulbar palsy. This is reversible with prompt treatment of thyroid storm.
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Acute Thyrotoxic Bulbar Myopathy with Encephalopathic Behaviour: An Uncommon Complication of Hyperthyroidism
2013Co-Authors: Neeraja Boddu, Sridhar Badireddi, Karl David Straub, John Schwankhaus, Rajani JaganaAbstract:Copyright © 2013 Neeraja J. Boddu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. Acute thyrotoxic bulbar palsy is rare, severe, and rapidly progressive. We describe a case of thyrotoxicosis with bulbar palsy, encephalopathy, and pyramidal tract dysfunction. Case Report. 64-year-old white male with toxic multinodular goiter presented with rapid atrial fibrillation. He had mild tremor, normal Cranial Nerve Examination, 4/5 strength in all extremities, normal reflexes, and down going plantars. TSH was low at 0.09 (normal: 0.34–5.6 uIU/mL), and free T4 was high at 5.22 (normal: 0.47–1.41 ng/dL). Despite optimal AVnodal blockade, he had persistent rapid atrial fibrillation. He later developed cervical dystonia, rigidity, clonus, dysarthria, dysphagia, vocal cord palsy, and absent gag reflex. Thyroid storm was suspected. Neuroimaging and cerebrospinal fluid cultures were nondiagnostic. Acetylcholine receptor antibodies were negative. Swallow ability was impaired with heavy secretions. Remarkable improvement in symptoms was noted after initiation of treatment for thyroid storm.Conclusion. Pyramidal tract symptoms and bulbar palsy may occur with thyrotoxicosis. Cranial Nerve involvement and encephalopathy raise a question of primary brain mechanism causing bulbar palsy. This is reversible with prompt treatment of thyroid storm. 1
Herman K - One of the best experts on this subject based on the ideXlab platform.
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A rare case of concomitant sicca keratopathy and ipsilateral central facial palsy in Wallenberg's dorsolateral medullary syndrome
German Medical Science GMS Publishing House; Düsseldorf, 2017Co-Authors: De Bruyn D, Van Aken E, Herman KAbstract:Objective: To describe a patient with a right-sided supranuclear facial palsy and concomitant sicca keratopathy of the right eye following right-sided dorsolateral medullary infarction. Methods: Our patient underwent a complete ophthalmologic and neurologic Examination including biomicroscopy, fundus Examination, Cranial Nerve Examination, Shirmer I test, and magnetic resonance imaging of the brain.Results: A 61-year-old woman presented in emergency with a central facial Nerve palsy on the right side and truncal ataxia. Neurologic assessment revealed a concurrent dysphagia, dysarthria, hypoesthesia of the right face, and weakness of the right upper limb. Magnetic resonance imaging of the brain showed an old left-sided cerebellar infarction, but a recent ischemic infarction at the level of the right dorsolateral medulla oblongata was the cause of our patient's current problems. One month after diagnosis of the right-sided dorsolateral medullary syndrome, there were complaints of ocular irritation and a diminished visual acuity in the right eye. Biomicroscopy showed a sicca keratopathy with nearly complete absence of tear secretion on the Shirmer I test, but with normal eye closure and preserved corneal reflexes and sensitivity.Conclusion: A dorsolateral medullary syndrome can have a variable expression in symptomatology. Our case is special because of the combination of an ipsilateral supranuclear facial palsy with normal upper facial muscle function together with an ipsilateral sicca keratopathy as a result of a nearly absent tear secretion. We hypothesized that the mechanism underlying the patient's sicca keratopathy ipsilateral to the supranuclear facial palsy involved the superior salivatory nucleus, which is situated in the caudal pons inferiorly of the motor facial nucleus and is most probably affected by a superior extension of the infarcted area in the right medulla oblongata
Herman Kristien - One of the best experts on this subject based on the ideXlab platform.
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A rare case of concomitant sicca keratopathy and ipsilateral central facial palsy in Wallenberg’s dorsolateral medullary syndrome
German Medical Science GMS Publishing House, 2017Co-Authors: De Bruyn Deborah, Van Aken Elisabeth, Herman KristienAbstract:Objective: To describe a patient with a right-sided supranuclear facial palsy and concomitant sicca keratopathy of the right eye following right-sided dorsolateral medullary infarction. Methods: Our patient underwent a complete ophthalmologic and neurologic Examination including biomicroscopy, fundus Examination, Cranial Nerve Examination, Shirmer I test, and magnetic resonance imaging of the brain.Results: A 61-year-old woman presented in emergency with a central facial Nerve palsy on the right side and truncal ataxia. Neurologic assessment revealed a concurrent dysphagia, dysarthria, hypoesthesia of the right face, and weakness of the right upper limb. Magnetic resonance imaging of the brain showed an old left-sided cerebellar infarction, but a recent ischemic infarction at the level of the right dorsolateral medulla oblongata was the cause of our patient’s current problems. One month after diagnosis of the right-sided dorsolateral medullary syndrome, there were complaints of ocular irritation and a diminished visual acuity in the right eye. Biomicroscopy showed a sicca keratopathy with nearly complete absence of tear secretion on the Shirmer I test, but with normal eye closure and preserved corneal reflexes and sensitivity.Conclusion: A dorsolateral medullary syndrome can have a variable expression in symptomatology. Our case is special because of the combination of an ipsilateral supranuclear facial palsy with normal upper facial muscle function together with an ipsilateral sicca keratopathy as a result of a nearly absent tear secretion. We hypothesized that the mechanism underlying the patient’s sicca keratopathy ipsilateral to the supranuclear facial palsy involved the superior salivatory nucleus, which is situated in the caudal pons inferiorly of the motor facial nucleus and is most probably affected by a superior extension of the infarcted area in the right medulla oblongata