BACKGROUND: The goal of haemodialysis treatment in end-stage renal disease (ESRD) patients is to correct the complications of the uraemic condition. Among the main complications are fluid overload and subsequent hypertension that are corrected by achievement of 'dry weight'. We report in this study the evolution of post-dialysis body-weight and blood pressure in patients who began their HD treatment in our unit. METHODS: We studied the monthly evolution of post-dialysis body-weight (expressed as a percentage of pre-dialysis body-weight at the first HD treatment) and predialysis mean arterial pressure (MAP) over 24 months in 61 patients (21 females, mean age 59.8 years; 20% diabetic), treated with cellulosic membranes for 8 h, 3 times a week. RESULTS: The post-dialysis body-weight decreased between the onset of HD and month 2 (M2) (-4.40+/-0.52%). Then it went up, reaching -1.56+/-0.96% at M6, +0.3+/-1.27% at M12, +1.27+/-1.38% at M18 and +1.64+/-1.33% at M24. The post-dialysis body-weight increased by 6% between M2 and M24. The mean arterial pressure (MAP) decreased from 111.3+/-2.5 mmHg at M0 to 94.4+/-1.7 at M6, and then remained stable after M6. Between M2 and M6 the post-dialysis body-weight increased, whereas the predialysis MAP continued to decline. The incidence of hypotension episodes was maximal during the first 4 months of HD treatment. CONCLUSIONS: After the second month of dialysis treatment, the simultaneous increase of post-dialysis body-weight and decrease of pre-dialysis MAP are related to the effects of two processes, i.e. increased weight as the result of anabolism induced by the HD treatment on the one hand and normalization of blood pressure by fluid removal on the other. Continuous clinical assessment of the patient is necessary to provide adequate prescription of post-dialysis body-weight. During the first months of HD treatment, the nephrologist, like Janus, is a double-faced gatekeeper: he must be willing to decrease post-dialysis weight to achieve 'dry weight' and to normalize blood pressure, but he must also be prepared to increase it to compensate for anabolism and to avoid episodes of hypotension. (+info)
Autosomal dominant muscle cramp syndrome in a Japanese family.
OBJECTIVES: To identify the clinical, electrophysiological, histological, and genetic characteristics of a Japanese family with a muscle cramp syndrome. METHODS: Fourteen patients (eight men, six women) were studied in four generations of a single family. Electrophysiological examinations were performed in four cases and muscle and nerve biopsies were performed on the propositus. RESULTS: The mode of inheritance seemed to be autosomal dominant. The cramps occurred during both exertion and at rest, and during sleep. Electromyographic examination indicated a neurogenic aetiology. There was a decreased number of large myelinated fibres in the sural nerve, and fibre type grouping in the quadriceps femoris muscle biopsy. CONCLUSIONS: The autosomal dominant muscle cramp syndrome in this family is probably caused by a polyneuropathy. (+info)
Nocturnal leg cramps in children: incidence and clinical characteristics.
The records of 2527 healthy children seen in an ambulatory care clinic were evaluated for nocturnal leg cramps in the preceding 12 months, frequency and duration of the cramps, whether the cramps affected one leg or both legs at a time, whether there was associated muscle cramps in feet, whether the cramps occurred when the child was awake or asleep, and whether there was residual tenderness in the affected muscles. Nocturnal leg cramps were present in 185 children for an overall incidence of 7.3%. Leg cramps were noted only in children aged > or = 8 years. The incidence increased at 12 years and peaked at 16 to 18 years of age. A majority (81.6%) of the affected children had nocturnal leg cramps 1 to 4 times per year. The mean duration of episodes was 1.7 minutes. Leg cramps were unilateral in 98.9% of cases and the ipsilateral foot also was involved in 18.9% of cases. One hundred thirty-five (73%) children had leg cramps while asleep, and the remaining 23 (12.4%) children had leg cramps in either state. Fifty-seven (30.8%) children had residual tenderness in the affected muscles. The mean duration of residual tenderness was 33.2 minutes (range: 2 minutes-1 day). We conclude that nocturnal leg cramps are common in children aged > 12 years. A majority of the affected children have leg cramps 1 to 4 times per year. The cramps are usually unilateral and occur when the children are asleep. Normal duration of the leg cramp is < 2 minutes. Residual tenderness is present in approximately 30% of the affected children. Residual tenderness, if present, usually lasts for half an hour. (+info)
Abnormal cortical processing of voluntary muscle relaxation in patients with focal hand dystonia studied by movement-related potentials.
In order to clarify the abnormality in cortical motor preparation for voluntary muscle relaxation of the hand in patients with focal hand dystonia, Bereitschaftspotentials (BPs) preceding voluntary muscle contraction and relaxation were recorded in eight patients (three with simple writer's cramp and five with dystonic writer's cramp), and were compared with those from 10 normal subjects. Voluntary muscle relaxation: after keeping the right wrist in an extended position for > 5 s, the subject let the hand drop by voluntarily terminating muscle contraction of the wrist extensor without any associated muscle contraction. Voluntary muscle contraction: the right wrist was flexed by voluntarily contracting the wrist flexor muscle. Scalp EEGs were recorded from 11 electrodes placed over the frontal, central and parietal areas. In the control group, the BP measured at the movement onset was maximal at the left central area (C1), and distributed predominantly over the left hemisphere equally in both the contraction and relaxation tasks. In the focal hand dystonia group, BP was maximal at C1 in the contraction task, whereas, in the relaxation task, it was maximal at the midline central area (Cz) and symmetrically distributed. At the left central area, the BP amplitude in the focal hand dystonia group was diminished significantly in the relaxation task compared with the contraction task (P < 0.05). The present results demonstrate for the first time that the cortical preparatory process for voluntary muscle relaxation, or motor inhibition, is abnormal in focal hand dystonia. (+info)
The wrist of the formula 1 driver.
OBJECTIVES: During formula 1 driving, repetitive cumulative trauma may provoke nerve disorders such as nerve compression syndrome as well as osteoligament injuries. A study based on interrogatory and clinical examination of 22 drivers was carried out during the 1998 formula 1 World Championship in order to better define the type and frequency of these lesions. METHODS: The questions investigated nervous symptoms, such as paraesthesia and diminishment of sensitivity, and osteoligamentous symptoms, such as pain, specifying the localisation (ulnar side, dorsal aspect of the wrist, snuff box) and the effect of the wrist position on the intensity of the pain. Clinical examination was carried out bilaterally and symmetrically. RESULTS: Fourteen of the 22 drivers reported symptoms. One suffered cramp in his hands at the end of each race and one described a typical forearm effort compartment syndrome. Six drivers had effort "osteoligamentous" symptoms: three scapholunate pain; one medial hypercompression of the wrist; two sequellae of a distal radius fracture. Seven reported nerve disorders: two effort carpal tunnel syndromes; one typical carpal tunnel syndrome; one effort cubital tunnel syndrome; three paraesthesia in all fingers at the end of a race, without any objective signs. CONCLUSIONS: This appears to be the first report of upper extremity disorders in competition drivers. The use of a wrist pad to reduce the effects of vibration may help to prevent trauma to the wrist in formula 1 drivers. (+info)
Superficial femoral artery branch avulsion after severe muscle cramping.
Avulsion of a muscular branch of a major artery without a history of major trauma has not been reported to our knowledge. Occasionally, blunt and even minor trauma can result in injuries that seem out of proportion to the level of injury. We report a case of an avulsed muscular branch of the superficial femoral artery in a patient with recent thigh cramping. This injury is likely related to the intense tetany the patient described having before he came to the hospital. (+info)
Possible mechanisms of muscle cramp from temporal and spatial surface EMG characteristics.
In this study, the initiation and development of muscle cramp are investigated. For this, we used a 64-channel surface electromyogram (EMG) to study the triceps surae muscle during both cramp and maximal voluntary contraction (MVC) in four cramp-prone subjects and during cramp only in another four cramp-prone subjects. The results show that cramp presents itself as a contraction of a slowly moving fraction of muscle fibers, indicating that either the spatial arrangement of the motoneurons and muscle fibers is highly related or that cramp spreads at a level close to the muscle. Spectral analyses of the EMG and peak-triggered average potentials show the presence of extremely short potentials during cramp compared with during MVC. These results can also be interpreted in two ways. Either the motoneurons fire with enlarged synchronization during MVC compared with cramp, or smaller units than motor units are active, indicating that cramp is initiated close to or even at the muscle fiber level. Further research is needed to draw final conclusions. (+info)
Excitability properties of motor axons in patients with spontaneous motor unit activity.
OBJECTIVES: Measures of nerve excitability provide information about biophysical properties of peripheral axons in disease states. One measure, the strength duration time constant (tau(SD)), was previously reported to be prolonged in motor axons of patients with acquired neuromyotonia. The present study used a new protocol that applies a more comprehensive and sensitive panel of measures of axonal excitability, to determine firstly whether changes in tau(SD) were present in a group of patients with evidence of spontaneous motor unit activity; and secondly, if such changes in tau(SD) were present, whether other parameters of axonal excitability were affected, to clarify the mechanism of the change in tau(SD). METHODS: Eleven patients with both symptoms and EMG evidence of spontaneous motor unit activity were studied. Eight patients had autoimmune associated acquired neuromyotonia (aNMT) and three had the cramp fasciculation syndrome. The protocol first measured stimulus-response behaviour using two stimulus durations (from which the distribution of strength-duration time constants was estimated), and then threshold tracking was used to determine threshold electrotonus to 100 ms polarising currents, a current-threshold relation (indicating inward and outward rectification), and the recovery of excitability after supramaximal activation. RESULTS: The results were compared with previously published normal data. The value for tau(SD) of motor axons in the patient group was 0.43 (0. 02) ms (mean (SEM)), identical with the control value. Most other indices of axonal excitability, including those dependent on fast potassium channels, were also found to be normal. When compared with age matched controls however, the patients with acquired neuromyotonia had significantly greater late subexcitability after an impulse, greater excitability overshoots after depolarisation or hyperpolarisation, and more accommodation. CONCLUSIONS: No clear evidence for the mechanism of ectopic discharge in these patients was obtained, probably because the activity was generated focally, and most often at the motor nerve terminals. The unexpected finding of increased excitability overshoots and accommodation compared with age matched controls, suggests a relative up regulation of slow potassium conductance, possibly as a consequence of the continuous motor unit activity. (+info)