(99m)Tc-TRODAT-1 SPECT study in evaluation of Holmes tremor after thalamic hemorrhage.

Holmes tremor is also known as rubral or midbrain tremor. The tremor usually involves lesions near the red nucleus and the nerve fiber tracts originating in the cerebellum and the substantia nigra. We report a case of a 62-year-old woman who presented with Holmes tremor 5 months after a left thalamic hemorrhage, with a partial recovery 3 years later. Sequential technetium-(99m)TRODAT-1 single-photon emission computed tomography (SPECT) of the patient's brain revealed partially improved tracer uptake reduction in the striatums, particularly on the left side. We propose that involvement of both the nigrostriatal and the dentate-rubro-thalamic pathways are essential in the pathogenesis of Holmes tremor after a thalamic lesion, and regeneration of the nigrostriatal system is possible in this type of tremor after the initial degeneration. The (99m)Tc-TRODAT-1 SPECT study is a useful and convenient tool for evaluating the nigrostriatal dopamine function in patients with Holmes tremor.

Effects of potassium supplementation on the recovery of thyrotoxic periodic paralysis.

Potassium supplements have been recommended to hasten recovery and prevent cardiopulmonary complications in patients with thyrotoxic periodic paralysis (TPP). However, this recommendation has not yet been proven efficacious. Thirty-two patients with acute attacks of TPP over a 3-year-period were divided into 2 groups. Group A (n = 12) was a control group treated with normal saline infusion 125 mL/hr only. Group B (n = 20) received intravenous KCl administration at a rate of 10 mmol/hr in normal saline 125 mL/hr. During the attack and for 6 hours after muscle recovery, hemodynamics were continuously recorded and muscle strength and plasma K(+) concentration were measured hourly. The sex, age, muscle strength, thyroid function, biochemical values including plasma K(+) levels, as well as the time from attack to therapy (3.6 +/- 1.6 v 3.3 +/- 1.0 hr) were not significant between the 2 groups. However, recovery time was significantly shorter in the KCl group than the control (6.3 +/- 3.8 v 13.5 +/- 7.5 hr, P < .01). Rebound hyperkalemia greater than 5.5 mmol/L occurred in 40% patients receiving KCl. The dose of KCl administered and peak K(+) concentration were positively correlated (r = 0.85, P < .001). In conclusion, KCl therapy proves to help the recovery of paralysis in TPP associated with rebound hyperkalemia. KCl supplementation should be given as small as possible (<10 mmol/hr) to avoid rebound hyperkalemia unless there are cardiopulmonary complications.