Study register · detailBeobachtungsstudie (CSF-Biomarker) · Psychosis · 2004
Cerebrospinal Anandamide Levels are Elevated in Acute Schizophrenia and are Inversely Correlated with Psychotic Symptoms
Giuffrida et al.·NeuropsychopharmacologyImpact 4.4
UnclearGRADELow477 citations
Samplen = 203 Pat.
Durationunclear
ControlHealthy controls, dementia patients…
EndpointCSF anandamide concentration
Blindingn.a.
DesignBeobachtungsstudie (CSF-Biomarker)
”Key finding
CSF anandamide levels are 8-fold elevated in untreated first-episode schizophrenics and correlate negatively with psychotic symptoms; the clinical significance and causality remain unclear.
Summary
n=203 (47 antipsychotic-naive first-episode paranoid patients, 84 healthy, 13 dementia, 22 affective disorder, 37 typical antipsychotics, 34 atypical antipsychotics). CSF anandamide levels 8-fold elevated in untreated acute paranoid-schizophrenic patients vs. controls (p<0.001). Negative correlation between CSF anandamide and psychotic symptoms (rS=-0.452, p=0.001). The elevation was absent under typical antipsychotic treatment.
P
PopulationPatients with acute paranoid schizophrenia (first-episode, antipsychotic-naive n=47; typically antipsychotically treated n=37; atypically treated n=34) as well as healthy controls (n=84), dementia patients (n=13) and patients with affective disorders (n=22)
I
InterventionMeasurement of anandamide levels in cerebrospinal fluid (CSF)
C
ControlHealthy controls, dementia patients, patients with affective disorders
O
OutcomeCSF anandamide levels 8-fold elevated in antipsychotic-naive first-episode patients vs. controls; inverse correlation with psychotic symptomatology (rS = -0.452, p = 0.001)
Confidence in the evidence
Very lowLowModerateHigh
Low
The second of four GRADE levels, the effect estimate is of limited reliability.
Quality profile
Sample size★★★★★
Blinding—
Effect size—
Citations / year★★★★★
Authors
Giuffrida A, Leweke FM, Gerth CW, Schreiber D, Koethe D, Faulhaber J, Klosterkötter J, Piomelli D
The endocannabinoids are a family of bioactive lipids that activate CB1 cannabinoid receptors in the brain and exert intense emotional and cognitive effects. Here, we have examined the role of endocannabinoid signaling in psychotic states by measuring levels of the endocannabinoid anandamide in cerebrospinal fluid (CSF) of acute paranoid-type schizophrenic patients. We found that CSF anandamide levels are eight-fold higher in antipsychotic-naive first-episode paranoid schizophrenics (n = 47) than healthy controls (n = 84), dementia patients (n = 13) or affective disorder patients (n = 22). Such an alteration is absent in schizophrenics treated with 'typical' antipsychotics (n = 37), which antagonize dopamine D2-like receptors, but not in those treated with 'atypical' antipsychotics (n = 34), which preferentially antagonize 5HT(2A) receptors. Furthermore, we found that, in nonmedicated acute schizophrenics, CSF anandamide is negatively correlated with psychotic symptoms (rS = -0.452, P = 0.001). The results suggest that anandamide elevation in acute paranoid schizophrenia may reflect a compensatory adaptation to the disease state.