Effect of Subthalamic Deep Brain Stimulation on Non-Motor Fluctuations in Parkinson’s Disease.

Effect of subthalamic deep brain stimulation on non-motor fluctuations in Parkinson’s disease.

Filed under: Depression Treatment

J Neural Transm. 2012 Dec 23;
Azulay JP, Witjas T, Eusebio A

The non-motor consequences of subthalamic stimulation are largely questioned. Cognition, motivation, anxiety, depression and even occurrence of suicides have been considered as a potential consequence of the surgical intervention. Non-motor fluctuations are present in all the patients with motor fluctuations and may sometimes be even more invalidating. Interestingly, subthalamic deep brain stimulation alleviates non-motor fluctuations allowing strikingly successful effects on sensory, dysautonomic and cognitive fluctuations while psychic fluctuations respond less consistently to this treatment. Nevertheless, severe mood fluctuations, oscillating from Off dysphoria to ON hypomania, are frequently associated with addictive behaviors and improve dramatically after subthalamic stimulation. This may be a further argument to support the indication of surgery for these patients.
HubMed – depression

 

Systemic lupus erythematosus activity and depression.

Filed under: Depression Treatment

Rheumatol Int. 2012 Dec 21;
Skare T, da Silva Magalhães VD, Siqueira RE

HubMed – depression

 

Hippocampal CLOCK protein participates in the persistence of depressive-like behavior induced by chronic unpredictable stress.

Filed under: Depression Treatment

Psychopharmacology (Berl). 2012 Dec 20;
Jiang WG, Li SX, Liu JF, Sun Y, Zhou SJ, Zhu WL, Shi J, Lu L

RATIONALE: Circadian disturbances are strongly linked with major depression. The circadian proteins CLOCK and BMAL1 are abundantly expressed but function differently in the suprachiasmatic nucleus (SCN) and hippocampus. However, their roles in depressive-like behavior are still poorly understood. OBJECTIVES: To investigate the alterations of CLOCK and BMAL1 in the SCN and hippocampus in rats subjected to chronic unpredictable stress (CUS) and to explore the relationship of circadian protein and the depressive-like behavior. RESULTS: Together with depressive-like behavior induced by CUS, CLOCK and BMAL1 in the SC were inhibited during the light period, and the peak expression of CLOCK in the hippocampus was shifted from the dark to light period. BMAL1 expression in the hippocampus was not significantly changed. Two weeks after the termination of CUS, abnormalities of CLOCK in the CA1 and CA3 endured, with unchanged depressive-like behavior, but the expression of CLOCK and BMAL1 in the SCN recovered to control levels. Knockdown of the Clock gene in CA1 induced depressive-like behavior in normal rats. CLOCK in the SCN and hippocampus may participate in the development of depressive-like behavior. However, CLOCK in the hippocampus but not SCN was involved in the long-lasting effects of CUS on depressive-like behavior. BMAL1 in the hippocampus appeared to be unrelated to the effects of CUS on depressive-like behavior. CONCLUSION: CLOCK protein in the hippocampus but not SCN play an important role in the long-lasting depressive-like behavior induced by CUS. These findings suggest a novel therapeutic target in the development of new antidepressants focusing on the regulation of circadian rhythm.
HubMed – depression

 

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