Introduction Obsessive‐compulsive disorder (OCD) is among the most disabling chronic psychiatric disorders and has a significant negative impact on multiple domains of quality of life. Deep brain stimulation (DBS) is a treatment option for severe therapy‐resistant OCD. Objective To provide a detailed clinical description and treatment outcome analysis in a cohort of eight refractory OCD patients receiving ventral capsule/ventral striatum (VC/VS) stimulation with the intention to validate discriminating fiber bundles previously associated with clinical response. Materials and Methods The primary outcome measure (the Yale‐Brown Obsessive Compulsive Scale [Y‐BOCS]) and secondary outcomes depressive symptoms, anxiety, and quality of life were retrospectively analyzed. DBS leads were warped into standard stereotactic space. A normative connectome was used to identify the neural network associated with clinical outcome. Results With a median stimulation duration of 26 months, patients exhibited a mean Y‐BOCS reduction of 10.5 resulting in a response rate of 63%. Modulation of a fiber bundle traversing the anterior limb of the internal capsule (ALIC) was associated with Y‐BOCS reduction. This fiber bundle connected the frontal regions to the subthalamic nucleus (STN) and was functionally identified as the hyperdirect pathway of the basal ganglia circuitry. Conclusion Our findings show that in VC/VS stimulation, the neural network associated with clinical outcome shows overlap with that of previously described for other targets namely the anterior limb of the internal capsula, the nucleus accumbens, or the STN, which supports the evolvement from the concept of an optimal gray matter target to conceiving the target as part of a symptom modulating network.

Introduction: The presence of neuroglial tissue is considered a hallmark in Limited Dorsal Myeloschisis (LDM). However, several reports have indicated that the presence of neuroglial tissue in LDM cannot always be demonstrated. Here, we present such a case of LDM and provide an alternative hypothesis for lacking the neuronal component. Case Description: An antenatal LDM suspected neonate was born with a cystic skin lesion and membranous sac typical for membranous LDM. Three days post-partum the otherwise healthy infant underwent surgery, during which the stalk was resected and the spinal cord was untethered. Histopathologically, no neuroglial tissue could be determined. Noteworthy, S-100 staining revealed numerous peripheral nerves. Discussion: The current paradigm explains the absence of neuroglial tissue in resected stalks of LDM by indicating that it should be present in the unresected part, more proximal to the dorsal spinal cord. We hypothesize a different mechanism in which following reopening of the neural tube, mesodermal invasion causes a tight and persistent strand between the cutaneous- and neuro-ectoderm. Elongation of this mesodermal strand during embryological development allows for the formation of a mesenchymal stalk without the presence of neuroglial tissue. Hydrodynamic forces can cause fistulation of the poorly differentiated mesodermal tissue and subsequently lead to a saccular defect.