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Query: UMLS:C0030552 (paresis)
5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vertebral body replacement after spondylectomy, combined with microsurgical decompression and anterior plating, was performed in 22 patients as an aggressive therapeutic approach to multisegmental cervical spondylosis. The patients were 13 men and 9 women, ranging in age from 32 to 74 years. In 19 patients, the typical signs of cervical myelopathy were present. In three patients, pain was the major symptom, accompanied by moderate spastic paresis and hyperreflexia. Apart from cervical myelography and computed tomographic scanning, which was performed in 10 patients, magnetic resonance imaging was the radiological procedure of choice in 12 patients. During spondylectomy, one vertebra was removed in 14 patients, two vertebrae in seven patients, and three vertebrae in one patient. The time of postoperative follow-up ranged from 8 to 46 months, with an average interval of 21 months. In all 22 patients, satisfactory bony fusion was achieved as demonstrated by radiological control examinations. Seventeen patients (77%) were symptom free or had only minor residual symptoms. Three (14%) patients had intermittent nuchal or cervicobrachial pain, which responded well to analgesic medication or the application of a soft collar. Two (9%) patients still had myelopathic but not incapacitating symptoms. Of 15 patients who were employed before surgery, 13 returned to a full-time job. The only severe complication of surgery was a prevertebral abscess that healed without sequelae. It is concluded that aggressive surgical therapy of multisegmental cervical spondylosis by a combination of vertebrectomy, decompression (using the surgical microscope), bone grafting, and osteosynthesis is a straightforward and promising procedure for the treatment of this debilitating disease.
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PMID:Multisegmental cervical spondylosis: treatment by spondylectomy, microsurgical decompression, and osteosynthesis. 194 28

Dissociated motor loss due to cervical spondylosis and disc herniation was evaluated in 10 patients who presented with left deltoid paresis in the absence of sensory deficits or myelopathy. All of these cases underwent cervical anterior decompression. Based on magnetic resonance imaging, computed tomography myelography, and computed tomography discography, patients were divided into two pathologic types: The first showed focal bony spur and disc herniation with axial cord rotation and nerve root compression, and the second demonstrated ventral cord flattening. Electrophysiologic studies included evoked spinal potentials, motor evoked potentials, and evoked muscle action potentials. Motor evoked potentials, recorded epidurally from the ventral aspect of the thecal sac and the nerve root within the anterior discectomy or vertebrectomy sites, proved clinically most useful. Combining the latest available neuroradiologic and electrophysiologic information, 4 types of neural injury associated with deltoid pareses were identified in the 10 patients. The first included isolated C5 nerve root lesions; the second, C6 nerve root lesions; the third, both C5 and C6 nerve root lesions, and finally, intrinsic cord pathology.
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PMID:Neuroradiologic and electrophysiologic assessment of cervical spondylotic amyotrophy. 815 99

Clinical symptoms and patho-anatomic changes in cervical myelopathy due to spondylotic changes are described. The leading symptoms are numbness and clumsiness of upper and lower extremity, mostly combined with gait disturbances. Muscle wasting primarily on the upper extremity leads to the myelopathic hand. Cervical myelopathy can be classified into five main groups: 1. Spastic tetraparesis with numbness and hyperreflexivity of upper and lower extremity. The majority of patients present with the myelopathic hand. 2. Spastic paraparesis with lesion below C6. 3. Spastic tetraparesis, mild or moderate, with deltoid muscle paresis. 4. Amyotrophic myelopathic hand with mild long tract signs. 5. Central cord syndrome due to cervical spondylosis combined with trauma. From the therapeutic aspect, conservative treatment is often unsuccessful. It is important to relieve pressure on the spinal cord, and decompressive procedures, especially posterior laminoplasty techniques, are required. Earlier surgery provides better results.
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PMID:[Symptoms and pathological anatomy of the degenerative cervical spine]. 899 3

A case of cervical epidural hematoma caused by cervical twisting after epidural anesthesia was reported. A 41-year-old man who had had anterior fusion of C5 - 7 using a plate due to cervical spondylosis fifteen months before admission, had undergone epidural anesthesia through the C7/T1 interspace without difficulty for shoulder pain in a pain clinic. Two hours after injection, he complained of severe pain in his neck and both shoulders just after cervical twisting as was his custom. Within minutes he noted paresis of his left extremities. Neurological examination on admission revealed left side dominant tetraparesis and loss of pain and temperature sensations below the level of T4 on his right side. Laboratory data analysis and coagulation tests were normal. CT scans and MRI demonstrated an epidural hematoma with a small amount of air extending from C3 to the upper margin of C7. Four hours after the onset, a laminoplasty was performed from C3 to C7 with total removal of the hematoma. No bleeding site or any vascular abnormality was found to account for the hematoma formation. He was discharged with good recovery after operation. Most of the reported epidural hematomas associated with epidural anesthesia were related to coagulopathy, anticoagulant therapy or difficult puncture. On review of the literature, this is the first case of spinal epidural hematoma cause by cervical twisting after spinal anesthesia and which was without impaired coagulation or difficult spinal puncture. Cervical epidural hematoma should be considered as a possible complication in patients with pain or neurological deficits after some cervical manipulations.
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PMID:[Cervical epidural hematoma caused by cervical twisting after epidural anesthesia: a case report]. 966 97

Cervical spondylotic myelopathy is a common disease caused by chronic segmental compression of the spinal cord. Despite the fact that the columns of the nuclei of the phrenic nerve are located between the 3rd and 5th cervical nerve segments, phrenic nerve paresis is not usually clinically significant. We present one case of cervical spondylotic myelopathy with bilateral phrenic paresis in whom magnetic resonance imaging and surgical findings confirmed intrinsic cord disease as being the cause of this syndrome. This case report suggests that one pathophysiology of clinical phrenic nerve paresis may be segmental damage to the anterior horns caused by cervical spondylosis.
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PMID:Phrenic paresis and respiratory insufficiency associated with cervical spondylotic myelopathy. 1501 56

This 60-year-old man with cervical spondylosis experienced bilateral arm pain and weakness. After anterior cervical fusion and posterior decompression at a local hospital his symptoms worsened and he was admitted to our hospital. On admission he manifested bilateral motor weakness, neuropathic pain, and numbness below the C5 level. Radiological findings showed spinal cord compression at the C4 to C7 level. He again underwent posterior decompression and anterior fusion. Although his paresis was improved, his severe neuropathic pain and numbness persisted. Because treatment with NSAIDs, clonazepam, and gabapentin failed to control his symptoms we administered ketamine (NMDA receptor antagonist) because his symptoms were alleviated upon ketamine test challenge. His severe symptoms improved and there were no complications. However, upon cessation of ketamine treatment they reappeared. Therefore, we continued daily ketamine treatment for 6 months, after which we changed to codeine phosphate. His symptoms were controlled without any complications. Ketamine is useful for the control of severe neuropathic pain, however, as long-term ketamine administration is inadvisable, we suggest that treatment be tailored to each patient's particular clinical status.
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PMID:[Ketamine treatment for severe neuropathic pain with cervical spondylotic myelopathy. A case report]. 2116 Jan 5

Clinical symptoms and patho-anatomic changes in cervical myelopathy due to spondylotic changes are described. The leading symptoms are numbness and clumsiness of upper and lower extremity, mostly combined with gait disturbances. Muscle wasting primarily on the upper extremity leads to the myelopathic hand. Cervical myelopathy can be classified into five main groups: 1. Spastic tetraparesis with numbness and hyperreflexivity of upper and lower extremity. The majority of patients present with the myelopathic hand. 2. Spastic paraparesis with lesion below C6. 3. Spastic tetraparesis, mild or moderate, with deltoid muscle paresis. 4. Amyotrophic myelopathic hand with mild long tract signs. 5. Central cord syndrome due to cervical spondylosis combined with trauma. From the therapeutic aspect, conservative treatment is often unsuccessful. It is important to relieve pressure on the myelon, and decompressive procedures, especially posterior laminoplasty techniques, are required. Earlier surgery provides better results.
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PMID:[Clinical symptoms and patho-anatomic changes in cervical myelopathy]. 2824 74

We report the case of a 53-year-old-man who developed human T-cell leukemia virus type-1-associated myelopathy (HAM) after ABO-incompatible liver transplantation for alcoholic liver cirrhosis. The living donor was seropositive for human T-cell leukemia virus type-1 (HTLV-1) and the recipient was seronegative for HTLV-1 before transplantation. After transplantation, the recipient developed steroid-resistant acute cellular rejection, which was successfully treated using anti-thymocyte globulin, and he was eventually discharged. He underwent spinal surgery twice after the transplantation for the treatment of cervical spondylosis that had been present for a period of 9 months before the transplantation. The surgery improved his gait impairment temporarily. However, his gait impairment progressed, and magnetic resonance imaging revealed multiple sites of myelopathy. He was diagnosed with HAM 16 months after the transplantation. Pulse steroid therapy (1000mg) was administered over a period of 3 days, and his limb paresis improved. Presently, steroid therapy is being continued, with a plan to eventually taper the dose, and he is being carefully followed up at our institution. Our case suggests that liver transplantation involving an HTLV-1-positive living donor carries the risk of virus transmission and short-term development of HAM after transplantation.
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PMID:Myelopathy due to human T-cell leukemia virus type-1 from the donor after ABO-incompatible liver transplantation. 3102 62