Placement of an electrode array as a dural substitute for dorsal column stimulation: technical note.

One the drawbacks of the dorsal column stimulation (DCS) method is that the electrode array and the subsequent electrical stimulation induce proliferation of connective tissue between the array and the dura. In this case report, a patient is presented in whom dural thickening after placement of a DCS electrode array at the C2-C3 level prevented sufficient electrical penetration and thus resulted in treatment failure. The thickened dura was excised and the electronic array was used as a dural substitute. This resulted in efficient DCS and resolution of the pain symptoms.

Electrical stimulation of auditory and somatosensory cortices for treatment of tinnitus and pain.

The efficacy of electrical stimulation of the auditory cortex using extradural implanted electrodes for treatment of tinnitus was studied in 12 patients suffering tinnitus. The effect of similar stimulation of the somatosensory cortex for treatment of neuropathic pain was studied in five patients. It was shown that patients with pure tone type of tinnitus experienced a significant 97% suppression on average while those who had noise type tinnitus only had non-significant 24% suppression. All patients with pain experienced a significant reduction of their pain (using a visual analog scale), and in four out of five it was clinically relevant, i.e., the patient is really helped by it. It is concluded that electrical stimulation of sensory cortices can be effective treatments of severe unilateral tinnitus and unilateral neuropathic pain in selected patients. The results suggest that similar pathophysiological mechanisms underlie some forms of these phantom sensations, and therefore, similar treatment such as electrical stimulation of the respective sensory cortices can suppress tinnitus and pain.

Somatosensory cortex stimulation for deafferentation pain.

Functional neuroimaging has demonstrated that a relationship exists between the intensity of deafferentation pain and the degree of deafferentation-related reorganization of the primary somatosensory cortex. It has also revealed that this cortical reorganization can be reversed after the attenuation of pain. Deafferentation pain is also associated with hyperactivity of the somatosensory thalamus and cortex. Therefore, in order to suppress pain, it seems logical to attempt to modify this deafferentation-related somatosensory cortex hyperactivity and reorganization. This can be achieved using neuronavigation-guided transcranial magnetic stimulation (TMS), a technique that is capable of modulating cortical activity. If TMS is capable of suppressing deafferentation pain, this benefit should be also obtained by the implantation of epidural stimulating electrodes over the area of electrophysiological signal abnormality in the primary somatosensory cortex. The first studies demonstrated a statistically significant pain suppression in all patients and a clinically significant pain suppression in 80% of them. This clinical experience suggests that somatosensory cortex stimulation may become a neurophysiology-based new approach for treating deafferentation pain in selected patients. In this chapter, we review the relevant recent reports and describe our studies in this field.

Auditory cortex stimulation for tinnitus.

Functional imaging techniques have demonstrated a relationship between the intensity of tinnitus and the degree of reorganization of the primary auditory cortex. Studies in experimental animals and humans have revealed that tinnitus is associated with a synchronized hyperactivity in the auditory cortex and proposed that the underlying pathophysiological mechanism is thalamocortical dysrhythmia; hence, decreased auditory stimulation results in decreased firing rate, and decreased lateral inhibition. Consequently, the surrounding brain area becomes hyperactive, firing at gamma band rates; this is considered a necessary precondition of auditory consciousness, and also tinnitus. Synchronization of the gamma band activity could possibly induce a topographical reorganization based on Hebbian mechanisms. Therefore, it seems logical to try to suppress tinnitus by modifying the tinnitus-related auditory cortex reorganization and hyperactivity. This can be achieved using neuronavigation-guided transcranial magnetic stimulation (TMS), which is capable of modulating cortical activity. If TMS is capable of suppressing tinnitus, the effect should be maintained by implanting electrodes over the area of electrophysiological signal abnormality on the auditory cortex. The results in the first patients treated by auditory cortex stimulation demonstrate a statistically significant tinnitus suppression in cases of unilateral pure tone tinnitus without suppression of white or narrow band noise. Hence, auditory cortex stimulation could become a physiologically guided treatment for a selected category of patients with severe tinnitus.

Frequency specific hearing improvement in microvascular decompression of the cochlear nerve.

BACKGROUND: Microvascular compressions of the cochlear nerve can lead to hearing loss. Due to the tonotopic organization of the cochlear nerve any focal compression of the cochlear nerve will result in a frequency specific hearing loss. Decompressing the cochlear nerve could result in a frequency specific hearing improvement, without improving overall hearing. METHOD: Thirty one patients underwent microvascular decompression operations of the vestibulocochlear nerve for vertigo or tinnitus. Preoperative audiograms were substracted from postoperative audiograms obtained 2 years after microvascular decompression. The frequencies of maximal hearing improvement postoperatively were determined. FINDINGS: Of the 31 patients studied, 19 had improvements of 5 dB or more at one or more frequencies postoperatively, and 15 patients had improvements of 10 dB or more. Three patients had improvements of 25 dB or more postoperatively. The postoperative hearing improvement was frequency-specific and related to the anatomical location of the vascular contact on the auditory nerve. The improvement of hearing becomes diluted when the difference between pre- and postoperative hearing thresholds are averaged over all audiometric frequencies. We therefore present results for each frequency that was tested. CONCLUSIONS: Microvascular decompression of the cochlear nerve can improve hearing in selected patients. The improvement seems too small to justify decompressive surgery for the sole purpose of hearing improvement, but it could be considered if associated short vertigo spells, ipsilateral tinnitus, otalgia and cryptogenic hemifacial spasm are present. Decompression should be performed early, before BAEP changes become noticeable. 3D-MRI could become a valuable tool for selecting good surgical candidates.

Validation of a closed head injury model for use in long-term studies.

To study pharmacotherapy of traumatic brain injury in rats, a modified closed head injury model was used that expresses clinically relevant features including intracranial hypertension and morphological alterations. Long-term survival under ethically acceptable conditions would greatly improve its clinical relevance. To ensure this goal with great reproducibility, the experimental protocol was adapted, in particular the impact-acceleration kinetics. Variations in impact-acceleration conditions were obtained by modifying the stiffness of the impact site and changing the height of a 400 g weight dropped from 51.5 to 31.5 cm (51.5/400; 31.5/400). Impact and acceleration were measured with a force sensor incorporated in a rigid dummy-rat and an accelerometer mounted on the platform onto which the animals are positioned. Significant correlation was shown between impact and acceleration. Accelerations obtained in rats were significantly lower than those in the dummy. Unlike the 51.5/400 group, in the 31.5/400 group no mortality or cranial fractures were observed. In both groups intracranial pressure rose to pathological values immediately after trauma and remained elevated longer than 24 h. Diffuse axonal injury developed in all groups and remained present for at least 7 days. By reducing the impact-acceleration conditions, post-traumatic complications were diminished, while the clinically important features were maintained.