Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 41-year-old man was doing well until July 1989, when he noted numbness over soles, followed 4 months later by difficulty in walking. These symptoms were progressively getting worse, and he was admitted to our department on June 12, 1990. General physical examination was unremarkable. Neurologically cranial nerves were intact except old right, traumatic strabismus. Muscle tone and deep tendon reflexes were normal throughout, but bilateral Babinski and Chaddock reflexes were present. Mild weakness of lower extremities were found on muscle testing (4/5). In sensory system, superficial sensory disturbance below T10 was seen, and markedly diminished vibration and position senses of lower extremities were noted. Cerebellar test was intact, although unsteadiness was found on heel-shin test. Romberg sign was definitely positive. His gait was wide-based and ataxic. Laboratory data showed no abnormalities in CBC, chemistry, urinalysis, serological tests and endocrinological examinations. Spinal MRI (Siemens 1.5 Tesla) showed abnormal deposition of epidural fatty tissues compressing spinal cord with flattening of cord from T4 to T8. Spinal ataxia as compressive myelopathy due to epidural lipomatosis was considered and he underwent laminectomy from T4 to T8 with improvement in walking. Epidural lipomatosis is an unusual cause of spinal cord compression, presenting compressive myelopathy, radiculopathy, cauda equina syndrome, intermittent claudication, or back pain. Most of cases were associated with long-term administration of adrenocortical steroid hormone, or underlying diseases, except only 3 cases including ours. This is the first case of spinal epidural lipomatosis presenting progressive gait disturbance due to spinal ataxia.
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PMID:[A case of epidural lipomatosis presenting spinal ataxia]. 206 Feb 46

We report about two cases of hemivertebrae in pigs. The malformations appeared in the T2/3, respectively in the T10. One case showed clinical apparent signs, namely ataxia and leg weakness. The productivity of the affected pig was reduced. Both cases are of unclear genesis. A hereditary predisposition could not be proved.
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PMID:[Wedge-shaped vertebral formation as the cause of leg weakness syndrome in swine--a case report]. 224 34

We have studied an unusual, spontaneous, intradural extramedullary spinal cord tumor in 12 dogs. Animals presented with paraparesis and ataxia early in life (11/12 ranged from 6 to 38 months of age) suggesting that these tumors may be congenital. Various breeds of dogs were represented with four cases in German Shepherds and three in retrievers; there was no sex predisposition. Post-mortem examinations revealed a single intradural mass consistently located between T10 and L2, which produced extensive compression of the spinal cord. Metastasis was never observed and significant pathological changes in other organs were lacking. Microscopic examination revealed solid sheets of ovoid to fusiform cells interspersed with areas of acinar and tubular differentiation. Some areas were rarified and focal squamous metaplasia was observed. Ultrastructural features included the presence of a continuous basal lamina, junctional complexes, microvilli and occasional cilia at the apices of acinar complexes. Immunocytochemical studies did not support a neurectodermal origin. At least 13 case reports of this entity have been previously published and have been designated ependymomas, medulloepitheliomas and neuroepitheliomas. A recent case was diagnosed as a nephroblastoma and we feel that this is an interesting and provocative diagnosis. These tumors could result from remnants of renal primordium which becomes trapped between the dura and the developing spinal cord. However, firm evidence of such a histogenesis is not yet at hand.
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PMID:A novel intradural extramedullary spinal cord tumor in young dogs. 245 49

The patient, a 30 year-old man, dentist, started having an influenza-like infection which lasted five days, with malaise, muscle pain throughout the body and fever. One day before the hospital admission he presented urinary retention followed in the next day by ataxia and numbness sensation in both feet and lower third of his legs. The neurological examination disclosed a thoracic spinal cord impairment at T9-T10 level and the diagnosis of a post- infectious transverse myelitis was made. The plain Rx of the spine showed a spina bifida oculta in the T7 vertebra, which is roughly at the same level of the T9-T10 spinal cord segment. An iodinated myelography showed no abnormalities. The CSF examination showed small increase in the white cells (6.4 cells/cu.mm). The patient received dexamethasone (4. 5g /day) and two weeks later was entirely free of symptoms. The authors think that the congenital bone defect (spina bifida) might have played a role in the development of the myelitis, probably because of an ontogenetically determined "vulnerable point" ("locus minor resistentia ") at that level, either anatomical or immunological.
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PMID:[Post-infectious transverse myelitis and thoracic spina bifida: report of a case]. 637 43

Sixty-six dogs suffering from intervertebral disk diseases on cervical and/or thoracolumbar disks were treated by a ventral fenestration. The breeds affected with disk diseases were Dachshund (65.1%), Beagle (15.2%), Shih Tsu (4.5%), Pekingese (4.5%), and others (18.2%). Sites suffered from disk diseases and received disk fenestration most frequently were from T10-11 to L2-3. However, other disks were also needed the operation in some cases. An average number of disks received fenestration was 6.0. Days to walk after the fenestration in 51 cases varied 1 to 120 days (average: 14.9 +/- 22.0 days, mean +/- S.D.) depending on their severity. The recovery rates from the follow-up study were as follows: In grade I (3 cases, able to walk with back pain) and grade II (14 cases, slight ataxia and paresis) it was 100%, respectively. The rates in grade III (23 cases, paraplegia with positive deep pain) and grade IV (26 cases, paraplegia with lack of deep pain) were 73.9% and 65.4%, respectively. A few recurrence after the operation were observed in this study. As a result, the ventral fenestration was extremely effective as a treatment for disk diseases in the dog.
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PMID:A retrospective study of ventral fenestration for disk diseases in dogs. 828 31

A 7-year-old neutered female domestic short hair cat was presented with hind limb ataxia. A subarachnoid cyst in the T10-T11 spinal cord region was identified by myelography as a collection of contrast medium in the subarachnoid space.
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PMID:Spinal subarachnoid cyst in a cat. 1022 19

A 12-year-old grey Warmblood stallion presented with fever of unknown origin, and anaemia. Five days later it had developed ataxia and become recumbent, and was humanely killed. At necropsy, malignant melanomas were identified in the perineal subcutis, spleen, and thoracic vertebral canal (T10-11). Populations of malignant melanoma cells were scattered throughout medullary cavities of the axial and appendicular skeleton, and were identified grossly as irregular areas of black to grey discoloration. To the authors' knowledge, this is the first report of disseminated intramedullary melanoma in a domestic species.
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PMID:Disseminated metastatic intramedullary melanoma in an aged grey horse. 1157 37

Primary solitary amyloidoma of spine is a rare subset of amyloidosis in which the amyloid deposition is focal and not secondary to a systemic process or plasma cell discrasia. Only seventeen cases of spine involvement have been reported. We report a 71-year-old man with 3 months history of ataxia and frequent falls. On the 4th month paraparesis developed. Magnetic resonance imaging of the dorsal spine revealed a lesion involving the T-9 vertebral level with significant spinal cord compression. Decompressive laminectomy with posterior instrumentation and fusion from T8 to T10 was performed. Histopathology revealed abundant amyloid deposits. No evidence of myeloproliferative disease or systemic amyloidosis was found. The patient showed marked neurological improvement with residual mild spastic gate 6 months after surgery. When occurring primarily in a localized anatomic area, the prognosis of amyloidoma is excellent, and cure can be expected by local resection. It is important to know that diagnosis requires a high index of suspicion and, ultimately, adequate tissue biopsy for histopathological studies.
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PMID:Primary solitary amyloidoma of thoracic spine: a case report and review of the literature. 1286 May 8

Subarachnoid blood has been reported as a cause of chronic spinal arachnoiditis. Although syringomyelia has been thought to be caused by spinal arachnoiditis, reports of syringomyelia following aneurysmal subarachnoid hemorrhage (SAH) are very rare. We describe two patients with syringomyelia associated with chronic spinal arachnoiditis following SAH. From January 2001 to December 2010, 198 patients with aneurysmal SAH were treated at Kinki University School of Medicine. Two of the 198 patients had syringomyelia following aneurysmal SAH; thus the rate of syringomyelia associated with aneurysmal SAH was 1.0%. Patient 1 was a 54-year-old woman who presented with back pain, back numbness and gait disturbance 20 months after SAH. Her MRI revealed syringomyelia of the spinal cord from C2 to T10. She underwent shunting of the syrinx to the subarachnoid space. Patient 2 was a 49-year-old man, who was admitted to the hospital with headache, diplopia, hoarseness, dysphagia and ataxia five months after SAH. MRI revealed syringomyelia from the medulla oblongata to C6, and an enlargement of the lateral and fourth ventricles. After foramen magnum decompression and C1 laminectomy, a fourth ventricle-subarachnoid shunt was placed by insertion of a catheter. Spinal arachnoiditis and spinal syringomyelia are rare but important chronic complications after SAH.
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PMID:Spinal syringomyelia following subarachnoid hemorrhage. 2228 78

Dorsal spinal cord herniation is reportedly a rare condition. Here, the authors report an unusual case of dorsal spinal cord herniation at the thoracolumbar junction presenting with scalloping of ossification of the ligamentum flavum (OLF). A 75-year-old woman with a 2-year history of bilateral leg dysesthesia presented with progressive gait ataxia. Neurological examination showed bilateral patellar tendon hyperreflexia with loss of vibratory sensation and proprioception in her bilateral lower extremities. CT myelography revealed a posterior kink and dorsal herniation of the spinal cord at T11-12, with OLF between T10-11 and T12-L1. In addition, scalloping of the OLF was observed at T11-12 at the site of the herniated spinal cord. This scalloping was first noted 9 years previously and had been gradually progressing. The patient underwent surgical repair of the spinal cord herniation. Subsequently, her spinal cord herniation and vibratory sensation and proprioception in both legs partly improved, but gait ataxia remained unchanged. Dorsal spinal cord herniation reportedly occurs under conditions of vulnerability of the dorsal dura mater. In this case, acquired vulnerability of the dorsal dura mater owing to previous epidural catheter placement into the thoracolumbar space may have resulted in dorsal spinal cord herniation.
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PMID:Dorsal spinal cord herniation at the thoracolumbar junction presenting with scalloping of ossification of the ligamentum flavum: case report. 3162 76


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