Application of scanning and transmission electron microscopy, x-ray energy spectroscopy, and x-ray diffraction to calcium pyrophosphate crystal formation in vitro.
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Biomedical subjects
Publications and source records attributed to P T Cheng.
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Using powder x-ray diffraction analysis, we studied calcium pyrophosphate crystal formation in silica and gelatin gels was well as in comparable aqueous solutions. We demonstrated that the physiological salts, monoclinic and triclinic calcium pyrophosphate dihydrate can be formed in gels and that gels do affect the type of crystals formed from ions in solution. These observations support our hypothesis that calcium pyrophosphate dihydrate crystal deposition in joints is regulated by the physical chemical gel state of the connective tissue matrix.
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A total of 61 traumatic cervical cord-injured patients were included in this study. Needle electromyography and nerve conduction study were performed at 6 to 24 weeks postinjury. Correlation between the presence of spontaneous electromyographic potentials and the presence of dysesthetic pain, as well as other clinical characteristics including age, gender, level of injury, severity of injury, spasticity, duration of injury, and performance of spinal surgery was statistically analyzed. Of the 31 patients who had spontaneous electromyographic potentials in their hands, 27 (87%) had dysesthetic pain in their limbs. Only 9 (30%) of the other 30 patients without spontaneous potentials developed dysesthetic pain. A significant correlation (P < 0.001) between the presence of spontaneous electromyographic potential and dysesthetic pain was found. The presence of spontaneous electromyographic potentials was also significantly (P < 0.05) correlated with severity of injury but not with age, gender, injury level, duration of injury, operation, and spasticity. In conclusion, the presence of spontaneous electromyographic potentials in cervical cord-injured patients was significantly related to the presence of dysesthetic pain. They occurred more often in patients with more severe injury.
This study was undertaken to explore whether we could provide supportive laboratory evidence for the clinical observations that a stroke patient has lost functional mobility/locomotion capability based on dynamic balance responses (center of force sway patterns) and motor control activities (electromyography patterns) during the motor task of sit-to-stand. A computerized controlled dynamic postural control assessment system was developed and used in this study. Various dynamic balance indexes were introduced and derived from center of force sway patterns expressed in four domains (space, time, force, and frequency). Motor control was assessed by multichannel surface electromyography of each side of the lower limb during the same motor task. The functional mobility capability was evaluated using the traditional FIM method. Fourteen stroke patients with right hemiplegia and nine healthy elderly individuals were recruited as the experimental and control groups, respectively. Muscle activity was recorded for quadriceps, hamstrings, anterior tibialis, and triceps surae muscles and was used for analysis. Center of force sway patterns and ground reaction forces were registered. All signals were synchronized at "seat-off." Surface electromyographic patterns of activities recorded during sit-to-stand and dynamic balance indexes computed from center of force sway patterns were categorized and compared with the functional mobility scores. Results show that both the motor control patterns and dynamic balance indexes correlated well to the extent of mobility impairment evaluated using the traditional FIM method. An important conclusion for rehabilitation medicine is that the functional mobility capability of stroke patients may be expressed numerically using dynamic balance indexes and visualized graphically through electromyographic motor patterns.
This study is designed to investigate the immediate effectiveness of electrotherapy on myofascial trigger points of upper trapezius muscle. Sixty patients (25 males and 35 females) who had myofascial trigger points in one side of the upper trapezius muscles were studied. The involved upper trapezius muscles were treated with three different methods according to a random assignment: group A muscles (n = 18) were given placebo treatment (control group); group B muscles (n = 20) were treated with electrical nerve stimulation (ENS) therapy; and group C muscles (n = 22) were given electrical muscle stimulation (EMS) therapy. The effectiveness of treatment was assessed by conducting three measurements on each muscle before and immediately after treatment: subjective pain intensity [(PI) with a visual analog scale], pressure pain threshold [(PT) with algometry], and range of motion [(ROM) with a goniometer] of upper trapezius muscle (lateral bending of cervical spine to the opposite side). When the effectiveness of treatment was compared with that of the placebo group (group A), there was significant improvement in PI and PT in group B (P < 0.01) but not in group C (P > 0.05). The improvement of ROM was significantly more in group C (P < 0.01) as compared with that in group A or group B. When each group was divided into two additional subgroups based on the initial PI, it was found that ENS could reduce PI and increase PT significantly (P < 0.05), but did not significantly (P > 0.05) improve ROM, as compared with the placebo group for both subgroups. EMS could significantly (P < 0.05) improve ROM, but not PT, better than the placebo groups, for either subgroup. It could reduce PI significantly more (P < 0.05) than placebo controls only for the subgroup with mild to moderate pain, but not with severe pain. For pain relief, ENS was significantly better (P < 0.05) than EMS; but for the improvement of ROM, EMS was significantly better (P < 0.05) than ENS. It is concluded that ENS is more effective for immediate relief of myofascial trigger point pain than EMS, and EMS has a better effect on immediate release of muscle tightness than ENS.
To explore the possible mechanisms of phantom limb discomfort after amputation, three amputees with phantom limb pain were studied. This study examined the change of regional cerebral blood flow using technetium-99m hexamethylpropyleneamine oxime-single photon emission computerized tomography, which was arranged at the time of severe phantom limb discomfort and after the discomfort subsided or was completely relieved. Nine representative transverse slices parallel to the orbitomeatal line were selected for quantification. The cortical ribbon (2-cm thickness) was equally subdivided into 12 symmetrical pairs of sector regions of interest in each slice. The irregularly shaped regions of interest were drawn manually around the right thalamus and basal ganglion and then mirrored to the left thalamus and basal ganglion. The contralateral to ipsilateral ratio of regional cerebral blood flow for each area was calculated. The intensity of phantom limb pain was evaluated on a 0 to 10 visual analog scale. In Cases 1 and 2, the contralateral to ipsilateral regional cerebral blood flow ratios of multiple areas of the frontal, temporal, or parietal lobes were increased at the time of more severe phantom limb pain, and the ratios were normalized or even decreased when the phantom limb pain subsided. In Case 3, increased contralateral to ipsilateral regional cerebral blood flow ratios were also found over the frontal, temporal, and parietal lobe. However, most of the increased regional cerebral blood flow ratios of regions of interest in the first study persisted in the follow-up study. Also, the regional cerebral blood flow ratios of greater number of regions of interest of the same gyrus and new gyrus were increased. There was no significant right-left difference of regional cerebral blood flow over bilateral thalami and basal ganglia in all three cases. The results suggested that phantom limb pain might be associated with cortical activation involving the frontal, temporal, or parietal cortex, and it may imply the possibility of the existence of an ascending polysynaptic pathway that conveys the uncomfortable phantom limb sensation to the cerebral cortex. These findings may also indicate that reorganization of the cortical blood flow occurs in amputees. However, it is still difficult to conclude that the changes in regional cerebral blood flow were attributable directly to pain. With no comparison group of amputees and because of the small number of cases, it is hard to generalize about cerebrocortical involvement in phantom pain, and it is possible that the findings represent a normal phenomenon seen after 'amputation. Another possibility is that the findings represent increased arousal caused by pain rather than an intrinsic pain pathway. Further study is worthwhile.
To assess the efficacy of electrical acupuncture in the rehabilitation of patients with hemiplegia in stroke, we randomized 128 patients within 2 wk of stroke onset to receive either comprehensive rehabilitation plus electrical acupuncture (n = 59) or comprehensive rehabilitation only (n = 59). Electrical acupuncture was administered by electrical stimulation of acupuncture points through adhesive surface electrodes five times per week. Neurological status (Brunnstrom's stage) and the Chinese version of the Functional Independence Measure were assessed before treatment and at discharge. Patients treated with electrical acupuncture had a shorter duration of hospital stay for rehabilitation and better neurological and functional outcomes than the control group had, with a significant difference in scores for self-care and locomotion (P = 0.02). This result did not postulate the previous study that acupuncture therapy for stroke patients should depend on needle manual and "de qi" response. We suggest that electrical acupuncture through adhesive surface electrodes in conjunction with current optimal rehabilitation programs is a convenient and effective therapy for stroke patients.
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The purpose of this study was to explore whether we could provide supportive laboratory evidence for clinical observations that a stroke patient has lost functional mobility/locomotion capability based on dynamic balance responses (centre of pressure, COP sway patterns) and motor control activities (EMG patterns) during the motor task of sit-to-stand. A computerized controlled dynamic postural control assessment system was developed and used in this study. Various dynamic balance indices were introduced and derived from COP sway patterns expressed in four domains (i.e. space, time, force, and frequency). Motor control was assessed by multi-channel surface electromyography of each side of the lower limb during the same motor task. The functional mobility capability was evaluated using a traditional FIM method. Fourteen stroke patients with right hemiplegia and nine healthy elderly were recruited as the experimental and control groups respectively. Muscle activity was recorded for quadriceps, hamstrings, anterior tibialis, and triceps surae muscles and used for analysis. Centre of pressure sway patterns and ground reaction forces were registered. All signals were synchronized at 'seat-off'. Surface electromyographic patterns of activities recorded during sit-to-stand and dynamic balance indices computed from centre of pressure sway patterns were categorized and compared with the functional mobility scores. The results show that both the motor control patterns and dynamic balance indices correlated well to the extent of mobility impairment evaluated using the traditional FIM method. An important conclusion for rehabilitation medicine is that the functional mobility capability of stroke patients may be quantified analytically using dynamic balance indices and visualized graphically through EMG motor patterns.
Pseudogout is characterized by the deposition of calcium pyrophosphate dihydrate, triclinic [CPPD(T)] and calcium pyrophosphate dihydrate, monoclinic [CPPD(M)] crystals in articular connective tissues. We studied aqueous solutions over a range of calcium chloride/sodium pyrophosphate concentrations to determine the ionic conditions under which these particular salts form. At 37 degrees C, CPPD(T) forms when [PPi]t greater than or equal to 10(-4), while formation of CPPD(M) occurs at 10(-3) M < [PPi]t less than or equal to 10(-2) M. When [Na+]t > 120 mM, calcium disodium pyrophosphates precipitate. With 1 mM Mg++, CPPD(M) forms at [PPi]t > 10(-3) M, mixed with a calcium magnesium pyrophosphate at [PPi]t greater than or equal to 10(-2) M. We conclude that CPPD(T) and CPPD(M) crystals form in a restricted ratio and range of [Ca++]t and [PPi]t and that other ions, particularly Mg++ and Na+, affect the nature of the crystal products formed.
We studied calcium pyrophosphate crystal formation in an in vitro cartilage system. Two parallel troughs were excavated in tibial plateau articular cartilage obtained postmortem. One well was filled with solid sodium pyrophosphate, the other with calcium chloride. After incubation for 24 h at either 10 degrees C or 37 degrees C the precipitate band between the troughs was analyzed for the size and nature of crystals present. In subsequent experiments, the cartilage was pretreated by laceration, contusion, trypsin or hyaluronidase denaturation. We found that cartilage denaturation resulted in formation of larger crystals but that the crystal product in all experiments was identical, alpha CaNa2P2O7.4H2O a nonphysiologic crystal.
Calcium pyrophosphate crystal formation has been associated clinically with hypercalcemic states (hyperparathyroidism) and hypomagnesemia. We studied aqueous solutions at pH 7.4, 37 degrees C, [Na+] = 140 nM over a range of calcium chloride/magnesium chloride/sodium pyrophosphate concentrations to determine the effect of calcium and magnesium ions on crystal formation. We found that CPPD(T) and CPPD(M) could form under different ionic conditions. Low [Mg++] and [PPi] favoured CPPD(T) whereas higher [Mg++] and [PPi] favoured CPPD(M). At [Mg++] = 1.0 mM a calcium magnesium pyrophosphate crystal phase designated CMPP2 formed. As [Mg++] affects the crystal phase formed more than equimolar [Ca++], we conclude that ionic magnesium deficiency may be a clinically important determinant in calcium pyrophosphate dihydrate crystal formation.
Cholesterol crystals were demonstrated in synovial fluids from 4 patients with knee osteoarthritis and recurrent synovial effusions. Large crystals (10-80 micros) were readily identifiable by their characteristic plate-like morphology. Some fluids also contained numerous smaller (1-5 microns) irregular, rod and needle shaped crystals. Identification of these crystals as cholesterol was established by x-ray diffraction analysis (2 fluids) and by ultrastructural studies (1 fluid). This study documents the occurrence of cholesterol crystals in osteoarthritic effusions, but their precise pathogenetic significance remains unclear.