RESUMO
The heterogeneity of mood states in bipolar disorders leads to some confusion in diagnostic and therapeutic strategies. Apart from the classical syndromes characterizing euphoric mania and melancholic depression, recent literature has pointed to alternative mood states associating both manic and depressive symptoms. This resulted in the definition of various syndromes including mixed states, dysphoric mania, agitated depression and more recently the depressive mixed state. This consequently raises the question of the best therapeutic strategies. As the boundaries between the various states associating both depressive and manic symptoms have yet to be clarified, there is a need to further discuss whether dimensional rather than categorical approaches could help to further refine their definitions and define the best therapeutic strategies. As stated by Kraepelin, mood episodes in manic-depressive illness were defined according to three dimensions: mood, cognitive processes, and motor and motivational drive. Cognitive and motor processes were regarded as quantitative items whose alterations may correspond to either an increase or a decrease. The current definitions are far from this dimensional approach. Thus, the current diagnostic criteria make it difficult to define mixed states. Such poorly convincing diagnostic criteria may account for the description of many other states exhibiting both manic and depressive symptoms. A dimensional approach could be useful to define mood states in bipolar disorders. These dimensions should progressive, from inhibition to excitation. Because tonality affects is not a dimension, the emotional reactivity (hyper-reactivity versus hypo-reactivity) represents an additional dimension that would help characterize these states better.
Assuntos
Transtorno Bipolar/epidemiologia , Transtorno Bipolar/psicologia , Depressão/epidemiologia , Depressão/psicologia , Psiquiatria/métodos , Humanos , SíndromeRESUMO
This study compares plasma, red cell, and cerebrospinal fluid (CSF) folate levels in subjects with mild or moderate Alzheimer's disease (AD) of senile onset and in non-demented control subjects. Twelve subjects with mild or moderate (Folstein's Mini-Mental-State-MMS--between 10 and 23) AD (DSM3 R criteria) and 12 control subjects without dementia and with MMS above 23 were included. To avoid any change in plasma folate levels due to dehydration, all dehydrated subjects were excluded. Were also excluded all subjects obviously suffering from malnutrition or alcoholism, or taking drugs likely to interfere with folate metabolism. Changes in folate levels due to posture or prolonged venous occlusion were carefully avoided. Patients with AD were 5 males and 7 females aged (Mean +/- SD) 80.2 +/- 5.7 years, MMS 14.8 +/- 2.6; controls were 7 males and 5 females aged 78.9 +/- 7.2 y, MMS 28.3 +/- 1.5. The two groups were not statistically different for these variables, except for the MMS. Plasma folate levels were lower (p < 0.006) in patients with AD (4.5 +/- 1.5 micrograms/l) compared with controls (7 +/- 2.2 micrograms/l). Red cell folate levels were lower (p < 0.007) in patients with AD (183.7 +/- 91.1 micrograms/l) compared with controls (300.4 +/- 96.1 micrograms/l). CSF folate levels were lower in AD (18.9 +/- 9.7 micrograms/l) than in controls (21.9 +/- 8.2 micrograms/l) but the difference was not statistically significant (p > 0.05). Our results indicate poorer nutrition in patients with AD.