Effects of Acute Low Back Pain on Postural Control

OBJECTIVE: To evaluate the changes in static and dynamic postural control after the development of acute low back pain. METHODS: Thirty healthy right-handed volunteers were divided into three groups; the right back pain group, the left back pain group, and the control group. 0.5 mL of 5% hypertonic saline was injected into L4-5 paraspinal muscle for 5 seconds to cause muscle pain. The movement of the center of gravity (COG) during their static and dynamic postural control was measured with their eyes open and with their eyes closed before and 2 minutes after the injection. RESULTS: The COGs for the healthy adults shifted to the right quadrant and the posterior quadrant during their static and dynamic postural control test (p<0.05). The static and dynamic instability index while they had their eyes closed was significantly increased than when they had their eyes open with and without acute back pain. After pain induction, their overall and anterior/posterior instability was increased in both the right back pain group and the left back pain group during the static postural control test (p<0.05). A right deviation and a posterior deviation of the COG still remained, and the posterior deviation was greater in the right back pain group (p<0.05). CONCLUSION: The static instability, particularly the anterior/posterior instability was increased in the presence of acute low back pain, regardless of the visual information and the location of pain.

Effect of Stimulation Polarity of Transcranial Direct Current Stimulation on Non-dominant Hand Function

OBJECTIVE: To evaluate motor excitability and hand function on the non-dominant side according to the polarity of transcranial direct current stimulation (tDCS) on the motor cortex in a healthy person. METHOD: tDCS was applied to the hand motor cortex for 15 minutes at an intensity of 1 mA in 28 healthy right-handed adults. Subjects were divided randomly into four groups: an anodal tDCS of the non-dominant hemisphere group, a cathodal tDCS of the non-dominant hemisphere group, an anodal tDCS of the dominant hemisphere group, and a sham group. We measured the motor evoked potential (MEP) in the abductor pollicis brevis and Jabsen-Taylor hand function test (JTT) in the non-dominant hand prior to and following tDCS. All study procedures were done under double-blind design. RESULTS: There was a significant increase in the MEP amplitude and a significant improvement in the JTT in the non-dominant hand following anodal tDCS of the non-dominant hemisphere (p<0.05). But there was no change in JTT and a significant decrease in the MEP amplitude in the non-dominant hand following cathodal tDCS on the non-dominant hemisphere and anodal tDCS of the dominant hemisphere. CONCLUSION: Non-dominant hand function is improved by increased excitability of the motor cortex. Although motor cortex excitability is decreased in a healthy person, non-dominant hand function is maintained. A homeostatic mechanism in the brain might therefore be involved in preserving this function. Further studies are warranted to examine brain functions to clarify this mechanism.

A Case of Hyponatremia Associated with Paroxetine: A case report

Paroxetine is a selective serotonin reuptake inhibitor (SSRI) widely used for depression in brain damaged patients as it is known for its few affects on cognition or psychomotor function. Major side effects observed for paroxetine are vertigo, headache and tremor. It is reported that hyponatremia is also rarely observed. In 69 year-old male with left hemiplegia due to cerebral infarction had started taking 20 mg/day of paroxetine for depression. Next day the patient showed severe generalized weakness and decreased consciousness. Laboratory tests showed that serum sodium level was decreased to 102 mEq/L. Paroxetine administration was stopped and 3% sodium and oral furosemide were administered under the diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH). We report a case of patient with severe hyponatremia due to SIADH within 2 days after use of paroxetine. This case emphasizes the need to monitor serum sodium level routinely at the initial treatment to prevent hyponatremia.