Remission of Major Depression Under Deep Brain Stimulation of the Lateral Habenula in a Therapy-Refractory Patient


Remission of Major Depression Under Deep Brain Stimulation of the Lateral Habenula in a Therapy-Refractory Patient


Alexander Sartorius a, , Karl L. Kiening b, Peter Kirsch c, Carl C. von Gall d, Uwe Haberkorn d, Andreas W. Unterberg e, Fritz A. Henn f and Andreas Meyer-Lindenberg g
a Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, J5, D-68159 Mannheim, Germany
b Department of Neurosurgery, Division of Stereotactic Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany
c Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany
d Department of Nuclear Medicine, University of Heidelberg, Heidelberg, Germany
e Department of Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany
f Brookhaven National Laboratory, Life Sciences, Long Island, New York
g Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany

Depression is a severe, common psychiatric illness with limited therapeutic options. Only approximately two-thirds of patients treated respond to standard antidepressants. Even with electroconvulsive therapy (ECT), a significant fraction remains therapy refractory.
For such cases deep brain stimulation (DBS) is currently under investigation: DBS of the subcallosal cingulate was successful in 7 of 20 patients after 6 months (1). Stimulating the ventral capsule/ventral striatum resulted in 3 of 15 remitted patients (2).
A possible novel target is suggested by anatomical implications of the long-standing monoamine hypothesis of depression (3): the serotonergic, noradrenergic, and dopaminergic system each have strong interactions and direct efferents from the lateral habenula (LHb) (to dorsal raphe nuclei, locus coeruleus, and ventral tegmental area) that in turn receives limbic and cortical inputs (4). During learned helplessness, an animal model of depression and anxiety (5), susceptible rats (6) showed striking LHb hypermetabolism (7). In humans, this area covaries with dorsal raphe nuclei activity during the induction of depression through tryptophan depletion ([8] and [9]), and shows selective volume reductions in brains of patients with depression (10). Recent primate work implicated the LHb in controlling reward through the ventral tegmental area, constituting a “circuit of disappointment” (11). In summary, convergent evidence indicates that overactivity in the LHb is present during depressed states, where it could drive the changes in midbrain activity linked to depression ([12] and [13]). This suggests that the LHb might prove to be a promising novel target for DBS in cases of intractable major affective disorder.
We report here the results on the first patient with treatment-resistant major depression undergoing bilateral DBS of the major afferent bundle (i.e., stria medullaris thalami) of the LHb.

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