Acute akathisia occur mostly during the neuroleptic and antidepressant treatment, but some other drugs like metoclopramide, some calcium channel blockers, dopamine agonists, antimalarials, buspirone and amphetamine may cause akathisia
(4). Stuppaeck et al. reported akathisia associated carbon monoxide intoxication
(7), Carrazzana et al. reported akathisia with subtalamic toxoplasmosis abscesses
(1).
Although the pathogenesis of this syndrome is still obscure, PET studies revealed D2 receptor blockade in striatum may play major role and noradrenergic and seronergic systems appear to be involved(4,9) This would explain akathisia and EPS induced by antidepressants and the positive response to 5-HT2 antagonists and beta blockers. Additionally there appears to be dopamine receptor blockade in the mesocortical dopamine system(2). The mesocortical pathway has an inhibitory effect on motor effect. Akathisia is thought to be a product of postsynaptic blockade of this pathway. The association between low serum iron level and akathisia has been not exactly showed(2). Drugs which have been found to have some efficacy in the treatment of akathisia are: Anticholinergics, Beta blockers, Benzodiazepines, Cyproheptadine, Clonidine, Mianserin. anticholinergics are probably most useful when akathisia is accompanied by parkinsonian side effects, thereby we treated the patient with Biperidene(4).
In our case; the initial brain MR images, high intensity images on diffusion-weighted MR and decreased blood flow in basal ganglia by SPECT showed that the lesions were associated with focal ischemia and edema. Ischemia and edema were limited to basal ganglia which may seen in cerebral hypoxic events(6). However, our patient has no history of hypotension or anoxia, and he had rapid improvement that may not seen by hypoxic events. DWI analysis revealed that alterations of the bilateral basal ganglia in the acute stage are not the result of extracellular edema, but rather the result of intracellular edema. As we know, uremic toxins impair basal ganglia metabolism such as dopamin turnover. This may be facilitated by uncontrolled hyperglicemia. Impaired dopamin turnover and increased sensitivity of postsynaptic dopamine receptors could lead to akathisia(2,4). Similar to our case, the neuroimaging changes of the syndrome regressed or disappeared in the majority of reported cases, after a period of several weeks.
Received by: 07 Ocak 2008
Revised by: 11 Nisan 2008
Accepted: 11 Nisan 2008
)
