Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human T-cell lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) has been associated with changes in extracellular matrix of neural tissue. HTLV-I infection has multiple other systemic effects. Extracellular matrix is important for bone mineral deposition. We examined bone mineral density (BMD) in patients with HAM/TSP. BMD was assessed by ultrasonographic calcaneous densitometry in 24 patients (7 males, 17 females) with HAM/TPS, and 23 healthy HTLV-I-seronegative controls matched by age and sex. Patients with HAM/TPS had a mean BMD T-score of -3.07 +/- 0.64 in males and -2.93 +/- 0.69 in females. Control patients revealed a T-score of -0.77 +/- 1.31 in males and -1.17 +/- 1.08 females. The difference in T-score between HAM/TSP patients and control groups is significant (P < 0.001). Of HAM/TPS patients, 7 of 24 (29.2%) had osteopenia (T-score between -1 and -2.5) and 17 of 24 (70.8%) were diagnosed with osteoporosis (T < -2.5). Respective figures for control patients were 10 of 23 (43.5%) with a normal T-score, 11 of 23 (47.8%) with osteopenia, and 2 of 23 (8.7%) with osteoporosis. After adjustment for age and sex, odds ratio of osteoporosis for HAM/TSP patients was 31.52 (95% confidence interval, 5.07 to 195.88). No correlation was found in HAM/TSP patients between T-score and age, menstrual status, gait functionality, or years of evolution of HAM/TSP. HAM/TSP patients have a significantly diminished BMD of the calcaneous that appears not to be explained by paresis, age, years of disease, menstrual status; may be the result of systemic alterations due to HTLV-1 infection.
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PMID:Osteoporosis in HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). 1449 52

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

An adult, captive-born Sumatran tiger (Panthera tigris sumatrae) had been ataxic for approximately 3 mo and had been self-mutilating after an acute onset of unilateral paresis and Homer's syndrome. Histologic lesions in the cervical spinal cord were consistent with fibrocartilaginous embolic myelopathy (FCEM), and they included the presence of cartilaginous occlusion of spinal blood vessels. This is the first reported case of FCEM in a large felid and specifically a Sumatran tiger.
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PMID:Fibrocartilaginous embolic myelopathy in a Sumatran tiger (Panthera tigris sumatrae). 1530 22

A 5-month-old Angus heifer with a history of acute hindlimb paresis that quickly progressed to lateral recumbency was necropsied. Gross lesions included a 6-cm segment of gray to brown discoloration and softening of the right ventrolateral spinal cord between T2 and T3. Microscopically, there was liquefactive necrosis of ventrolateral white and gray matter, and multiple intravascular emboli partially or completely occluded many intralesional and adjacent spinal and meningeal arteries and veins. Emboli were alcian blue positive, consistent with fibrocartilage of the nucleus pulposus of the intervertebral disk. No gross abnormalities were detected in the vertebrae or intervertebral disks. Fibrocartilaginous embolic myelopathy appears to be very rare in cattle; however, it should be considered in cases of acute, nonprogressive spinal cord dysfunction.
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PMID:Fibrocartilaginous embolic myelopathy in a calf. 1530 54

This retrospective study aims to discuss and compare our results with those previously mentioned in the literature with regard to C5-C6 radiculopathy that occurs after decompression carried out for cervical spondylotic myelopathy. There are few reports in the literature referring to the incidence of the C5-C6 radiculopathy following cervical decompression procedures. Some authors believe that the postoperative cord shift is the most likely cause. From January 1994 to November 2002, 121 patients underwent cervical corpectomies for cervical spondylotic myelopathy. The preoperative and the postoperatively discovered paresis have been assessed according to the criteria of the British Medical Council. The Nurick Scale was used to grade the severity of the myelopathic changes. The follow-up period varied from 4 to 111 months with an average of 50 months. Symptoms of C5 and/or C6 radiculopathy appeared in 10 patients (8.2%) postoperatively. Aggravation of a preoperative C5 and/or C6 radiculopathy was seen in 3 patients, while 7 patients developed a new C5 and/or C6 radiculopathy in the immediate postoperative period. These motor deficits resolved completely in 7 patients within 7 months of surgery, whereas a residual motor weakness remained in the other 3 patients. The postoperative C5 motor deficit is not infrequently associated with partial involvement of the C6 root. The lesions can be either unilateral or bilateral with a statistically average frequency of 8%. The prognosis is generally favorable. Our results did not support the hypothesis that the claimed cord shift phenomenon is a possible aetiology.
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PMID:The incidence of C5-C6 radiculopathy as a complication of extensive cervical decompression: own results and review of literature. 1537 14

Today, posterior stabilization of the cervical spine is most frequently performed by lateral mass screws or spinous process wiring. These techniques do not always provide sufficient stability, and anterior fusion procedures are added secondarily. Recently, transpedicular screw fixation of the cervical spine has been introduced to provide a one-stage stable posterior fixation. The aim of the present prospective study is to examine if cervical pedicle screw fixation can be done by low risk and to identify potential risk factors associated with this technique. All patients stabilized by cervical transpedicular screw fixation between 1999 and 2002 were included. Cervical disorders included multisegmental degenerative instability with cervical myelopathy in 16 patients, segmental instability caused by rheumatoid arthritis in three, trauma in five and instability caused by infection in two patients. In most cases additional decompression of the spinal cord and bone graft placement were performed. Pre-operative and post-operative CT-scans (2-mm cuts) and plain X-rays served to determine changes in alignment and the position of the screws. Clinical outcome was assessed in all cases. Ninety-four cervical pedicle screws were implanted in 26 patients, most frequently at the C3 (26 screws) and C4 levels (19 screws). Radiologically 66 screws (70%) were placed correctly (maximal breach 1 mm) whereas 20 screws (21%) were misplaced with reduction of mechanical strength, slight narrowing of the vertebral artery canal (<25%) or the lateral recess without compression of neural structures. However, these misplacements were asymptomatic in all cases. Another eight screws (9%) had a critical breach. Four of them showed a narrowing of the vertebral artery canal of more then 25%, in all cases without vascular problems. Three screws passed through the intervertebral foramen, causing temporary paresis in one case and a new sensory loss in another. In the latter patient revision surgery was performed. The screw was loosened and had to be corrected. The only statistically significant risk factor was the level of surgery: all critical breaches were seen from C3 to C5. Percutaneous application of the screws reduced the risk for misplacement, although this finding was not statistically significant. There was also a remarkable learning curve. Instrumentation with cervical transpedicular screws results in very stable fixation. However, with the use of new techniques like percutaneous screw application or computerized image guidance there remains a risk for damaging nerve roots or the vertebral artery. This technique should be reserved for highly selected patients with clear indications and to highly experienced spine surgeons.
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PMID:Complications of transpedicular screw fixation in the cervical spine. 1591 52

We present a case of a patient who received nitrous oxide on two occasions within a period of 8 weeks and who subsequently developed a diffuse myelopathy, characterized by upper extremity paresis, lower extremity paraplegia and neurogenic bladder. Laboratory testing revealed hyperhomocysteinaemia and low levels of vitamin B(12). Because of this uncommon clinical presentation, we analysed the patient's DNA, and found a polymorphism in the MTHFR gene that is associated with the thermolabile isoform of the 5,10-methylenetetrahydrofolate reductase enzyme, which explained the myelopathy experienced by the patient after being exposed to nitrous oxide. Soon after initiating supplementary therapy with folic acid and vitamin B(12), the neurological symptoms subsided.
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PMID:Reversible nitrous oxide myelopathy and a polymorphism in the gene encoding 5,10-methylenetetrahydrofolate reductase. 1636 Dec 98

Calcification of the cervical ligamentum flavum is a rare entity observed exclusively in Japanese people. We report a new case in a 65-year-old man from Tunisia who presented with symptoms of cervical myelopathy with mild tetra paresis, sensory abnormalities and dysuria. Magnetic resonance imaging (MRI) showed a posterior compression of the spinal cord at C3-C4. CT-scan showed a calcification of the ligamentum flavum at level C3-C4, compressing the left postero-lateral aspect of the spinal cord. C3-C4 laminectomy was performed with removal of abnormal ligamentum flavum tissue. The postoperative course was uneventful and all symptoms resolved. Calcification of the cervical ligamentum flavum is a rare entity; the diagnosis is easy but the pathogenesis remains unclear. Literature regarding this pathology is reviewed.
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PMID:[Calcification of the cervical ligamentum flavum. Case report and review of the literature]. 1655 32

Five cats had clinical signs, radiographic findings, and cerebrospinal fluid analyses consistent with fibrocartilaginous embolic myelopathy. All cats had an acute onset of nonpainful, asymmetrical spinal cord signs (paresis or paralysis of one or more limbs). Magnetic resonance imaging was performed in three cats. On T2-weighted images, an intramedullary lesion was revealed that was hyperintense to normal spinal cord gray matter. On T1-weighted images, the lesion was isointense. Three of the cats were euthanized, and postmortem examination confirmed myelomalacia with intralesional fibrocartilaginous emboli. Two cats survived and were clinically improved within 3 weeks.
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PMID:Fibrocartilaginous embolic myelopathy in five cats. 1661 36

Portosystemic encephalopathy (PSE) is a well-known, common complication of portal hypertension. It is thought to be caused by nitrogenous substances such as ammonia, which are normally cleared from the blood stream by the liver. In cirrhosis and other hepatic disorders with portosystemic shunting (PSS)-- either surgical portosystemic anastomoses (PSA) or spontaneous PSS-- the collateral vessels bypass the liver allowing the accumulation of toxic, ammoniacal substances in the blood and tissues. PSE is characterized by encephalopathy; portosystemic myelopathy (PSM) is characterized by paresis of the extremities, Babinski signs and muscle spasticity in patients with cirrhosis and/or PSS. Usually only the lower extremities are involved. This report presents the first case of this syndrome observed 5 years after a transjugular intrahepatic portosystemic shunt. The 31 year old man with chronic Hepatitis B developed complete spastic paraparesis within 4 weeks after onset of clinical/neurological symptoms, accompanied by an episode of severe hepatic encephalopathy. The transcortical magnetic stimulation showed normal motoric stimulation times to the abductor digiti minimi muscles but no stimulation to the tibialis muscles was seen. Lumbar stimulation to the tibialis muscles, however, was normal. This indicates loss of motor neurons in the spinal cord, a characteristic finding in patients with portosystemic myelopathy. We performed a search of the literature for all reported cases of cirrhosis and/or PSS that developed PSM. However, the intervals between the construction of a shunt and the diagnosis of portosystemic myelopathy were shorter in total portacaval shunts (median 16 months) than in partial, non-portacaval shunts (median 60 months, p < 0.01). This suggests that not only the shunt itself but also the shunted volume contributes to the development of the syndrome Sixty-one patients with PSM have been reported in the literature since 1944. PSE had developed before PSM in almost all cases. PSM occurred from 1 month to 10 years after the creation of portacaval anastomoses (PCA) or splenorenal shunts (SRS) or in cirrhotic patients without shunts. No one type of liver disease or type of shunt appears to predispose to PSM. The mechanisms of PSE and PSM are thought to be similar and of nitrogenous origin, but their pathogenesis remains unknown. Lathyrism, a toxic syndrome with similar symptoms and signs, is caused by the ingestion of a legume, Lathyrus sativa, which contains beta-N-oxalo-L amino-L-alanine (BOAA). This animal model with or without BOAA appears to offer a reliable way of studying PSM experimentally.
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PMID:Portosystemic myelopathy: spastic paraparesis after portosystemic shunting. 1663 7


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