Kava and dopamine antagonism.

Abstract

Clinical course ofpatients I and 2. 1' = high dosage intravenous immunoglobulins (HIG); = HIG maintenance; * = plasmapheresis; P = prednisone, (alternate day dosage (mm) in parentheses); A = azathioprine; Cy = cyclosporin (daily dosage in parentheses); IFN-a = interferon-a (weekly dosage in miUion IU).temporary improvement during and after a flu like syndrome. In July 1992 solo treatment with interferon-a-2a (Roferon-A) at a dosage of 3 million intemational units (MIU) twice weekly was begun. On the third day after the first injection a dramatic improvement was seen and during 11 days the patient progressively recovered to normal. Serial nerve conduction studies showed progressive reduction of conduction blocks. Seven days after the reduction of interferon-a to 1 MIU/week, progressive weakness of distal muscles occurred that paralleled an increase in multiple conduction blocks. Reinstitution of interferon-a-2a treatment at a dosage of 2 MIU twice weekly, produced a complete recovery within six days. Again the dose of interferon was gradually reduced to 1 MIIU twice weekly, without clinical changes.Only minor adverse effects, such as fever and arthromyalgia, were seen during interferon treatment.Patient 2 was a healthy 3 year old boy who developed a waddling gait and muscle pain in his legs 20 days after an upper respiratory tract infection. The patient had recovered spontaneously after 15 days. During the next three months he had another three episodes of leg weakness lasting 10-15 days. Brain and spinal cord MRI was normal; electrophysiological studies showed delayed motor conduction velocity with multiple conduction blocks in all the nerves tested and normal sensory conduction velocities. The CSF contained 96 mg/dl protein and 3 white blood cells/ml, but no oligoclonal bands.During the fifth attack the child became unable to walk unaided and was admitted to our neurological department. He was treated with IVIg at a dose of 1 g/kg daily for two days and prednisone (at a dose of 50 mg every other day) and after three days he regained the ability to walk. Neurography showed disappearance of conduction blocks in two of three motor nerves. Twenty days later the boy had another relapse. Again treatment with IVIg improved motor symptoms in a few days. In the next 15 months he showed relapses every 13 to 20 days despite treatments with azathioprine and cyclosporin. All the episodes responded to IVIg. During three relapses the patient was treated with plasma exchange and showed improvement comparable with IVIg treatment. Treatment with interferon-a-2a (Roferon-A) (2-5 MUIIday)) was given. After this treatment the child regained normal strength within 15 days. The dose of interferon-a was reduced to 2 MIU twice a week after three months. The patient showed no relapses during the subsequent months and no adverse effects were seen. Neurography performed two months after interferon treatment showed improvement of motor conduction velocity in all nerves with pronounced reduction of conduction blocks.On the basis of the rese...

Saccade and Cognitive Function in Chronic Kava Users

“…In kava users, the current results show no cognitive indicators of dysfunction that may precede, or lead to the choreoathetotic movements reported among kava users in the literature (Schelosky et al, 1995;Spillane et al, 1997;Clough et al, 2001). This suggests that these involuntary movement reactions occur from acute rather than chronic changes.…”

“…For example, there have been several case reports of severe choreoathetosis following kava use (Schelosky et al, 1995;Spillane et al, 1997) and we have recently raised the possibility of an association between heavy kava use and seizures, either from toxicity or on withdrawal (Clough et al, 2001). In addition, the use of kava has been associated with hallucinations (Brunton, 1988) and an improvement in psychotic symptoms among psychiatric patients (Cawte, 1986).…”

Toxicity of Kava Kava

“…Acute kava usage caused reversible anesthesia of the mouth and skin, euphoria, sedation, muscle weakness, ataxia and, eventually, intoxication. Schelosky et al (55) reported that four patients took kava and confronted with central dopaminergic antagonism. Kava is a spinal depressant, causing transient ataxia or uncoordinated walk (53).…”

Herbal and alternative medicine: the impact on anesthesia

“…51,52 Since their effects are mediated by GABA receptor activation or by serotonin re-uptake inhibition (amongst other mechanisms), there is great potential for interaction with anaesthetic agents. 53 Apart from prolonged sedation or the risk of serotonin syndrome, some of these drugs may also precipitate seizures 54 (due to direct inhibition of anticonvulsive therapy, accelerated anti-convulsive metabolism, or additive excitatory effects with mood stabilizers like trazondone, buspirone and fluoxetine). L-Dopa efficacy may be compromised, resulting in worsening symptoms of Parkinsonism.…”