Cervical spinal cord injury (cSCI) disrupts bulbospinal projections to motoneurons controlling the upper limbs, resulting in significant functional impairments. Ongoing clinical and experimental research has revealed several lines of evidence for functional neuroplasticity and recovery of upper extremity function after SCI. The underlying neural substrates, however, have not been thoroughly characterized. The goals of the present study were to map the intraspinal motor circuitry associated with a defined upper extremity muscle, and evaluate chronic changes in the distribution of this circuit following incomplete cSCI. Injured animals received a high cervical (C2) lateral hemisection (Hx), which compromises supraspinal input to ipsilateral spinal motoneurons controlling the upper extremities (forelimb) in the adult rat. A battery of behavioral tests was used to characterize the time course and extent of forelimb motor recovery over a 16 week period post-injury. A retrograde transneuronal tracer -pseudorabies virus -was used to define the motor and pre-motor circuitry controlling the extensor carpi radialis longus (ECRL) muscle in spinal intact and injured animals. In the spinal intact rat, labeling was observed unilaterally within the ECRL motoneuron pool and within spinal interneurons bilaterally distributed within the dorsal horn and intermediate gray matter. No changes in labeling were observed 16 weeks post-injury, despite a moderate degree of recovery of forelimb motor function. These results suggest that recovery of the forelimb function assessed following C2Hx injury does not involve recruitment of new interneurons into the ipsilateral ECRL motor pathway. However, the functional significance of these existing interneurons to motor recovery requires further exploration.

A 57-year-old woman presented with a 1-year history of major depressive disorder. She was started on venlafaxine XR 75 mg orally daily and a few days later developed severe dysosmia to foods she used to enjoy. She never had previous problems with smell or taste. At her 1-month follow-up, her depressive symptoms had improved, but she reported persistent dysosmia and was found to have associated weight loss due to decreased oral intake. She was advised to switch medications, but due to financial constraints she continued taking the same dose. At follow-up 48 days later, she reported complete resolution of her dysosmia and was eating normally again, but she had persistence of some depressive symptoms so her dose was gradually increased to venlafaxine XR 225 mg orally daily until her depressive symptoms and postmenopausal hot flashes were well controlled. There were no changes with continued use over the following 8 years.