Impact of Mesial Temporal Lobe Resection on Brain Structure in Medically Refractory Epilepsy.

OBJECTIVE: Surgical resection can decrease seizure frequency in medically intractable temporal lobe epilepsy. However, the functional and structural consequences of this intervention on brain circuitry are poorly understood. We investigated structural changes that occur in brain circuits after mesial temporal lobe resection for refractory epilepsy. Specifically, we used neuroimaging techniques to evaluate changes in 1) contralesional hippocampal and bilateral mammillary body volume and 2) brain-wide cortical thickness. METHODS: Serial T1-weighted brain magnetic resonance images were acquired before and after surgery (1.6 ± 0.5 year interval) in 21 patients with temporal lobe epilepsy (9 women, 12 men; mean age, 39.4 ± 11.5 years) who had undergone unilateral temporal lobe resection (14 anterior temporal lobectomy; 7 selective amygdalohippocampectomy). Blinded manual segmentation of the unresected hippocampal formation and bilateral mammillary bodies was performed using the Pruessner and Copenhaver protocols, respectively. Brain-wide cortical thickness estimates were computed using the CIVET pipeline. RESULTS: Surgical resection was associated with a 5% reduction in contralesional hippocampal volume (P < 0.01) and a 9.5% reduction in mammillary body volume (P = 0.03). In addition, significant changes in cortical thickness were observed in contralesional anterior and middle cingulate gyrus and insula (Pfalse discovery rate < 0.01) as well as in other temporal, frontal, and occipital regions (Pfalse discovery rate < 0.05). Postoperative verbal memory function was significantly associated with cortical thickness change in contralesional inferior temporal gyrus (R2 = 0.39; P = 0.03). CONCLUSIONS: These results indicate that mesial temporal lobe resection is associated with both volume loss in spared Papez circuitry and changes in cortical thickness across the brain.

Deep brain stimulation for stroke: Current uses and future directions.

BACKGROUND: Survivors of stroke often experience significant disability and impaired quality of life related to ongoing maladaptive responses and persistent neurologic deficits. Novel therapeutic options are urgently needed to augment current approaches. One way to promote recovery and ameliorate symptoms may be to electrically stimulate the surviving brain. Various forms of brain stimulation have been investigated for use in stroke, including deep brain stimulation (DBS). OBJECTIVE/METHODS: We conducted a comprehensive literature review in order to 1) review the use of DBS to treat post-stroke maladaptive responses including pain, dystonia, dyskinesias, and tremor and 2) assess the use and potential utility of DBS for enhancing plasticity and recovery from post-stroke neurologic deficits. RESULTS/CONCLUSIONS: A large variety of brain structures have been targeted in post-stroke patients, including motor thalamus, sensory thalamus, basal ganglia nuclei, internal capsule, and periventricular/periaqueductal grey. Overall, the reviewed clinical literature suggests a role for DBS in the management of several post-stroke maladaptive responses. More limited evidence was identified regarding DBS for post-stroke motor deficits, although existing work tentatively suggests DBS-particularly DBS targeting the posterior limb of the internal capsule-may improve paresis in certain circumstances. Substantial future work is required both to establish optimal targets and parameters for treatment of maladapative responses and to further investigate the effectiveness of DBS for post-stroke paresis.