Efficacy of a low-dose subcutaneous lisuride infusion in Parkinson's disease.

Five parkinsonian patients with motor fluctuations and dyskinesia after long-term treatment with levodopa were treated with subcutaneous lisuride infusion (0.24-0.42 mg/day) together with oral levodopa for a mean period of 27 (range 13-36) months. All 5 patients showed marked initial improvement in mobility. Mild psychiatric side effects were observed in three patients; however, these side effects disappeared with reduction in the dosage of lisuride to 0.06 mg per day without a significant increase in motor fluctuations. A low dose of subcutaneous lisuride infusion with oral levodopa is an effective treatment for fluctuations of motor performance in parkinsonian patients without adverse psychiatric effects.

Three-Hertz postural oscillation in patients with brain stem or cerebellar lesions.

Postural instability was quantitatively studied in patients with lesions in the 1) pontine tegmentum, 2) deep cerebellar nuclei, or 3) cerebellar hemisphere. As compared to controls, patients with each lesion demonstrated a characteristic 3 Hertz (Hz) body oscillation. Cross-correlation functions revealed a strong correlation between the body sway and activities in the lower leg muscles. Based on these findings, we conclude that the 3 Hz body oscillation may be the result of any disturbance in the loop of long-latency reflexes mediated by the cerebellum.

Impaired modulation of tonic muscle activities and H-reflexes in the soleus muscle during standing in patients with Parkinson's disease.

The presence of postural disturbance in patients with Parkinson's disease (PD) was assessed by the displacement of the centre of foot pressure (CFP) and by changes in the amplitude of the soleus H-reflex when patients maintained an upright standing posture, followed by a forward-leaning posture. Thirteen patients and 13 age-matched normal controls (N) were studied. PD patients showed the following differences when compared to normal subjects: (1) the range of displacement of the CFP associated with forward leaning was significantly smaller (P<0.01); (2) the ratio of the increase in the soleus EMG activity to the CFP displacement (deltaEMG/deltaCFP) was larger (P<0.01), and the value of the deltaEMG/deltaCFP increased significantly in relation to the scale of clinical severity (P<0.01); and (3) the ratio of the increase in the amplitude of the soleus H-reflex to the soleus muscle EMG activity (deltaH-reflex/deltaEMG) was significantly lower in PD patients (P<0.05). The value of the deltaH-reflex/deltaEMG decreased significantly with the scale of clinical severity among the patients (P<0.05). These results suggest that the modulation of both the tonic stretch reflex and the phasic stretch reflex in the soleus muscle during standing are impaired in PD patients, and these impairments may partly cause their disability in the maintenance of a standing posture. Abnormalities in Ib inhibition and presynaptic inhibition are considered to be possible mechanisms in the disturbed modulation of the tonic stretch reflex and the phasic stretch reflex in PD patients during standing.

Comparison of amplitude of human soleus H-reflex during sitting and standing.

The modulation of the H-reflex in the human soleus muscle under conditions of different length or of background EMG activity was compared in 7 healthy subjects under three conditions: sitting, standing with support, and standing without support. The amplitude of the H-reflex increased when the muscle was shortened in both the sitting and standing conditions. The degree of increase in H-reflex was smaller during standing than sitting for the same change in muscle length. The H-reflex was augmented according to the increase of the background EMG. The "reflex gain", the ratio of the increase in amplitude of the H-reflex to soleus muscle EMG activity, decreased on sitting, standing with support and standing without support, ranked in that order. From these observations, it is concluded that the H-reflex is modulated by both muscle length and the degree of postural stability. The modulation of the reflex could be interpreted in terms of gain compensation and would serve to stabilize posture. A decrease in reflex gain may be appropriate in stabilizing the spinal reflex feedback loop during standing, especially without support.

Myotonic and repetitive discharges in hypokalemic myopathy associated with glycyrrhizin-induced hypochloremia.

Electromyographic studies were performed in two patients with hypokalemic myopathy induced by the administration of glycyrrhizin, 270-273 mg per day for a period of two and eight months, respectively. Myotonic and repetitive discharges were observed when the serum chloride level fell below 90 mEq/l. Following the administration of potassium chloride, when the chloride level rose above 90 mEq/l, these discharges disappeared. These findings support the causal role of hypochloremia in myotonic discharges. A serum chloride level below 90 mEq/l appears to be critical in producing the myotonic and repetitive discharges.

Spinal cord sarcoidosis: MRI findings in response to treatment.

The unusual case of a 64-year-old female with sarcoidosis involving the spinal cord is reported. Diffuse swelling of the cord with nodular lesions was observed on MRI. The lesions showed a low intensity area on the T1-weighted image. Following the administration of gadolinium-diethylenetriamine pentaacetic acid, the spinal cord, especially the nodular lesions, was diffusely enhanced. Serum levels of anti-endothelial cell antibodies and antinuclear antibodies were elevated. The diagnosis was confirmed by transbronchial lung biopsy which revealed noncaseating granulomas with giant epithelioid cells. The administration of prednisolone, 40 mg/day for 4 weeks, induced a remission.

Disturbed modulation of the stretch reflex gain during standing in cerebellar ataxia.

The postural control disturbance in patients with spino-cerebellar degeneration (SCD) was evaluated by the displacement of the center of foot pressure (CFP) and the amplitude of the triceps surae muscle H reflex in various standing postures. Twelve patients and 8 age-matched normal subjects (NL) were studied. The CFP, surface electromyograms (EMG) in the lower leg and the soleus H reflex were recorded in all subjects. The CFP displacement area was recorded in 10 patients. The following results were obtained: (1) the range of displacement of CFP from forward to backward leaning as a fraction of foot length was significantly smaller in the patients than in the controls (mean +/- S.D.; SCD = 52.8 +/- 12.7%; NL = 62.3 +/- 9.9%; P less than 0.05%, Student's t test); (2) the ratio of the increase in amplitude of the H reflex to soleus muscle EMG activity when the subjects leaned forward from an upright posture was significantly higher in the patients than in the controls (SCD = 0.41 +/- 0.40; NL = 0.17 +/- 0.15, P less than 0.05); (3) this ratio correlated with the area of CFP displacement during upright standing in the patients (r = 0.75, n = 10, P less than 0.05). These results indicate that the suppression of the stretch reflex observed in normal controls during standing is impaired in patients with SCD. We conclude that a decreased suppression of the stretch reflex is one of the mechanisms responsible for the instability on standing in patients with SCD.

Reciprocal Ia inhibition in patients with spinal spasticity.

Reciprocal Ia inhibition from ankle flexors to extensors was studied in five patients with spasticity due to incomplete traumatic spinal cord lesions. Nine healthy subjects were tested as controls. Excitability of the soleus motoneuron pool was estimated by H-reflex testing in the resting state. Ia inhibition was activated by conditioning stimuli to the peroneal nerve. Ia inhibition was detected in all patients tested, the amount of inhibition ranging from 8% to more than 50% of the test H-reflex size. In the control subjects only weak Ia inhibitory effects were present. These findings indicate increased excitability of the Ia inhibitory pathway to ankle extensor motoneurons in patients with spasticity due to spinal cord injury.