Jan Verlooy

Transcranial magnetic stimulation for tinnitus: influence of tinnitus duration on stimulation parameter choice and maximal tinnitus suppression.

Objective: Tinnitus is a distressing symptom for which few treatments exist. It leads to an important decrease in quality of life in 2 to 3% of the population. Tinnitus is considered a phantom sound, the result of cortical reorganization. Transcranial magnetic stimulation (TMS) is a noninvasive method to modulate cortical reorganization and has been shown to be able to influence tinnitus perception. Study Design: Retrospective analysis. Setting: Tertiary referral center. Patients: The effect of TMS of the contralateral auditory cortex in 114 patients with unilateral tinnitus is investigated as one of the selection criteria used for surgical implantation of electrodes on the auditory cortex. Intervention: TMS is performed at 90% of motor threshold at 1, 3, 5, 10, and 20 Hz, with each stimulation session consisting of 200 pulses. Results were classified as no effect (0-19% improvement), partial effect (20-79% improvement), and good effect (80-100 suppression). Main Outcome Measures: TMS had a good effect in 25% of the patients studied, partial effect in 28% patients, and no effect in 47%. Results: TMS at 200 pulses is capable of tinnitus suppression for seconds only. The results were influenced by tinnitus duration: the longer the tinnitus exists, the lower the stimulation frequency that yields maximal tinnitus suppression (p < 0.001). The maximal amount of tinnitus suppression decreases in time (p < 0.01), resulting in a 2% decrease of potential tinnitus suppression per year. Conclusion: TMS of the auditory cortex is capable of modifying tinnitus perception for a very short time. The maximal amount of suppression and best stimulation frequency depends on the tinnitus duration.

Imaging findings in diffuse axonal injury after closed head trauma

Abstract. Even in patients with closed head trauma, brain parenchyma can be severely injured due to disruption of axonal fibers by shearing forces during acceleration, deceleration, and rotation of the head. In this article we review the spectrum of imaging findings in patients with diffuse axonal injuries (DAI) after closed head trauma. Knowledge of the location and imaging characteristics of DAI is important to radiologists for detection and diagnosis. Common locations of DAI include: cerebral hemispheric gray-white matter interface and subcortical white matter, body and splenium of corpus callosum, basal ganglia, dorsolateral aspect of brainstem, and cerebellum. In the acute phase, CT may show punctate hemorrhages. The true extent of brain involvement is better appreciated with MR imaging, because both hemorrhagic and non-hemorrhagic lesions (gliotic scars) can be detected. The MR appearance of DAI lesions depends on several factors, including age of injury, presence of hemorrhage or blood-breakdown products (e. g., hemosiderin), and type of sequence used. Technical aspects in MR imaging of these patients are discussed. Non-hemorrhagic lesions can be detected with fluid attenuated inversion recovery (FLAIR), proton-density-, or T2-weighted images, whereas gradient echo sequences with long TE increase the visibility of old hemorrhagic lesions.

Primary and Secondary Auditory Cortex Stimulation for Intractable Tinnitus

Introduction: Recent research suggests tinnitus is a phantom phenomenon based on hyperactivity of the auditory system, which can be visualized by functional neuroimaging, and transiently modulated by transcranial magnetic stimulation (TMS). We present the results of the first implanted electrodes on the primary and secondary auditory cortex after a successful TMS suppression. Methods and Materials: Twelve patients underwent an auditory cortex implantation, 10 for unilateral and 2 for bilateral tinnitus, based on >50% suppression applying TMS. Results were analyzed for pure tone tinnitus and white noise tinnitus. Results: TMS results in 77% pure tone tinnitus and 67% white noise reduction. Electrical stimulation via an implanted electrode results in a mean of 97% pure tone tinnitus and 24% white noise suppression. Mean Visual Analogue Scale score decreases from 9.5 to 1.5 for pure tone and from 8.8 to 6.8 for white noise postoperatively. Discussion: Pure tone tinnitus might be the conscious percept of focal neuronal hyperactivity of the auditory cortex. Once visualized, this hyperactivity can be modulated by neurostimulation. Conclusion: The preliminary results of the first implantations suggest that patients with unilateral pure tone tinnitus are good surgical candidates for electrode implantation and permanent electrical stimulation of the auditory cortex, provided that the tinnitus is of recent origin and can be suppressed by TMS.

Is the root entry/exit zone important in microvascular compression syndromes?

OBJECTIVE Microvascular compression syndromes such as trigeminal neuralgia, hemifacial spasm, and disabling positional vertigo involve an artery or vein compressing a cranial nerve. A cranial nerve is composed of a central nervous system (CNS) segment and a peripheral nervous system (PNS) segment separated by the root entry/exit zone (REZ). Although vascular compression can occur at any point along the cranial nerve, it has been generally assumed that only vascular contact at the REZ of the affected cranial nerve can cause symptoms. On the basis of personal surgical experience, we propose that vascular compression of the CNS segment alone causes symptoms. This has important repercussions for the future diagnosis and treatment of microvascular compression syndromes, especially the cochleovestibular compression syndrome. METHODS For the anatomic study, four autopsy specimens and one surgical biopsy specimen of the vestibulocochlear nerve were microscopically and ultramicroscopically analyzed for structural differences between the CNS and PNS segments. For the clinical study, five patients with the clinical picture of cochleovestibular compression syndrome were treated by microsurgical decompression at the level of the CNS segment and not the REZ. One patient underwent reoperation for recurrent symptoms 4 years later, and a 4-mm vestibular neurectomy was performed at that stage. We performed an epidemiological analysis to demonstrate that the known incidences of trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia are related to the length of their respective CNS segments. RESULTS Histological differences between the PNS and CNS segments suggest that the PNS segment is more resistant to compression. This was confirmed by neurophysiological data from intraoperative monitoring in posterior fossa surgery and experimental studies. We found a clear epidemiological correlation between the length of the CNS segment, which differed among cranial nerves, and the incidence of the microvascular compression syndrome. Successful decompression of the CNS segment in patients without compression at the REZ of the vestibulocochlear nerve for disabling positional vertigo provides clinical support for this hypothesis. CONCLUSION The evidence we present supports the hypothesis that vascular compression syndromes arise from vascular contact along the CNS segment of the cranial nerves.

Impaired autoregulation of cerebral blood flow in an experimental model of traumatic brain injury.

In order to study the pathophysiology and the intracranial hemodynamics of traumatic brain injury, we have developed a modified closed-head injury model of impact-acceleration that expresses several features of severe head injury in humans, including acute and long-lasting intracranial hypertension, diffuse axonal injury, neuronal necrosis, bleeding, and edema. In view of the clinical relevance of impaired autoregulation of cerebral blood flow after traumatic brain injury, and aiming at further characterization of the model, we investigated the autoregulation efficiency 24 h after experimental closed-head injury. Cortical blood flow was continuously monitored with a laser-Doppler flowmeter, and the mean arterial blood pressure was progressively decreased by controlled hemorrhage. Relative laser-Doppler flow was plotted against the corresponding mean arterial blood pressure, and a two-line segmented model was applied to determine the break point and slopes of the autoregulation curves. The slope of the curve at the right hand of the break point was significantly increased in the closed head injury group (0.751 +/- 0.966%/mm Hg versus -0.104 +/- 0.425%/mm Hg,p = 0.028). The break point tended towards higher values in the closed head injury group (62.2 +/- 20.8 mm Hg versus 46.9 +/- 12.7 mm Hg; mean +/- SD, p = 0.198). It is concluded that cerebral autoregulation in this modified closed head injury model is impaired 24 h after traumatic brain injury. This finding, in addition to other characteristic features of severe head injury established earlier in this model, significantly contributes to its clinical relevance.

Brainstem hemorrhage in descending transtentorial herniation (Duret hemorrhage)

Objectives: To review clinical and radiological findings in patients with Duret hemorrhages and to discuss the pathophysiology and differential diagnosis of these lesions. Patients and methods: We reviewed the case records of four patients with Duret hemorrhages who had been admitted to the neurological intensive care unit with supratentorial mass lesions. Results: Descending transtentorial and subfalcine herniations were present in all cases. Three patients were admitted with acute subdural hematoma and one with intraparenchymal hemorrhage. Computed tomography revealed the presence of blood in the mesencephalon and upper pons. Three patients died; one survived with severe disabilities. Discussion: Duret hemorrhages are typically located in the ventral and paramedian aspects of the upper brainstem (mesencephalon and pons). The pathophysiology of Duret hemorrhage remains under debate: arterial origin (stretching and laceration of pontine perforating branches of the basilar artery), versus venous origin (thrombosis and venous infarction). Multifactorial causation seems likely. Conclusion: Duret hemorrhages are delayed, secondary brainstem hemorrhages. They occur in craniocerebral trauma victims with rapidly evolving descending transtentorial herniation. Diagnosis is made on computed tomography of the brain. In most cases the outcome is fatal. On the basis of our observations we believe that arterial hypertension and advanced age are risk factors for the development of Duret hemorrhage.

Functional anatomy of the human cochlear nerve and its role in microvascular decompressions for tinnitus.

OBJECTIVEThe functional anatomy (i.e., tonotopy) of the human cochlear nerve is unknown. A better understanding of the tonotopy of the central nervous system segment of the cochlear nerve and of the pathophysiology of tinnitus might help to ameliorate the disappointing results obtained with microvascular decompressions in patients with tinnitus. METHODSWe assume that vascular compression of the cochlear nerve can induce a frequency-specific form of hearing loss and that when the nerve is successfully decompressed, this hearing loss can recuperate. Thirty-one patients underwent a microvascular decompression of the vestibulocochlear nerve for vertigo or tinnitus. Preoperative audiograms were subtracted from postoperative audiograms, regardless of the surgical result with regard to the tinnitus and vertigo, because the hearing improvement could be the only sign of the vascular compression. The frequency of maximal improvement was then correlated to the site of vascular compression. A tonotopy of the cochlear nerve was thus obtained. RESULTSA total of 18 correlations can be made between the site of compression and postoperative maximal hearing improvement frequency when 5-dB hearing improvement is used as threshold, 13 when 10-dB improvement is used as threshold. A clear distribution can be seen, with clustering of low frequencies at the posterior and inferior side of the cochlear nerve, close to the brainstem, and close to the root exit zone of the facial nerve. High frequencies are distributed closer to the internal acoustic meatus and more superiorly along the posterior aspect of the cochlear nerve. CONCLUSIONThe tonotopic organization of the cisternal segment of the cochlear nerve has an oblique rotatory structure as a result of the rotatory course of the cochlear nerve in the posterior fossa. Knowledge of this tonotopic organization of the auditory nerve in its cisternal course might benefit surgeons who perform microvascular decompression operations for the vestibulocochlear compression syndrome, especially in the treatment of unilateral severe tinnitus.

The value of MRI in the diagnosis of postoperative spondylodiscitis

Abstract We evaluated the role of MRI in the diagnosis of postoperative spondylodiscitis. Spondylodiscitis is a serious complication of surgery, and the diagnosis frequently depends on a combination of clinical, laboratory and imaging findings. We compared the MRI findings in six patients with biopsy- or surgery-proven spondylodiscitis with those in 38 asymptomatic postoperative patients. Contrast enhancement and signal changes in the intervertebral disc or the vertebral endplates are not specific for spondylodiscitis, being also seen in the asymptomatic patients. However, absence of Modic type 1 changes, of contrast enhancement of the disc or of enhancing paravertebral soft tissues suggests that the patient does not have spondylodiscitis. MRI appears more useful for exclusion than for confirmation of postoperative spondylodiscitis.

Continuous measurement of intracranial pressure in awake rats after experimental closed head injury

The present study validates a method for continuous measurement of intracranial pressure (ICP) in freely moving rats after experimental induction of impact-acceleration injury. Rats subjected to either mild or moderate trauma were individually placed in a Bas-Ratturn system, equipped with a sensor that synchronously turns the cage in response to the locomotor activity of the animal. In this way correct probe positioning is permanently assured and damage due to coiling is avoided. The evolution of ICP and mean arterial blood pressure (MABP) in injured rats was compared with that of a non-traumatized sham group. Since the animals regained consciousness after surgery, interference of anaesthesia on these sensitive parameters should be minimised. The results showed that immediately after induction of neurotrauma, ICP was significantly higher in traumatized rats (sham: 7.7 +/- 0.5 mmHg; mild trauma: 10.4 +/- 0.7 mmHg; moderate trauma: 14.9 +/- 2.4 mmHg; P<0.05). Regression analysis showed a stable ICP up to 3 h post-insult for all three conditions. From 4 h onwards till the end of the experiment at 10 h post-insult, a significant increase in ICP was seen for sham-operated and mildly traumatized rats (16.1 +/- 3.4 and 30.5 +/- 6.9 mmHg, respectively; P<0.05), but not for moderately traumatized rats (47.3 +/- 11.9 mmHg). The method allows observation of ICP for a critical period up to 3 h. As such the method can be regarded as clinically relevant to study early pathological aspects of intracranial hypertension and to define a therapeutic window for pharmacological intervention after traumatic brain injury (TBI).

The Association of Meningioma and Pituitary Adenoma: Report of Seven Cases and Review of the Literature

Seven patients with the co-occurrence of meningioma and pituitary adenoma are reported. Diagnosis was based on histological examination and if not available on MR imaging. Extensive review of the literature reveals only 18 other cases with this association if meningiomas appearing after radiation therapy for pituitary tumors are excluded. As in isolated meningiomas, the female-to-male ratio is high. A preponderance of perisellar meningiomas is apparent. Another distinct characteristic of this combination is not revealed, since no specific typing of the meningioma and no specific endocrine syndrome is uncovered. Two patients presented with multiple meningiomas, of which one showed two histologically different tumor types. The presence of other tumors in association with pituitary adenomas and meningiomas in our series is striking and could suggest a genetic dysregulation leading to the development of these tumors.