We investigated the dopamine metabolite plasma homovanillic acid (plas
ma HVA) levels in 37 catatonic patients on the day of admission before
initial medication as well as in 17 healthy controls. In a prospectiv
e study catatonic syndrome was diagnosed according to criteria of Lohr
and Wiesniwski (1987) and Rosebush et al (1990) whereas comorbid diag
nosis was made by Diagnostic and Statistical Manual of Mental Disorder
s, 3rd ed, revised (DSM III/R) (APA 1987). On the day of admission blo
od samples were taken before initial medication. Compared to controls
(80.1 +/- 40.1 pmol/ml) catatonic patients showed significantly (p = 0
.0286) increased plasma HVA (140.9 +/- 53.6 pmol/ml). Catatonic patien
ts free of neuroleptic medication (n = 21) differed significantly (p =
0.0416) from controls whereas neuroleptically treated catatonics (n =
16) did not. Our findings of increased plasma HVA in catatonia are ex
plained by an alteration in either mesolimbic or mesocortical dopamine
rgic function, as is assumed in the case of schizophrenia. As an alter
native, it may be due to increased nigrostriatal function, which can l
ead, as shown in animal experiments with the dopamine agonist amphetam
ine, to hypokinetic states resembling catatonia in humans.