1/41. Subacute sensory neuropathy associated with Epstein-Barr virus.A 35-year-old man experienced severe sensory loss, pseudoathetosis, and areflexia during recovery from a severe viral illness. Sensory nerve action potentials were absent, motor conduction velocities were mildly slowed, and blink reflexes were normal. magnetic resonance imaging (MRI) revealed abnormal signal within the central and dorsal aspects of the thoracic cord. Acute and convalescent Epstein-Barr virus (EBV) titers suggested EBV as the etiology. Subacute sensory neuropathy, with peripheral and central nervous system involvement, is a rare complication of EBV infection.- - - - - - - - - - ranking = 1keywords = nervous system (Clic here for more details about this article) |
2/41. iliac artery aneurysm causing isolated superior gluteal nerve lesion.Lesions of the superior gluteal nerve (SGN) lead to weakness of hip abduction, manifesting itself as a gait abnormality, with contralateral tilting of the pelvis with each step. Causes are numerous and may occur at different anatomical locations before the nerve enters the suprapiriform foramen, in the foramen itself, or after the nerve has exited the foramen. This case report describes an SGN lesion by a large iliac artery aneurysm in a patient presenting with a gait disorder.- - - - - - - - - - ranking = 0.015825323688006keywords = lead (Clic here for more details about this article) |
3/41. Painless limp as a presentation of pelvic eosinophilic granuloma in a child.Painless limp in children continues to pose a diagnostic challenge. In the majority of the cases transient synovitis of the hip is the cause. However, bone tumours should be considered as a possibility and specifically looked for when a child continues to have ongoing symptoms. Failure to diagnose tumours at an early stage can lead to a poorer outcome. This case report describes a child with eosinophilic granuloma who presented with a progressive painless limp. It emphasises the need to look carefully at the pelvic bones when evaluating a hip radiograph.- - - - - - - - - - ranking = 0.015825323688006keywords = lead (Clic here for more details about this article) |
4/41. Lumbar spinal stenosis causing congenital clubfoot.Congenital lumbar spinal stenosis is believed to rarely cause neurologic symptoms during childhood. We present a 16-year-old boy with bilateral congenital clubfeet surgically corrected by tendo Achillis releases at 2 years of age who presented with progressive, bilateral footdrop. magnetic resonance imaging of his lumbosacral spine showed severe spinal stenosis at the L3-5 vertebrae. Congenital lumbar spinal stenosis is probably an under-recognized cause of lower extremity neurologic abnormalities, including clubfoot deformity. magnetic resonance imaging has made this eminently treatable disorder easier to recognize.- - - - - - - - - - ranking = 4.7329777821869keywords = neurologic (Clic here for more details about this article) |
5/41. Brainstem conundrum: the Chiari I malformation.PURPOSE: To describe the Chairi I Malformation in relation to the anatomy of the brain and spinal cord, the common manifestations of the condition, diagnostic considerations, and management for the primary care provider. DATA SOURCES: Extensive review of the world-wide scientific literature on the condition, supplemented with actual case studies. CONCLUSIONS: The adult Chairi I Malformation is an insidious congenital brainstem anomaly that consists of caudal displacement of the cerebellar tonsils, brainstem and fourth ventricle into the upper cervical space, resulting in overcrowding of the posterior fossa. IMPLICATIONS FOR PRACTICE: Due to the vague, and often ambiguous presenting symptoms of Chiari I Malformation, many patients are misdiagnosed with conditions such as multiple sclerosis, fibromyalgia, chronic fatigue syndrome, or psychiatric disorders. patients frequently experience symptoms months to years prior to accurate diagnosis and often incur irreversible neurologic deficits.- - - - - - - - - - ranking = 2.3664888910935keywords = neurologic (Clic here for more details about this article) |
6/41. Treatment of craniocervical spine lesion with osteogenesis imperfecta: a case report.STUDY DESIGN: A case report of craniocervical spine lesions including basilar impression, atlantoaxial dislocation, and syringomyelia, with osteogenesis imperfecta is presented, and the literature is reviewed. OBJECTIVE: To discuss the problems involved in the surgical management of craniocervical spine lesion with osteogenesis imperfecta. SUMMARY OF BACKGROUND DATA: osteogenesis imperfecta is known to have various spine lesions as complications. However, few reports have described craniocervical lesions associated with osteogenesis imperfecta. methods: A 14-year-old girl with osteogenesis imperfecta, Silence classification IVB, experienced difficulty walking, with marked motor disturbance and muscle weakness in the extremities. Deep tendon reflexes were exaggerated bilaterally in the upper and lower extremities, and positive Babinski reflex and ankle clonus were observed bilaterally. Basilar impression, atlantoaxial dislocation, and syringomyelia were shown by plain radiography, tomography, three-dimensional computed tomography, and magnetic resonance imaging. RESULTS: In the reported patient, posterior fossa decompression and atlantoaxial posterior fusion could not be performed because the foramen magnum and upper cervical spine invaginated to the base of the skull. Therefore, occipitocervical spine fusion using titanium loop and wires was performed at the reduced position of the atlantoaxial dislocation, resulting in improvement of neurologic deficits. CONCLUSIONS: For patients with atlantoaxial dislocation, syringomyelia, and basilar impression without clinical symptoms or signs of brain stem compression, occipitocervical spine fusion alone at the reduction of the atlantoaxial dislocation may be indicated because these procedures improve neurologic deficits and prevent postoperative development of basilar impression and enlargement of syringomyelia.- - - - - - - - - - ranking = 4.7329777821869keywords = neurologic (Clic here for more details about this article) |
7/41. Quantification of circulating anti-Hu antibody in serial samples from patients with paraneoplastic neurological syndromes: possible correlation of antibody concentration and course of neurological symptoms.Serial samples, spanning an observation period of 4 to 10 years, from five patients with anti-Hu associated paraneoplastic neurological syndromes (PNS) were investigated with an enzyme linked immunosorbent assay (ELISA) employing recombinant HuD protein as antigen. In one patient the anti-Hu antibody concentration converted from negative to highly positive levels after the onset of neurological symptoms. These findings argue in favour of the idea that an autoimmune process, which is generated at the beginning of the neurological disease, causes the anti-Hu associated PNS. serum samples obtained shortly after the beginning of the PNS were available from two other patients. The anti-Hu antibody levels in these latter patients increased from modest to highly positive anti-Hu antibody in follow up samples. In two patients a clear decrease of the anti-HuD antibody concentration together with an improvement of paraneoplastic neurological symptoms after successful tumour treatment were seen. overall these data suggest that there might be a correlation between the anti-HuD antibody level and the clinical course of paraneoplastic neurological symptoms which supports further the hypothesis that an autoimmune process is responsible for the anti-Hu associated paraneoplastic neurological symptoms.- - - - - - - - - - ranking = 33.130844475308keywords = neurologic (Clic here for more details about this article) |
8/41. Exertional myelopathy in type 2 congenital kyphosis.STUDY DESIGN: A case of lower-extremity myelopathy induced by physical exertion in a patient with Type 2 (failure of segmentation) congenital kyphosis is reported. OBJECTIVE: To describe the uncommon presentation of neurologic sequelae in a patient with Type 2 congenital kyphosis. SUMMARY OF BACKGROUND DATA: Various reports have described neurologic sequelae in patients with Type 1 (failure of formation) congenital kyphosis. To the authors' knowledge, no case of Type 2 congenital kyphosis leading to neurologic symptoms has been reported. methods: A 17-year-old boy presented with a 3-year history of progressively worsening midthoracic back pain. During exertion, numbness developed along the posterior aspects of his legs, and he experienced a wobbly sensation in his lower extremities that prevented his participation in athletic activities. His static and dynamic neurologic examination was unremarkable. However, he developed a wide-based clumsy myelopathic gait when he was asked to run in the halls of the clinic. magnetic resonance imaging demonstrated that the spinal cord was draped over the posterior vertebral body of T10. Anterior thoracic spinal cord decompression and fusion were performed through a seventh rib thoracotomy using a structural rib graft to fill the defect. The anterior 1 cm of bone was left intact so as not to cause any additional instability. RESULTS: The patient tolerated the procedure well and had complete resolution of his exertionally dependent myelopathic symptoms. At this writing, 3 years after surgery, he is involved in the Navy ROTC program. CONCLUSIONS: Although Type 2 congenital kyphosis is a rare entity, it should be followed carefully and corrected surgically when appropriate. A history of exertional myelopathy may be an early sign of spinal cord impingement and is an indication for surgical decompression.- - - - - - - - - - ranking = 9.4817808880618keywords = neurologic, lead (Clic here for more details about this article) |
9/41. Congenital spondylolysis of the axis with associated myelopathy. Case report.Cervical spondylolysis is a rare clinical entity and occurs predominantly at the C-6 level. The authors describe a patient with congenital spondylolysis of the axis that caused myelopathy. The patient was a 57-year-old woman with long-standing gait disturbance. Plain cervical radiography revealed a radiolucent defect across the pedicle of the axis. magnetic resonance imaging of the cervical spine in the neutral, flexion, and extension neck positions as well as a computerized tomography myelography in the neutral neck position failed to demonstrate any spinal cord compression. When she rotated her neck, however, the spinal cord was caught between the hypertrophic anterior arch of the atlas and posterior part of the slipped pedicle of the axis on the contralateral side. The spinal cord was transformed into a pear shape. Mechanical injury to the spinal cord seemed to explain her neurological presentation. This is, to the authors' knowledge, the 15th case of axial spondylolysis and the sixth case of spinal cord involvement of the cervical spondylolysis. No cases involving myelopathy secondary to such a unique mechanism have been reported previously in the literature.- - - - - - - - - - ranking = 2.3664888910935keywords = neurologic (Clic here for more details about this article) |
10/41. vincristine-induced neuropathy as the initial presentation of charcot-marie-tooth disease in acute lymphoblastic leukemia: a Pediatric Oncology Group study.PURPOSE: After profound peripheral neurotoxicity during induction chemotherapy for acute lymphoblastic leukemia (ALL) in the index patient with Charcot-Marie-Tooth hereditary neuropathy (CMT), study coordinators of the Pediatric Oncology Group (POG) front-line ALL protocols reviewed patient registrations to identify any other patients with possible CMT. The goal was to provide preliminary information about patients with undiagnosed CMT who develop ALL. patients AND methods: Five children with ALL who were enrolled in POG B-precursor or T-cell ALL protocols from 1994 to 1999 subsequently were determined to have CMT hereditary neuropathy. Their clinical presentations and treatment records were reviewed in detail. Records of all patients entered on POG 9201 (lesser-risk ALL) were reviewed to identify all cases of significant vincristine toxicity noted in the first 6 months of treatment. RESULTS: The five identified patients all had substantial peripheral neurotoxicity that required alteration in treatment and/or orthopedic/physical therapy evaluation and follow-up. The POG 9201 review identified 25 of 686 patients (3.6%) with significant peripheral neuropathy. Three of 25 were diagnosed with CMT; the others have had no testing reported. CONCLUSIONS: A family history of CMT or other peripheral neuropathy should be sought at the time of diagnosis of ALL. Testing for CMT should be considered in any child with substantial vincristine-induced peripheral neurotoxicity. Treatment of such patients must be individualized. Testing of all patients with significant peripheral neuropathy would be necessary to determine the percentage of such neuropathy explained by underlying CMT.- - - - - - - - - - ranking = 1.760278616877keywords = neurotoxicity, toxicity (Clic here for more details about this article) |
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