We observed a case of withdrawal after abrupt discontinuation of mianserin. A 41‐year‐old woman was treated according to a diagnosis of depression, which was her 6th episode. Mianserin 30 mg/day, etizolam 1 mg/day and flunitrazepam 1 mg/day were administered. When the patient discontinued taking the drugs by herself because of subsiding of these symptoms, severe panic anxiety appeared. This panic anxiety was not relieved by taking etizolam and flunitrazepam again, but subsided rapidly by the re‐administration of mianserin 30 mg/day, and because of that the depressive symptom also disappeared. From these experiences panic anxiety seemed to be a withdrawal symptom, and involvement of the noradrenergic system in panic anxiety as well as serotonergic system was suggested.
We have had experience in treating two patients with parkinsonism of which the first manifestation was depression. Case 1 was a 61‐year‐old woman. A diagnosis of depression had been made and repeated medication consisting mainly of antidepressants was given. However, the depressive state persisted and the signs of parkinsonism gradually became evident. The initial treatment with antidepressant drugs was replaced with one based on L‐DOPA (400 mg a day). Subsequently, the symptoms of parkinsonism and depression diminished relatively rapidly. Case 2 was a 66‐year‐old man. His parkinsonism was suspected shortly after the onset, although the symptoms of depression were predominant. Similarly, the treatment based on L‐DOPA (400 mg a day) relieved the symptoms of depression and parkinsonism rapidly. The present study described above indicates that parkinsonism should be suspected in cases of persistent depression and in patients who have depressive symptoms resistant to antidepressants, since parkinsonism may first manifest itself as depression.
Clonazepam was administered to nine patients with tardive akathisia which could not be controlled by antiparkinsonian drugs, and a good response was obtained in all cases. The daily dose of clonazepam given was only 1.0-3.0 mg. In two of the nine patients, akathisia recurred when the dose of clonazepam was reduced, but disappeared again after the dose was increased again. Clonazepam appears to be worth trying in patients with tardive akathisia, and is effective at relatively low doses. However, a dose reduction should be performed with caution, since there is the possibility that akathisia will recur.KEY woms-Clonazepam, tardive akathisia, neuroleptic-induced akathisia.
The case of a 25-year-old male with methamphetamine dependence indicating the presence of synergism between methamphetamine and alcohol was reported. The three clinical features observed in the present case were: First, ingesting large quantities of alcohol after an intravenous injection of the psychostimulant induced psychomotor excitement, indicating that alcohol itself could potentiate the psychosis-inducing action of the psychostimulant. Second, repetition of the alcohol intake without the drug injection reactivated a psychotic state, suggesting that there is a cross-reverse tolerance phenomenon to alcohol. Third, drug injection alone, twice aggavated the psychiatric symptoms, indicating the presence of reverse tolerance to the psychostimulant.
A 56‐year‐old woman was admitted to our hospital because of insomnia and psychomotor retardation. This is her second admission. She was diagnosed as having depression and began to receive antidepressants. Her conditions got better after the treatment but the depressive state occurred again after she stopped taking those drugs. As EEG showed some spike discharges at the nondominant temporal lobe area, she was given anticonvulsants this time. Her depressive state improved rapidly by taking anticonvulsants instead of the antidepressants. The spike discharges at the nondominant temporal lobe area disappeared when the clinical symptoms improved.
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