Cases reported "Muscle Spasticity"

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11/93. Breathlessness associated with abdominal spastic contraction in a patient with C4 tetraplegia: a case report.

    A tetraplegic patient with C4 cervical cord injury reported breathlessness during episodes of spastic contraction of the abdominal muscles. To determine the mechanism, we performed electrophysiologic testing of the phrenic nerves. We measured abdominal pressure, esophageal pressure, and transdiaphragmatic pressure (Pdi) during a maximal inspiratory effort (Pdi max), a maximal sniff maneuver (sniff Pdi) during resting breathing, and during the episodes of breathlessness. Electrophysiologic testing of the phrenic nerves showed axonal neuropathy on the left. Sniff Pdi and Pdi max were 38cmH(2)O and 42cmH(2)O, respectively. Transient spastic contractions of abdominal muscles were associated with an increase in abdominal pressure greater than 30cmH(2)O, with a decrease in abdominal volume; this rise in abdominal pressure was transmitted to the esophageal pressure. Inspiration became effective only when esophageal pressure fell below the resting baseline value. Achieving this decrease required an increase in inspiratory effort, characterized by swings in esophageal pressure and Pdi of 30cmH(2)O and 40cmH(2)O (approximately 100% of Pdi max), respectively. During these periods, minute ventilation was markedly reduced. This is the first report that spastic abdominal muscle contractions can impose a significant load on the diaphragm, uncovering moderate diaphragmatic weakness. This has important clinical implications; abolition of the spastic abdominal muscle contraction in this patient completely resolved her intermittent respiratory symptoms.
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ranking = 1
keywords = neuropathy, nerve
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12/93. Atypical paraneoplastic syndrome associated with anti-Yo antibodies.

    OBJECTIVE: Polyneuropathy, myopathy and spasticity have not been described as a manifestation of a neurologic paraneoplastic syndrome (NPS) associated with anti-Yo antibodies (anti-Yo). CASE history: The patient is a 60-year-old woman with a history of ovarectomy, salpingectomy, hysterectomy and omentectomy because of ovarian cancer with peritoneal carcinosis. From May to September 1999, she received chemotherapy with carboplatin and docetaxel. In June 1999, weaknesses of the lower limbs began to appear. Neurologic investigation revealed bilateral ptosis with right-sided predominance, exaggerated deep tendon reflexes, discrete distal weakness, wasting of the upper limbs and diffuse weakness of the lower limbs. She had slight CK elevation, elevated lactate dehydrogenase and aldolase levels. Testing for anti-neuronal antibodies revealed high serum titers of antibodies against the cytoplasm of purkinje cells, confirmed as anti-Yo by immunoblot with recombinant proteins. CSF investigations showed 12/3 cells and positive oligoclonal bands. MRI of the brain showed bilateral, old ischemic basal ganglia lesions exclusively. Visually evoked potentials gave prolonged P100 latencies bilaterally. Nerve conduction studies and electromyography revealed motor polyneuropathy of the lower limbs. Muscle biopsy from the right anterior tibial muscle showed non-specific myopathic features. CONCLUSION: Polyneuropathy, myopathy and tetraspasticity may be the exclusive manifestations of an atypical NPS associated with anti-Yo. Anti-Yo may persist for years without relapse of the primary tumor.
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ranking = 1.5993201093374
keywords = neuropathy
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13/93. Chronic neurodegenerative disease associated with HTLV-II infection.

    Although human T-cell leukemia virus (HTLV) type I is known to cause a number of diseases, there has been no convincing evidence of pathological changes after infection with the related virus, HTLV-II. We have found an endemic focus of HTLV-II infection among members of an American Indian population in new mexico, USA. We set out to determine the pathological consequences of HTLV-II infection in this population and identified two sisters (aged 59 and 46 years) with a disease superficially resembling the myeloneuropathy induced by HTLV-I. These women had a syndrome similar to the olivopontocerebellar atrophy variant of multiple system atrophy, and HTLV-II infection was confirmed by western blot and the polymerase chain reaction. Thus, HTLV-II may, like HTLV-I, cause a progressive neurodegenerative disease.
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ranking = 0.53310670311247
keywords = neuropathy
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14/93. phenol block for hip flexor muscle spasticity under ultrasonic monitoring.

    Hip flexor spasticity, which is often associated with central nervous system (CNS) diseases, is a major impediment in rehabilitation. In order to cope with this problem, lumbar nerve blocking techniques developed by Meelhuysen and major and minor psoas muscle blocking techniques developed by Awad have been used in combination with physical therapies. Based on these techniques, we conducted major and minor psoas muscle phenol block (motor point block or intramuscular nerve block) under ultrasonic monitoring. phenol block was conducted in nine patients with cerebral infarction (13 blocking procedures) and three with spinal cord injuries (six blocking procedures) while keeping them in a lateral position with the operation side upside. The beginning of the femoral nerves and part of the lumbar artery were visualized by ultrasound in some patients. As a result of the improvement of hip flexor spasticity, the range of hip joint motion (determined by the Mundale technique, prone hip extension and Thomas test) improved shortly after blocking. When physical therapy was conducted after blocking, improvement of skin care management was observed in eight cases, ability to keep in a stable sitting position in nine, improvement of a standing posture in three, increases in the ability to walk in two and alleviation of pain in three. Although nerve block is reported to result in hematoma, decreases in muscle force, pain, cystic/rectal disorders and hypogonadism, we have observed no such complication in our patients.
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ranking = 1.1450382249522
keywords = nerve, nervous system
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15/93. Hereditary spastic dystonia with Leber's hereditary optic neuropathy: neuropathological findings.

    Neuropathological findings in a 59-year-old male case of hereditary spastic dystonia with Leber's hereditary optic atrophy included: marked depletion of myelinated nerve fibres in the posterior funiculi, corticopontine tracts and striatum; practically complete neuronal depletion in the putamen and lateral part of the caudate, and mild cell loss in the substantia nigra. The putamina had changed into a spongy fibrillary scar, the pallidal fibres and laminae were practically all degenerated. Moreover, there was generalised mild fibre degeneration of the white matter. The optic nerve showed marked, predominantly central, loss of nerve fibres with demyelination.
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ranking = 2.8327667577812
keywords = neuropathy, nerve
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16/93. Identification of a SACS gene missense mutation in ARSACS.

    The authors describe two patients in a Japanese family with autosomal recessive spastic ataxia of Charlevoix-Saguenay. They presented early onset spastic ataxia, sensorimotor neuropathy, nystagmus, slurred speech, and hypermyelinated retinal nerve fibers. The authors identified a homozygous missense mutation (T7492C) in the SACS gene, which resulted in the substitution of arginine for tryptophan at amino acid residue 2498 (W2498R).
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ranking = 0.76655335155624
keywords = neuropathy, nerve
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17/93. Clinical variability in maternally inherited leber hereditary optic neuropathy with the G14459A mutation.

    Spasticity and dystonia have been associated with mitochondrial (mt) dna mutations at A11696G, G14459A, and T14596A. We describe the clinical features and molecular analysis of two Caucasian pedigrees with the 14,459 guanosine (G) --> adenine (A) transition. The maternally inherited Leber hereditary optic neuropathy (LHON) phenotypes showed extreme clinical variability and the only screening test that was abnormal in the patient with spasticity/dystonia was a high T2 signal in the putamen bilaterally. The male patient in the second pedigree showed features of optic neuropathy without spasticity/dystonia. These results further support that the 14,459 G --> A transition mutation is causally related to LHON and spasticity/dystonia.
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ranking = 3.1986402186748
keywords = neuropathy
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18/93. Variable clinical manifestation of homoplasmic G14459A mitochondrial dna mutation.

    Leber hereditary optic neuropathy (LHON)/pediatric onset dystonia is associated with a G to A transition at nucleotide position (np) 14459, within the mitochondrial dna (mtDNA)-encoded ND6 gene. This mutation has been reported in families presenting with LHON alone, LHON plus dystonia, or pediatric dystonia with typical age of onset less than 5 years. The mutation changes a moderately conserved alanine to a valine at amino acid residue 72, which is within the most evolutionarily conserved region of the ND6 protein. Pediatric onset disease is associated with basal ganglia dysfunction, spasticity, and encephalopathy. We report a family with G14459A mtDNA mutation and a broad spectrum of clinical manifestation. The proband was a 3-year-old girl with anarthria, dystonia, spasticity, and mild encephalopathy. MRI of the brain demonstrated bilateral, symmetric basal ganglia lucencies associated with cerebral and systemic lactic acidosis. Her maternal first cousin presented with a new onset limp and mild hemiparesis along with similar MRI findings with a much milder phenotype. Additional investigation of the family members with the mutation has revealed both asymptomatic and symptomatic individuals with variable clinical and laboratory features of mitochondrial disease. This study re-emphasizes the heterogeneous clinical manifestation of homoplasmic G14459A mtDNA mutation even within the same family, and supports the hypothesis that nuclear genes may play a role in modifying the clinical expression of mitochondrial disease. Published 2003 Wiley-Liss, Inc.
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ranking = 0.53310670311247
keywords = neuropathy
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19/93. phenol reduces hypertonia and enhances strength: a longitudinal case study.

    Phenyl alcohol blocks are used to relieve spasticity. Such nerve conduction blocks result from phenol-induced axonotmesis and could potentially affect muscle properties related to the ability to generate, maximize, and reduce force. This study assessed the 12-week longitudinal effect of phenol on position (stiffness) and velocity (damping) components of hypertonia, in addition to strength (peak torque and times to generate and reduce torque) in an individual with chronic elbow flexor spasticity following stroke. phenol motor point injections of flexor muscles paradoxically increased the magnitude of flexion torque and decreased the times required to generate and reduce flexion and extension joint torques, in addition to reducing elbow extension stiffness and damping. Large reductions in the velocity-related component of hypertonia (damping changes > 90%) occurred immediately following injection, which is a finding that supports the velocity-dependent definition of spasticity. Although the changes in damping were large and transient, changes in stiffness and strength variables were small, slower to occur, and maintained. This suggests secondary changes following nerve block, possibly facilitated by regular elbow use subsequent to spasticity reduction.
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ranking = 0.46689329688753
keywords = nerve
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20/93. MRI of a very rare hereditary ectodermal dysplasia: PIBI(D)S.

    PIBI(D)S is a acronym for a very rare autosomal recessive syndrome consisting of photosensitivity, mild non-congenital ichthyosis, brittle cystine-deficient hair, impaired intelligence, occasionally decreased fertility and short stature. We report a 12-year-old female patient affected by PIBI(D)S with previously unreported MRI findings of central nervous system dysmyelination.
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ranking = 0.21125163117715
keywords = nervous system
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