location and its relation to hypothalamic structures. Large pedunculated HHs, mostly located outside the hypothalamus, are rarely associated with catastrophic epilepsy, whereas small unilateral intrahypothalamic lesions (Valdueza Types I and II) can be associated with severe seizures that lead to behavioral and cognitive deterioration. 1 , 15 The epileptogenesis of intrahypothalamic HHs is linked to their extensive connections with limbic neuronal networks, which can highly facilitate the spread of epileptic activity and the propagation of seizures. Electrophysiological
Pantaleo Romanelli, Alexander Muacevic and Salvatore Striano
Sarah K. B. Bick and Emad N. Eskandar
fornix and alters upstream and downstream signaling in memory circuitry, creating changes in metabolism and structure via alteration of network signaling and perhaps neurogenesis. Neurogenesis induced by DBS may contribute new neurons that integrate into functional circuits and improve function in the neuronal network underlying memory. 62 Although studies of forniceal DBS in humans have demonstrated promising metabolic changes in networks associated with memory, further studies are needed to determine whether these will be associated with durable clinical results
Jorge A. González-Martínez, William E. Bingaman, Steven A. Toms and Imad M. Najm
cortical mantle (IZ and cortex), and to lead to generation of differentiated neurons. This pattern of temporospatial progression was absent in controls. Discussion Our results suggest that the SVZ of postnatal human epileptic brain has the ability to proliferate and spontaneously generate new neurons, which migrate to superficial layers of the cortical mantle. It was previously suggested that neurogenesis in the postnatal human brain may constitute an evolutionarily undesired biological process in an already established neuronal network. 33 Here we demonstrated
Chris Kao, Jonathan A. Forbes, Walter J. Jermakowicz, David A. Sun, Brandon Davis, Jiepei Zhu, Andre H. Lagrange and Peter E. Konrad
T halamocortical oscillations are generated by both intrinsic oscillatory properties of individual neurons and reciprocal connections within the thalamocortical network. These oscillations likely play an important role in the regulation of consciousness in the mammalian brain and are an integral component of the electrical activity that is recorded from the cortical surface on electroencephalography. 14 , 20 , 31 In mild to moderate TBI, damage to underlying thalamocortical circuits and other neuronal networks may result in alterations in EEG activity
Hae Yu Kim, Yun Jung Hur, Heung-Dong Kim, Kang Min Park, Sung Eun Kim and Tae Gyu Hwang
Thalamic stimulation can provoke electroencephalography (EEG) synchronization or desynchronization, which can help to reduce the occurrence of seizures in intractable epilepsy, though the underlying mechanism is not fully understood. Therefore, the authors investigated changes in EEG electrical activity to better understand the seizure-reducing effects of deep brain stimulation (DBS) in patients with intractable epilepsy.
Electrical activation patterns in the epileptogenic brains of 3 patients were analyzed using classical low-resolution electromagnetic tomography analysis recursively applied (CLARA). Electrical activity recorded during thalamic stimulation was compared with that recorded during the preoperative and postoperative off-stimulation states in patients who underwent anterior thalamic nucleus DBS for intractable epilepsy.
Interictal EEG was fully synchronized to the β frequency in the postoperative on-stimulation period. The CLARA showed that electrical activity during preoperative and postoperative off-stimulation states was localized in cortical and subcortical areas, including the insular, middle frontal, mesial temporal, and precentral areas. No electrical activity was localized in deep nucleus structures. However, with CLARA, electrical activity in the postoperative on-stimulation period was localized in the anterior cingulate area, basal ganglia, and midbrain.
Anterior thalamic stimulation could spread electrical current to the underlying neuronal networks that connect with the thalamus, which functions as a cortical pacemaker. Consequently, the thalamus could modify electrical activity within these neuronal networks and influence cortical EEG activity by inducing neuronal synchronization between the thalamus and cortical structures.
Cristina V. Torres, Guillermo Blasco, Marta Navas García, Elena Ezquiaga, Jesús Pastor, Lorena Vega-Zelaya, Paloma Pulido Rivas, Silvia Pérez Rodrigo and Rafael Manzanares
Initial studies applying deep brain stimulation (DBS) of the posteromedial hypothalamus (PMH) to patients with pathological aggressiveness have yielded encouraging results. However, the anatomical structures involved in its therapeutic effect have not been precisely identified. The authors’ objective was to describe the long-term outcome in their 7-patient series, and the tractography analysis of the volumes of tissue activated in 2 of the responders.
This was a retrospective study of 7 subjects with pathological aggressiveness. The findings on MRI with diffusion tensor imaging (DTI) in 2 of the responders were analyzed. The authors generated volumes of tissue activated according to the parameters used, and selected those volumes as regions of interest to delineate the tracts affected by stimulation.
The series consisted of 5 men and 2 women. Of the 7 patients, 5 significantly improved with stimulation. The PMH, ventral tegmental area, dorsal longitudinal fasciculus, and medial forebrain bundle seem to be involved in the stimulation field.
In this series, 5 of 7 medication-resistant patients with severe aggressiveness who were treated with bilateral PMH DBS showed a significant long-lasting improvement. The PMH, ventral tegmental area, dorsal longitudinal fasciculus, and medial forebrain bundle seem to be in the stimulation field and might be responsible for the therapeutic effect of DBS.
Theodore G. Sarphie, Michael E. Carey, June F. Davidson and Joseph S. Soblosky
Object. Respiratory dysfunction including apnea frequently follows head injury in humans. The purpose of this study was to identify any structural alterations in the region of brainstem respiratory nuclei that might account for immediate postinjury respiratory abnormalities in anesthetized experimental animals.
Methods. Using scanning electron microscopy, the authors examined the floor of the fourth ventricle in injured rats after a piston strike to the sensorimotor cortex that depressed the dura 1, 2, or 4 mm. The rats were killed within minutes of injury. Cortical impact depths measuring either 1 or 2 mm (eight rats) produced no respiratory abnormalities, and the structural integrity of the ependymal lining of the ventricular floor in these animals was not compromised. Thirteen rats were subjected to impact to a 4-mm depth and 10 of these exhibited immediate temporary or permanent apnea. The medullae of nine of these rats were studied using scanning electron microscopy, and the fourth ventricular floors of all nine rats showed tears. Four rats that exhibited immediate, permanent apnea had tears in the caudal fourth ventricle floor near the obex, whereas five rats with no or only transient apnea had tears located more anteriorly, near the aqueduct or laterally. Changes in cerebrospinal fluid flow or pressure dynamics may have caused these tears. Light microscopy, focused near the area postrema, revealed a shearing defect through the ependyma of the fourth ventricular floor into the subjacent neuropil with a disruption of axonal pathways.
Conclusions. Respiratory neuronal network components lying within 2 mm of the area postrema may well have been disrupted by the caudal tears producing permanent apnea. A similar phenomenon could account for the transient or permanent postinjury apnea seen in humans with severe head injury.
Sunil Patel, Vibhor Krishna, Joyce Nicholas, Charles M. Welzig and Cristian Vera
Pulsatile arterial compression (AC) of the ventrolateral medulla (VLM) is hypothesized to produce the hypertension in a subset of patients with essential hypertension. In animals, a network of subpial neuronal aggregates in the VLM has been shown to control cardiovascular functions. Although histochemically similar, neurons have been identified in the retro-olivary sulcus (ROS) of the human VLM, but their function is unclear.
The authors recorded cardiovascular responses to electrical stimulation at various locations along the VLM surface, including the ROS, in patients who were undergoing posterior fossa surgery for trigeminal neuralgia. This vasomotor mapping of the medullary surface was performed using a bipolar electrode, with stimulation parameters ranging from 5- to 30-second trains (20–100 Hz), constant current (1.5–5 mA), and 0.1-msec pulse durations. Heart rate (HR) and blood pressure (BP) were recorded continuously from baseline (10 seconds before the stimulus) up to 1 minute poststimulus. In 6 patients, 17 stimulation responses in BP and HR were recorded.
The frequency threshold for any cardiovascular response was 20 Hz; the stimulation intensity threshold ranged from 1.5 to 3 mA. In the first patient, all stimulation responses were significantly different from sham recordings (which consisted of electrodes placed without stimulations). Repeated stimulations in the lower ROS produced similar responses in 3 other patients. Two additional patients had similar responses to single stimulations in the lower ROS. Olive stimulation produced no response (control). Hypotensive and/or bradycardic responses were consistently followed by a reflex hypertensive response. Slight right/left differences were noted. No patient suffered short- or long-term effects from this stimulation.
This stimulation technique for vasomotor mapping of the human VLM was safe and reproducible. Neuronal aggregates near the surface of the human ROS may be important in cardiovascular regulation. This method of vasomotor mapping with measures of responses in sympathetic tone (microneurography) should yield additional data for understanding the neuronal network that controls cardiovascular functions in the human VLM. Further studies in which a concentric bipolar electrode is used to generate this type of vasomotor map should also increase understanding of the pathophysiological mechanisms of neurogenically mediated hypertension, and assist in the design of studies to prove the hypothesis that it is caused by pulsatile AC of the VLM.
Howard M. Eisenberg, Charles Y. Liu and Oren Sagher
” presents a single case and reviews the topic, including a discussion of more standard methods for localization coregistered with molecular information from AMT-PET. The paired reports on hypothalamic hamartomas review this entity in detail as well as management strategies. Epilepsy surgery sits at the juncture of classic anatomical neurosurgery and functional neurosurgery. Surgery to treat epilepsy also provides us with an opportunity to understand neuronal networks. The papers in this issue illustrate some of the issues, challenges, and exciting developments in the
James T Rutka
central nervous system, and the fine histoarchitecture of the neuronal networks within the cerebral cortex. Of course, the work of Penfield 2 , 3 in the 1930s set the stage for the modern revolution of surgical techniques applied to the study of human epilepsy. In this special issue of Neurosurgical Focus, we have provided an update on the state-of-the-art management of epilepsy from both medical and surgical perspectives. We begin with a description of pharmacologically intractable epilepsy and proceed to a review of imaging strategies to identify neurosurgical