Neuromuscular Disease

Neuromuscular disease mainly manifests itself as fatigue and weakness, especially in the proximal muscles of the lower extremities.5,93 Aching muscles, paresthesias, and unsteadiness of gait have also been reported.5,89 The incidence of these symptoms varies from 30% to 80%,83,93 probably due to the criteria used, diligence of the respective observers, and patient selection.

Muscle weakness and fatigability are subjective symptoms. Both symptoms can be explained by decreased muscle strength on the one hand or lack of mental energy from depression and lethargy on the other hand. Hedman and associates94 studied an unselected series of PHPT patients to assess the association between these symptoms and muscle strength before and after surgery. A significant increase in the isokinetic strength of knee extension and knee flexion at higher angular velocities was found 3 months after surgery, suggesting that type II (fast twitch) muscle fibers were predominantly affected. The results of this study support the clinical impression that PHPT surgery is beneficial to patients with muscular symptoms.94,95 Joborn and colleagues,96 however, were unable to find any significant abnormalities of nerve conduction velocity or neuromuscular transmission in unselected PHPT patients.97

Joborn and coworkers documented that even patients with mild to moderate HPT without apparent muscular symptoms had impaired muscle function. Reinvestigation 6 months postoperatively showed improvement in only one patient who had severe preoperative muscular symptomatology.95,96 A 1988 study95 showed no significant difference in muscle strength between those patients with subjective impairments and the control patients. Seven months postoperatively, the PHPT patients had increased their muscle strength by 8%. These studies demonstrate that patients with PHPT, especially those with neuromuscular symptoms and muscle weakness, improve their muscle strength slightly after parathyroidectomy.

Patten and associates93 concluded, on the basis of the clinical, electromyographic, and biopsy evidence, that the neuromuscular abnormality in PHPT is probably neuropathic in origin.97 Electromyograms of 12 patients showed short-duration, low-amplitude motor unit potentials in some patients and abnormally high-amplitude, long-duration polyphasic potentials in others. Motor nerve conduction velocities and distal sensory latencies were normal. The major finding on muscle biopsy was atrophy of both type I (slow twitch) and type II muscle fibers, with type II fibers being more extensively involved. With the restoration of normocalcemia, neuromuscular symptoms improved within days to weeks after surgery.88

In contrast, Turken and colleagues98 demonstrated that 22 (52%) of 42 patients had neuromuscular symptoms consisting either of muscle cramps (45%), paresthesias (45%), or both (18%). No patient showed classic hyperparathyroid neuromuscular disease (muscle weakness, atrophy, hyperreflexia, abnormal gait, or tongue fasciculations). Electromyographic and nerve conduction studies were performed in 9 patients with neurologic abnormalities.98 None showed myopathy or signs of motor unit denervation. These results differed significantly from those reported earlier.99 There is clearly a trend toward subtle, earlier neuropathy that also manifests itself among so-called asymptomatic patients. Unfortunately, Turken and colleagues did not report the postoperative results.98

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