Treatment of myotonia with antiarrhythmic drugs. The treatment of myotonia: a controlled clinical trial. A pilot controlled study of the use of imipramine to reduce myotonia. The treatment of myotonia: evaluation of chronic oral taurine therapy. A comparative study of disopyramide and procainamide in the treatment of myotonia in myotonic dystrophy. Safety, tolerability, and efficacy of orally administered cannabinoids in MS. A double blind placebo RCT to investigate the effects of serotonergic modulation on brain excitability and motor recovery in stroke patients. Nifedipine in the treatment of myotonia in myotonic dystrophy. Therapy of myotonia. A double-blind evaluation of diphenylhydantoin, procainamide, and placebo.
The effects of disopyramide, phenytoin, mexiletine, and tocainide were compared in 30 patients with myotonic disorders. The severity of myotonia was assessed by clinical and electromyographic criteria at the end of each treatment phase lasting four weeks. Mexiletine (MXT) and tocainide (TCD) were found to be the most potent antimyotonic agents. The antimyotonic efficacy of MXT and TCD is explained by their fast-blocking effect on voltage-dependent sodium channels in the muscle membrane. The benefits of myotonia control with pharmacological agents must be weight against the risk of therapy in the individual patient. Because of the risks of hematologic problems, TCD is not recommended by us for the treatment of myotonia. nan It has been hypothesized that myotonic dystrophy is caused by a generalized disorder of membrane aminergic and petidergic receptors. A single uncontrolled study has suggested that the affective symptomatology and muscular disability of this disorder might be improved by tricyclic antidepressant treatment. In the present study, 12 adult patients with myotonic dystrophy (age range 18-55 yr) were treated with imipramine and placebo in a double-blind crossover paradigm. Both grip and percussion myotonia were significantly improved by imipramine treatment independent of change in depressive symptomatology. Serum drug levels revealed nonlinear elimination kinetics for imipramine in this patient population. A double-blind, single crossover study of chronic oral taurine administration versus placebo was conducted on nine patients with dystrophia myotonica. The severity of myotonia was assessed by clinical and electromyographic criteria and by testing the sensitivity of myotonic muscles to the intra-arterial infusion of potassium chloride. Confirming the antimyotonic effect of acute parenteral taurine, chronic treatment induced significant improvement of myotonia and a decreased sensitivity to the arterial potassium load as well as an enhancement of electrolyte movements across the membrane of the studied muscles. No significant side effects were noted. Ten patients with myotonic dystrophy were allocated at random to treatment with disopyramide and procainamide in a cross-over trial. Disopyramide was found to be at least as effective as procainamide in the relief of myotonia; and two patients who could not tolerate procainamide both tolerated disopyramide. The authors conducted a randomized, double-blind, placebo-controlled, twofold crossover study in 16 patients with MS who presented with severe spasticity to investigate safety, tolerability, and efficacy of oral Delta(9)-Tetrahydrocannabinol (THC) and Cannabis sativa plant extract. Both drugs were safe, but adverse events were more common with plant-extract treatment. Compared with placebo, neither THC nor plant-extract treatment reduced spasticity. Both THC and plant-extract treatment worsened the participant's global impression. Motor excitability is increased in both hemispheres in stroke patients during motor recovery. Pharmacologically controlled changes of cortical excitability might be beneficial for synaptic plasticity and therefore facilitate functional recovery after a brain lesion. In particular, it has been suggested that antidepressant drugs can modulate motor excitability. Several recent reports suggest the possibility of monitoring pharmacological effects on brain excitability through transcranial magnetic stimulation (TMS). The aim of this study was to investigate motor area excitability in patients with stroke after oral administration of citalopram. We conducted a prospective randomised placebo controlled study. Twenty patients with unilateral stroke were included in the study: ten patients treated by antidepressive drug and ten patients with placebo. A selective serotonergic drug (citalopram) or a placebo was administered using a mean dosage of 10 mg/day in combination with physiotherapy. Motor cortex excitability was studied by single and paired transcranial magnetic stimulation. TMS recording was tested before (T1) and 1 month after (T2) beginning drug treatment. Patients treated by the serotonergic drug, compared to patients that received a placebo, showed a significant improvement in neurological status as measured by NIHSS and a decrease of motor excitability over the unaffected hemisphere, while no differences were observed over the affected hemisphere. Our findings suggest that treatment with serotonergic drugs can bring about a significant decrease of the motor cortex excitability in stroke patients with effects on both the affected and unaffected hemispheres associated with a better motor recovery. Abnormal calcium transport may be implicated in the membrane defect in myotonic dystrophy. A single blind crossover trial of placebo (t.i.d.), nifedipine 10 mg (t.i.d.) and nifedipine 20 mg (t.i.d.), was performed in 10 patients with myotonic dystrophy. The severity of myotonia was assessed by measuring finger extension time after maximum voluntary finger flexion. A significant improvement in myotonia, after nifedipine, was recorded by this technique and supported by a subjective improvement in 50% of patients and clinical improvement of greater than 20% in five patients. Initial grip strength and muscle fatiguability measured by grip strength ergometry were not significantly altered. nan
Due to insufficient good quality data and lack of randomised studies, it is impossible to determine whether drug treatment is safe and effective in the treatment of myotonia. Larger, well-designed randomised controlled trials are needed to assess the efficacy and tolerability of drug treatment for myotonia.