Posted by ed_uk on October 29, 2004, at 13:34:57
In reply to doc screwed me over? redirected my DA?, posted by lostforwards on October 29, 2004, at 11:39:43
Hello,
I've posted the following study and case report because I felt that it was relevant to you and perhaps a few other people on psychobabble as well. It has been adapted (by me) from a study presented in The Journal of Neurology, Neurosurgery and Psychiatry. I can supply you with the full report if you would like.
Your lack of arm swing suggests that you are experiencing some residual parkinsonism despite the fact that you are no longer taking Risperdal. Contrary to popular belief, Parkinsonism doesn't always resolve rapidly when an antipsychotic(neuroleptic) such as risperidone(Risperdal) has been stopped. The case report below describes the case of a woman who treated with an antipsychotic. Even after the neuroleptic was discontinued, Parkinsonism and numbed emotions persisted for a long time. Nevertheless, the patient did eventually get back to normal though :)EXTRAPYRAMIDAL SIDE EFFECTS OF ANTIPSYCHOTICS/NEUROLEPTICS
Neuroleptic medications are among the most commonly used drugs for treating patients with serious mental illness. These agents, which for the most part act by blocking the D2 subtype of dopamine receptor, are associated with acute or subacute neurological side effects, which generally resolve when the medication is discontinued. These so-called "extrapyramidal" side effects, which include dystonia, parkinsonism, and akathisia, are thought to arise as a direct consequence of the dopamine receptor blockade in the striatum.Neuroleptic drugs are also, however, associated with delayed onset, or tardive, syndromes, which typically begin after the patient has been taking the medication for some time, and which can persist for months, or even years, after the drug is discontinued. The existence of these tardive syndromes indicates that neuroleptic drugs are capable of producing long lasting changes in brain function. The nature of these long term changes, and the pathophysiology of the tardive syndromes, continue to be poorly understood.
Among the tardive syndromes which have been described are tardive dyskinesia, tardive dystonia, and tardive akathisia. There has been little attention to the potential of neuroleptic drugs to produce tardive parkinsonism.
CASE REPORT
A 37 year old married woman with no personal or family history of psychiatric or neurological illness consulted her family physician with complaints of anxiety, insomnia, sadness, inertia, and restlessness. Despite there being no evidence of psychosis, she was treated (inappropriately) for five months with intramuscular injections of the neuroleptic fluphenazine decanoate (10-35 mg every two to four days), supplemented by oral fluphenazine (5-55 mg/day). On this regimen she became very slowed down, with a shuffling gait, mask-like face, cogwheel rigidity, and difficulty in writing. (All signs of Parkinsonism). Because of her continuing parkinsonism the neuroleptic drugs were stopped, whereupon she developed pelvic rocking and gyrating (a rare form of tardive dyskinesia). Six months later the patient was admitted to hospital. **Examination at that time showed a flat affect(numbed emotions), expressionless voice, and staring expression.** There was cogwheel rigidity at the elbows and wrists, slowness and freezing during performance of alternate motion rate tasks, and micrographia. (ie. her parkinsonism had persisted). She maintained a stooped posture and had a slow shuffling gait with flexion at the elbows and no arm swing. The patient described an inner compulsion to move (akathisia) but displayed no spontaneous gesturing or movement, aside from constant pelvic rocking. Extensive laboratory investigations, including MRI, EEG, and evoked potentials, were all negative.Over the ensuing five months the patient had trials of lorazepam(Ativan), propranolol(Inderal), and benztropine(Cogentin), with minimal response. Treatment with levodopa/carbidopa(Sinemet) and a course of electroconvulsive therapy(ECT) given for her depression produced noticeable improvement in her parkinsonism, although she continued to have severe akathisia and pelvic dyskinesia. Eighteen months after her last dose of neuroleptic drugs there was still evidence of mild parkinsonism, mild akathisia, and minimal pelvic dyskinesia. ***At a two and a half year follow up she had no evidence of parkinsonism, dyskinesia, or akathisia.***
Study Title: Persistent loss of tyrosine hydroxylase immunoreactivity in the substantia nigra after neuroleptic withdrawal.
(Tyrosine hydroxylase is an enzyme which has an important role in dopamine synthesis in the body).
Summary of animal study performed.
The case described above prompted a study of the effect of an eight week course of haloperidol (an antipsychotic) followed by two week withdrawal, on dopaminergic neurons of the substantia nigra in rats. Animals treated with haloperidol showed a highly significant 32%-46% loss of tyrosine hydroxylase immunoreactive neurons in the substantia nigra, and 20% contraction of the tyrosine hydroxylase stained dendritic arbour. Neuroleptic drug induced downregulation of nigral dopaminergic neurons may help to explain the persistent parkinsonism found in many patients after withdrawal of medication.Discussion of the results of the animal study.
These results indicate that neuroleptic medications can produce a persistent down regulation of tyrosine hydroxylase in dopaminergic neurons in the substantia nigra. Animals exposed to haloperidol for eight weeks and then withdrawn from the medication had a 32%-44% reduction in the number of tyrosine hydroxylase immunoreactive nigral cell bodies, and a 20% decrease in nigral cross sectional area, two weeks after the drug had been discontinued.
***The ability of neuroleptic drugs to induce persisting suppression of tyrosine hydroxylase in nigrostriatal neurons suggests that these agents may be capable of producing tardive parkinsonism.*** Melamed et al reported on two 35 year old patients with schizophrenia who, after many years of neuroleptic treatment, developed progressive parkinsonism that continued to worsen after discontinuation of the neuroleptic medication. Hardie and Lees found that 14 of 16 patients with neuroleptic drug induced parkinsonism (median age 61) had incomplete resolution of the parkinsonism after prolonged withdrawal from neuroleptic drugs. In another series, five of 48 elderly patients with drug induced parkinsonism had persistent parkinsonian features seven weeks after stopping the drug, and another five initially improved but later went on to develop idiopathic parkinsonism. The patient whom we studied, despite being young and despite having no previous neurological symptoms, had parkinsonism for at least 18 months after completing a five month course of high dose neuroleptic treatment.
Ed
poster:ed_uk
thread:408750
URL: http://www.dr-bob.org/babble/20041029/msgs/408789.html