1/54. Fisher syndrome with tetraparesis and antibody to GQ1b: evidence for motor nerve terminal block.A Fisher syndrome (FS) patient with antibody to tetrasyaloganglioside GQ1b (GQ1b) developed late limb weakness. Serial motor conduction velocities (MCVs) showed a marked reduction of distal compound muscle action potential (CMAP) amplitudes, worse at 2-3 weeks, followed by a dramatic increase in week 5. Motor conduction velocities were always in the normal range, distal motor latencies changed only slightly, and conduction block in intermediate nerve segments was absent. These electrophysiological data might suggest an axonal neuropathy or a distal demyelinating conduction block. However, the dramatic increase of distal CMAP amplitudes over a short time without significant changes of distal motor latencies, CMAP duration, and morphology indicate that weakness in this FS patient might be due to a block of acetylcholine release from motor terminals, possibly mediated by anti-GQ1b antibodies.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
2/54. neuromuscular blockade after ingestion of tree tobacco (Nicotiana glauca).Two patients presented with life-threatening motor paresis after ingestion of leaves from the tree tobacco plant (Nicotiana glauca ). In addition to severe muscle weakness, bulbar palsies, flexor muscle spasm, hypertension, nausea, vomiting, and respiratory compromise were reported or observed. These are the fourth and fifth reported cases of a toxicologic emergency apparently caused by the alkaloid, anabasine, an isomer of nicotine found in the tobacco tree plant. The effects of this plant ingestion can mimic other better-known causes of paresis or paralysis. In areas of the country where the plant is indigenous, this toxicologic condition should be considered in the differential diagnosis of patients presenting with paresis or paralysis.- - - - - - - - - - ranking = 2keywords = muscle (Clic here for more details about this article) |
3/54. Hyper-reflexia without spasticity after unilateral infarct of the medullary pyramid.Whether or not a lesion confined to the pyramidal tract produces spasticity in humans remains an unresolved controversy. We have studied a patient with an ischemic lesion of the right medullary pyramid, using objective measures of hyper-reflexia, spasticity, and weakness. Electromyographic activity (EMG) of the biceps muscles was recorded under the following conditions: (1) in response to a tendon tap with an instrumental reflex hammer, (2) in response to imposed quick stretch with motion analysis, and (3) during an isometric holding task. Hyper-reflexia of the involved arm in response to tendon tap was shown to be due primarily to an increase in the gain of the reflex arc. No velocity-dependent increase in the response to quick stretch of the involved arm was present. This was consistent with the absence of detectable spasticity on the clinical exam. These findings suggest that a lesion confined to the medullary pyramid can give rise to weakness and hyper-reflexia without causing spasticity. Moreover, these findings suggest that different anatomical substrates may underlie the clinical phenomena of hyper-reflexia and spasticity.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
4/54. ulnar nerve injuries of the hand producing intrinsic muscle denervation on magnetic resonance imaging.Muscle and nerve injuries in the hand may be difficult to detect and diagnose clinically. Two cases are reported in which magnetic resonance imaging showed ulnar nerve injury and intrinsic hand muscle denervation. The clinical, anatomical and radiological features of injury to the deep motor branch of the ulnar nerve and associated muscle denervation are discussed and illustrated.- - - - - - - - - - ranking = 6keywords = muscle (Clic here for more details about this article) |
5/54. Blue rubber bleb nevus syndrome with central nervous system involvement.An 11-month-old female patient presented with focal seizures. She was born at term with multiple scattered tiny protuberances and dark purple soft compressible nevi over her entire body. She had clumsiness and decreased muscle power in her left extremities. magnetic resonance imaging and magnetic resonance angiography revealed cerebral atrophy of the right central area around the anomalous venous sinus and multiple small enhancing lesions throughout the brain with gadolinium-diethylenetriamine pentaacetic acid enhancement. Despite right partial neonatal seizures, she had no further seizures for 3 years while receiving carbamazepine, and no change was observed in the number and size of the nevi. At last evaluation, language and psychomotor development were normal for her age.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
6/54. Zoster paresis of the shoulder. Case report and review of the literature.More than 95% of people in the united states are infected with the varicella zoster virus at some time in life, and this infection usually is manifested as chicken pox during childhood. The virus then establishes a latent infection of sensory ganglia, from which it may reactivate many years later to cause herpes zoster (shingles), a cutaneous painful rash along a dermatomal distribution. Less commonly, the varicella zoster virus may result in myotomal motor weakness or paralysis in addition to a painful dermatomal rash. A case of unilateral left C5-C6 segmental paresis attributable to herpes zoster in an otherwise healthy individual and a current review of the literature are presented. A case of zoster paresis of the shoulder muscles is presented to remind the orthopaedic community that this diagnosis may be confused with other diagnoses, including rotator cuff tear, and should be considered in the differential diagnosis of shoulder pain and shoulder girdle muscle weakness.- - - - - - - - - - ranking = 2keywords = muscle (Clic here for more details about this article) |
7/54. Axillary nerve injuries in children.Isolated axillary nerve injury is uncommon, particularly in children. The motor deficit of shoulder abduction may not recover spontaneously and can be a substantial handicap. Detection may be difficult initially, as the injury is masked by trauma such as head injury, and concomitant shoulder injury requiring immobilization. After mobilization, patients learn to partially compensate by using alternate muscles. There are few reports of surgical management of this nerve injury. Most concern predominantly adults, and the results are mixed with on average slightly greater than half having a good recovery (defined as grade 4-5 Medical research Council muscle power). We present our experience with 4 pediatric patients who had axillary nerve injury. Three patients had an interposition nerve graft, and 1 patient underwent neurolysis. All patients recovered to grade 4-5 deltoid muscle power. Children with an axillary nerve injury which fails to recover spontaneously by 4-6 months should strongly be considered for surgical exploration.- - - - - - - - - - ranking = 3keywords = muscle (Clic here for more details about this article) |
8/54. Myoadenylate deaminase deficiency with progressive muscle weakness and atrophy caused by new missense mutations in AMPD1 gene: case report in a Japanese patient.A 46-year-old woman with exertional myalgia developed slowly progressive weakness in her lower extremities. She had slight muscle weakness in her facial and upper extremities, and severe muscle weakness and atrophy in lower extremities more marked in the proximal portions. serum creatine kinase was slightly elevated. After ischemic forearm exercise test, blood ammonia had no elevation although lactate level increased normally. The computed tomography revealed that a characteristic distribution of skeletal muscle involvement with proximal and flexor muscles more severely affected than distal and extensor in the lower extremities. In addition, the left sternocleidomastoid muscle showed marked atrophy with an asymptomatic weakness of over 20 years duration suggesting abnormal development. Needle EMG examination showed a large number of easily recruited, short-duration, low-amplitude motor unit potentials in all extremities. Muscle biopsy showed absence of adenosine monophosphate deaminase activity with normal cytochrome c oxidase and phosphorylase activity. With the muscle enzyme activity assay, adenosine monophosphate deaminase activity was found to be lower than 0.2% of the controls. The dna analysis revealed that she was compound heterozygote involving two missense mutations (R388W and R425H) in exon 9 and exon 10 of AMPD1 gene. This is the first report of primary myoadenylate deaminase deficiency with progressive weakness and atrophy caused by novel compound heterozygous mutations of AMPD1 gene, and suggests that adenosine monophosphate deaminase is closely related not only to energy metabolism but also to the development of skeletal muscle.- - - - - - - - - - ranking = 11keywords = muscle (Clic here for more details about this article) |
9/54. High-intensity cycling exercise after a stroke: a single case study.Aerobic exercise training has demonstrated positive effects after brain injury. However, therapists express concern regarding the use of effortful exercise in individuals presenting with spasticity or involuntary muscle activity. This study aimed to address this concern and to evaluate whether an intervention of maximal intensity cycling exercise impaired an individual's ability to actively extend his hemiparetic elbow. Using a single case design, it was shown that active elbow extension improved during the period of this investigation, and was not impaired immediately following maximal cycling exercise.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
10/54. Spontaneous carotid dissection presenting lower cranial nerve palsies.Cranial nerve palsy in internal carotid artery (ICA) dissection occurs in 3--12% of all patients, but in 3% of these a syndrome of hemicranias and ipsilateral cranial nerve palsy is the sole manifestation of ICA dissection, and in 0.5% of cases there is only cranial nerve palsy without headache. We present two cases of lower cranial nerve palsy. The first patient, a 49-year-old woman, developed left eleventh and twelfth cranial nerve palsies and ipsilateral neck pain. The angio-RM showed an ICA dissection with stenosis of 50%, beginning about 2 cm before the carotid channel. The patient was treated with oral anticoagulant therapy and gradually improved, until complete clinical recovery. The second patient, a 38-year-old woman, presented right hemiparesis and neck pain. The left ICA dissection, beginning 2 cm distal to the bulb, was shown by ultrasound scanning of the carotid and confirmed by MR angiogram and angiography with lumen stenosis of 90%. Following hospitalisation, 20 days from the onset of symptoms, paresis of the left trapezius and sternocleidomastoideus muscles became evident. The patient was treated with oral anticoagulant therapy and only a slight right arm paresis was present at 10 months follow-up. Cranial nerve palsy is not rare in ICA dissection, and the lower cranial nerve palsies in various combinations constitute the main syndrome, but in most cases these are present with the motor or sensory deficit due to cerebral ischemia, along with headache or Horner's syndrome. In the diagnosis of the first case, there was further difficulty because the cranial nerve palsy was isolated without hemiparesis, and the second case presented a rare association of hemiparesis and palsy of the eleventh cranial nerve alone. Compression or stretching of the nerve by the expanded artery may explain the palsies, but an alternative cause is also possible, namely the interruption of the nutrient vessels supplying the nerve, which in our patients is more likely.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
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