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)

A rare case of mesenchymal chondrosarcoma originating from the thoracic spinal dura was reported. A 10-year-old girl complained of paresis of the right leg in June 1977. Then she became unable to walk early in August, and a complete paraparesis developed on August 18. She was admitted to our department on August 22. On admission she had complete paraparesis, bilateral ankle clonus, upward plantar reflexes, sensory disturbance below T7, shincter disturbance and neck stiffness. Plain thoracic X-ray revealed bilateral decalcification of pedicles of T6. Myodil myelography showed a complete block between T6 and lower end of T7 vertebrae. Bilateral laminectomy from T3 to T8 was performed. A tumor originating from the spinal dura was located in the right dorsal extradural space. The tumor was totally removed together with a small area of the affected dura. Light microscopy showed mesenchymal chondrosarcoma. Her recovery from neurological deficiencies was excellent and now she can run 14 months after surgery. Metastasis or recurrence has not yet been seen.
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PMID:[A case of mesenchymal chondrosarcoma originating from the spinal dura (author's transl)]. 49 58

From July 1984 to June 1990, seven cases of spontaneous spinal epidural hematoma (SSEH) were studied. The common clinical pictures in these cases were rather typical with an apoplectic onset of severe spinal pain followed in hours (median: four hours) by signs of progressive spinal cord compression. All cases underwent myelography and computed tomographic (CT)-myelographic studies which showed in all cases a block by a posterior extradural lesion in the spinal column; however, the correct diagnosis of SSEH was made preoperatively in only three cases. The neurologic deficits prior to surgery were complete or nearly complete paraplegia in five cases and a high grade of paraparesis in the other two. The median interval of paralysis or paresis before surgery was 28 hours. The final outcome was evaluated by the grade of functional recovery, and the following were found to be the favorable factors: 1) incomplete preoperative neurologic deficits; 2) a slow course of clinical progression, especially a long duration of pain before the onset of paralysis; 3) no delay in surgery; 4) involvement of short spinal segments; and 5) lumbosacral lesions. Particular emphasis is made on early diagnosis and prompt surgery for a favorable outcome.
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PMID:Spontaneous spinal epidural hematoma: report of seven cases. 136 22

Paraparesis (paraplegia) refers to partial (-paresis) or complete (-plegia) loss of voluntary motor function in the pelvic limbs. Similar involvement of all four limbs is termed tetraparesis (tetraplegia). Paraparesis generally results from spinal cord lesions caudad to the second thoracic spinal cord segment, whereas tetraparesis occurs because of lesions craniad to this segment (see discussion of spinal cord lesion localization in The Neurologic Examination and Lesion Localization, on page 328). The limbs may be affected equally; however, asymmetric lesions cause greater clinical involvement on the ipsilateral side. Strictly unilateral lesions at C1-T2 result in clinical involvement on only the affected side of the body (hemiparesis, hemiplegia). Monoparesis (monoplegia) occurs subsequent to unilateral T2-S1 lesions. Trauma and neoplasia are the most common spinal cord diseases affecting cats. Urinary and fecal incontinence often occur concomitant with paresis. General concepts relating to disorders of micturition are discussed at the conclusion of this chapter.
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PMID:Paraparesis (paraplegia), tetraparesis (tetraplegia), urinary/fecal incontinence. Spinal cord diseases. 180 59

Three patients with spinal dural arteriovenous fistula presented with acute and/or progressive myelopathy. The thoracic cord was focally enlarged and poorly defined on MR images in two of the patients. One individual showed focal cord atrophy, and one demonstrated abnormal intrathecal vessels. In all patients MR studies revealed cord enhancement after IV administration of gadopentetate dimeglumine. The MR findings are believed to represent disruption of the blood-cord barrier associated with cord ischemia and/or infarction, which, in turn, is caused by venous stasis resulting from the fistula. The diagnosis in each case was confirmed by the combined results of myelography, spinal arteriography, and surgery. Surgical excision or embolization of the fistula produced a poor return of lost function but an arrest in the progression of paresis. One of the patients had constant severe back and leg pain postoperatively, and a follow-up MR study 5 months after surgery showed focal atrophy and persistent enhancement of the thoracic cord. The patient with preoperative focal cord atrophy had an MR examination 1 year prior to surgery, which revealed enhancement of the cord similar to that seen on the immediate preoperative MR study. This patient also had severe pain in the back and lower extremities preoperatively, which accompanied her progressive paraparesis. It is believed that long-standing enhancement of the spinal cord in patients with dural arteriovenous fistula probably results from chronic progressive venous ischemia, which may be irreversible and cause pain of a central type.
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PMID:Venous infarction of the spinal cord resulting from dural arteriovenous fistula: MR imaging findings. 188 56

Six AIDS patients with progressive cytomegalovirus (CMV) polyradiculomyelitis were treated with ganciclovir in an open study. The diagnosis was based on the presence of a distinct clinical syndrome with progressive flaccid paraparesis, preserved proprioception and urinary retention with specific cerebrospinal fluid (CSF) findings. Ganciclovir therapy, 5-10 mg/kg per day, instituted 3-6.5 weeks after onset of symptoms, was ineffective in four patients with severe paraparesis. One patient developed CMV polyradiculomyelitis while receiving ganciclovir and further deteriorated during foscarnet therapy. One patient however, showing minor paresis of one leg, improved after institution of ganciclovir therapy 1 week after onset of symptoms. It is concluded that a presumptive diagnosis of CMV polyradiculomyelitis can be made on the basis of distinct clinical findings and CSF pleocytosis with predominance of polymorphonuclear leukocytes in patients with AIDS. Ganciclovir therapy does not appear to be beneficial for patients with advanced paresis in the doses used. Further investigations are needed in order to determine if early intervention with ganciclovir, when paresis is mild, or higher doses in advanced paresis, might be of some benefit.
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PMID:Therapy for cytomegalovirus polyradiculomyelitis in patients with AIDS: treatment with ganciclovir. 216 19

To determine the distribution of weakness in the lower limb after upper motoneuron lesions the strength of 8 muscle groups was measured. Four groups of patients were studied: 22 control subjects, 16 patients with unilateral leg paresis, 4 patients with severe unilateral paralysis and 5 patients with paraparesis. In the testing posture (seated), patients with cerebral upper motoneuron lesions showed no selective loss of power in flexors or extensors on the contralateral side. Gravitational torques were included in the measurements. However, proximal muscles (acting at hip and knee) were significantly less severely affected than more distal muscles (acting at ankle and hallux). At any particular joint, physiological flexors and extensors were affected equally in both the hemiparetic and paraparetic subjects. As in the upper limb (Colebatch and Gandevia, 1989), the strength of muscles on the clinically unaffected side was reduced compared with control subjects, although no muscle groups were especially affected.
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PMID:The distribution of muscle weakness in upper motoneuron lesions affecting the lower limb. 224 6

Interhemispheric subdural hematoma (ISDH), although not infrequent in children, has been rarely encountered in adults. Spread of CT, ISDH has been reported sporadically, and so far more than 40 cases have been reported. But bilateral ISDH is an extremely rare lesion, with only 5 cases reported in the literature. We report a sixth case of bilateral ISDH in adults. A 68-year-old woman was admitted because of headache and vomiting. Two days before admission she had fallen, striking her occiput, and had lost consciousness for a few minutes. Neurological examination on admission revealed hyperreflexia of her extremities, especially in her left leg. However, motor weakness was not recognized. There was no fracture visible on the plain X ray films of the skull. Axial CT scan demonstrated a high density lesion along the falx and its extension down over the tentorium. Coronal CT scan also demonstrated a convexo-convex high density lesion beside the falx, and its extension onto the tentorium. Cerebral angiogram showed lateral displacement of the callosomarginal artery, and an avascular area beside the falx and onto the tentorium. After admission she was managed conservatively, but on the 14th day after head trauma, paraparesis and left arm paresis were recognized. This condition deteriorated and she developed an inability to stand. On the 19th day parasagittal craniotomy and evacuation of the hematoma were performed. Her postoperative course was uneventful and she was discharged with no neurological deficits.
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PMID:[A case of bilateral interhemispheric subdural hematoma]. 235 80

In patients with spastic paraparesis, increased extensor tonus can be decreased by stimulation of flexor reflex afferents. This should improve dorsiflexion of the foot and reduce the sense of effort. We therefore examined ability to maintain stable firing of a single motor unit (SMU) in tibialis anterior muscle and force of dorsiflexion in 17 normal subjects and 9 with spastic paresis, during several minutes of tonic nonpainful stimulation (20 Hz, 0.1 msec) of the sural nerve at the ankle (SNS). Subjects were asked to maintain stable SMU firing first with, then without auditory feedback of the motor unit potential. SNS was then applied for several minutes. In normal subjects, the force of dorsiflexion increased 33 +/- 26% with SNS and 2.5% +/- 5% without SNS (p less than 0.0005). Most subjects noted increased resistance to dorsiflexion during SNS that resulted in greater innervation of tibialis anterior muscle. In six abnormal subjects, the force of dorsiflexion increased 30 +/- 30% with SNS, but no increase was recorded without SNS. In normal subjects and those with spastic paresis of the legs, SNS increased innervation of tibialis anterior muscle and awareness of greater effort required to maintain constant innervation. The altered proprioception may depend on facilitation of motor neurons.
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PMID:Sural nerve stimulation and motor control of tibialis anterior muscle in spastic paresis. 379 38

Motor lesions following herpes zoster are quite common. Hemiparesis, paraparesis, pareses of the facial and other cranial nerves as well as segmental pareses can be observed. We report on a patient suffering from zoster ophthalmicus complicated by paresis of the third cranial nerve. As a cause, a partial brain stem-encephalitis was diagnosed. The patient recovered after antiviral treatment (Aciclovir, Inosiplex).
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PMID:[Motor function loss in zoster neuritis versus encephalitis--clinical case and review of literature]. 620 68

Activation of leg musculature on both sides following a unilateral displacement was studied during stance on separate see-saws, or on stable force-measuring platforms, in patients with spastic hemiparesis and paraparesis. During balancing the movements on the spastic side were damped and the degree of muscle activation reduced. Whereas in healthy subjects the tibialis anterior muscles of both sides were activated, following a unilateral displacement, with the same strength and latency (see-saws 55 ms, platforms 85 ms), in hemispastic patients the EMG responses were delayed (by about 20 to 30 ms) and of reduced strength on the spastic leg, irrespective of whether the unaffected or the spastic side was displaced. In addition, the compensatory movements on the spastic side were damped in both conditions, although the amplitude of displacement was the same bilaterally. Although there was no correlation between the delay and the reduction in EMG response, the latter was correlated with the severity of paresis. In patients with spastic paraparesis quite similar results were obtained with delayed and reduced EMG responses on both sides. It is concluded that in spasticity the impaired regulation of quick compensatory movements is due to a dysfunction of a spinal interneuronal system by which the early EMG responses are mediated. This could be explained by loss of supraspinal control. In addition to the impaired neural activation of leg muscles, changes in the mechanical properties of muscle can be assumed to contribute to the damped movements on the spastic side.
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PMID:Interlimb coordination of posture in patients with spastic paresis. Impaired function of spinal reflexes. 647 85


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