F. Gerstenbrand

Mild Traumatic Brain Injury

Traumatic brain injury (TBI) is one among the most frequent neurological disorders. Of all TBIs 90% are considered mild with an annual incidence of 100–300/100 000. Intracranial complications of mild traumatic brain injury (MTBI) are infrequent (10%), requiring neurosurgical intervention in a minority of cases (1%), but potentially life threatening (case fatality rate 0.1%). Hence, a true health management problem exists because of the need to exclude the small chance of a life‐threatening complication in a large number of individual patients. The 2002 EFNS guideline used the best evidence approach based on the literature until 2001 to guide initial management with respect to indications for computed tomography (CT), hospital admission, observation and follow‐up of MTBI patients. This updated EFNS guideline for initial management in MTBI proposes a more selective strategy for CT when major [dangerous mechanism, Glasgow Coma Scale (GCS) < 15, 2 points deterioration on the GCS, clinical signs of (basal) skull fracture, vomiting, anticoagulation therapy, post‐traumatic seizure] or minor (age, loss of consciousness, persistent anterograde amnesia, focal deficit, skull contusion, deterioration on the GCS) risk factors are present based on published decision rules with a high level of evidence. In addition, clinical decision rules for CT now exist for children as well. Since 2001, recommendations, although with a lower level of evidence, have been published for clinical observation in hospitals to prevent and treat other potential threats to the patient including behavioural disturbances (amnesia, confusion and agitation) and infection.

EFNS guideline on mild traumatic brain injury: report of an EFNS task force.

In 1999, a Task Force on Mild Traumatic Brain Injury (MTBI) was set up under the auspices of the European Federation of Neurological Societies. Its aim was to propose an acceptable uniform nomenclature for MTBI and definition of MTBI, and to develop a set of rules to guide initial management with respect to ancillary investigations, hospital admission, observation and follow‐up.

Human brain structures related to plantar vibrotactile stimulation: a functional magnetic resonance imaging study.

The purpose of this study was to investigate the sensorimotor cortex response to plantar vibrotactile stimulation using a newly developed MRI compatible vibration device. Ten healthy subjects (20-45 years) were investigated. Vibrotactile stimulation of the sole of the foot with a frequency of 50 Hz and a displacement of 1 mm was performed during fMRI (echo-planar imaging sequence at 1.5 T) using an MRI compatible moving magnet actuator that is able to produce vibration frequencies between 0 and 100 Hz and displacement amplitudes between 0 and 4 mm. The fMRI measurement during vibrotactile stimulation of the right foot revealed brain activation contralaterally within the primary sensorimotor cortex, bilaterally within the secondary somatosensory cortex, bilaterally within the superior temporal, inferior parietal, and posterior insular region, bilaterally within the anterior and posterior cingular gyrus, bilaterally within the thalamus and caudate nucleus, contralaterally within the lentiform nucleus, and bilaterally within the anterior and posterior cerebellar lobe. The advantages of the new MRI compatible vibration device include effective transmission of the stimulus and controlled vibration amplitudes, frequencies, and intensities. The results indicate that plantar vibration can be a suitable paradigm to observe activation within the sensorimotor network in fMRI. Furthermore, the method may be used to determine the optimal responsiveness of the individual sensorimotor network.

Mild traumatic brain injury

In 1997, the Brain Injury Association defined traumatic brain injury (TBI) as an insult to the brain which is not of a degenerative or congenital nature but caused by external physical force [1]. After this definition, brain injury may produce a disturbance of consciousness resulting in an impairment of cognitive abilities or physical functions, but can result in a disturbance of behaviour or emotional functioning. The disorders may be temporary or permanent and may cause partial or total functional disability or psychosocial maladjustment. The American Brain Injury Association recommends a classification into three degrees of TBI, mild, moderate, and severe [2]. Frowein [3] proposed, in addition, s̀everest’ as a fourth category. Generally, one must differentiate between open and closed brain injury. Traumatic brain damage is caused by an impact on the head. The localization and the severity of the traumatic brain lesion depends on the direction, the intensity of the acting force and on the mobility of the head during the impact, with possibilities of defence movements. For the documentation of the acting force on the head, the impact scheme after SPATZ, adapted to the INNSBRUCK scheme [4], is useful. A blunt impact on the head causes a certain pattern of brain lesions in connection with acting forces and the position of the head. Neuro-pathological findings and the documentation of clinical data allow one to differentiate between three types of TBI, the linear outer TBI [4], with four subgroups depending on the direction of the impact (Type I occipital, Type II frontal, Types III and IV lateral, and with more intensive damage at the contre-coup area) in the brain tissue, the linear inner TBI with the inner upper brain trauma (lesions around the lateral ventriclesÐ butterfly lesions) [5], the lower inner brain trauma (lesions mainly in the upper brain stem) [6], and the rotational brain trauma (intraand extracerebral heamatomas, dilacerations of brain tissue) [7]. The neuropathological findings are fully confirmed by examinations with MRI [5, 6]. For mild brain trauma in the international literature, different terms are found [2]Ð minor head injury, mild head injury, traumatic head syndrome, post-brain injury syndrome, mild concussion syndrome, post-concussional syndrome, traumatic cephalgia, post-traumatic syndrome. In the continental European

Variability of BOLD response evoked by foot vibrotactile stimulation: influence of vibration amplitude and stimulus waveform.

The aim of the present was study to evaluate cortical and subcortical neural responses on vibrotactile stimulation of the food and to assess somatosensory evoked BOLD responses in dependence of vibration amplitude and stimulus waveform. Sixteen healthy male subjects received vibrotactile stimulation at the sole of the right foot. The vibration stimulus was delivered through a moving magnet actuator system (MMAS). In an event-related design, a series of vibration stimuli with a duration of 1 s and a variable interstimulus interval was presented. Four stimulation conditions were realized using a 2 (amplitudes 0.4 mm or 1.6 mm) x 2 (waveform sinusoidal or amplitude modulated) factorial design. Stimulating with 0.4 mm amplitude compared to 1.6 mm stimulus amplitude more strongly activated the pre- and postcentral gyrus bilaterally and the right inferior, medial and middle frontal gyrus. In the reverse comparison significant differences were observed within the left inferior parietal lobule, the left superior temporal gyrus, and the left temporal transverse gyrus. In the comparison of sinusoidal versus modulated waveform and vice versa no significant activation differences were obtained. The inter-subject variability was high but when all four stimulation conditions were jointly analyzed, a significant activation of S1 was obtained for every single subject. This study demonstrated that the BOLD response is modulated by the amplitude but not by the waveform of vibrotactile stimulation. Despite high inter-individual variability, the stimulation yielded reliable results for S1 on the single-subject level. Therefore, our results suggest that vibrotactile testing could evolve into a clinical tool in functional neuroimaging.

Contact force- and amplitude-controllable vibrating probe for somatosensory mapping of plantar afferences with fMRI

To study cerebral responses evoked from mechanoreceptors in the human foot sole using a computer‐controlled vibrotactile stimulation system.

Somatosensory Stimulation in Functional Neuroimaging: A Review

Functional brain imaging of the somatosensory system has evolved over the past two decades and it has become an important tool in the preoperative planning in neurosurgery, in the monitoring in neurorehabilitation and for the understanding of motor recovery after brain damage for the planning and optimization of neurorehabilitation strategies. Mapping of movement related cortical areas and areas that are related to body sensation was initially performed during neurosurgical procedures using direct cortical stimulation (Penfield, 1937). Several functional brain mapping techniques have subsequently evolved (Toga and Mazziotta, 2002). The era of functional brain imaging began in the 1980s with the implementation of the Positron Emission Tomography (PET) which provided a measure of the regional cerebral blood flow. Since the 1990s functional brain imaging is dominated by the rise of functional magnetic resonance imaging (fMRI) based on the blood oxygenation level dependant (BOLD) effect that was discovered 1990 by Ogawa et al. (Ogawa et al., 1990;Ogawa et al., 1992). Subsequently continuous evolution and progress of fMRI as well as its increasing popularity and spreading clinical use as a highly sensitive diagnostic neuroimaging instrument suitable for the assessment of a large variety of neurological and neurosurgical indications made fMRI to the leading functional neuroimaging modality. In this chapter we review somatosensory stimulation in PET and fMRI during the past decades, their advantages and disadvantages, optimal stimulation protocols as well as corresponding brain maps of different approaches of somatosensory stimulation in functional brain imaging and their clinical and neurophysilogical applications.

Association of ganglioneuroblastoma with syringomyelia

The association of a syndrome of a degenerative nature such as syringomyelia and a neuroblastoma can be of clinical interest. We will describe the case of a young female suffering from a retroperitoneal neuroblastoma and secondary development of syringomyelia. The possible pathogenetic link between these two pathologies will be discussed. Firstly, the dysontogenetic interpretation will be underlined. Other hypotheses will concentrate on the presence of tumors within the cord, which tend to cavitate, and furthermore, on the association between the edema and some diseases such as neoplasma, traumas, and on arachnoiditis as a major pathogenetic factor in syringomyelia. The existence of a possible link between arachnoiditis and the radiotherapy received by the patient after the surgical excision of the retroperitoneal neuroblastoma, will be discussed. Lastly a further pathogenetic hypothesis will be pointed out: an intramedullary softening due to disturbed blood supply, caused by the extramedullary neoplasm.

Functional magnetic resonance imaging under anaesthesia of a patient with severe chronic disorders of consciousness

CLINICAL CASE We report on a 19-year old male patient who is recovering from near-drowning. The patient was admitted for re-evaluation in a Minimally Conscious State. METHOD A regular functional Magnetic Resonance Imaging was not possible due to complex motor tics of the patient with sudden flexion and extension movements of arms and legs as well as opisthotonic retroflexion of the head and trunk. Thus, the patient was anaesthetised and functional Magnetic Resonance Imaging was performed under general anaesthesia which was introduced and maintained with Sevoflorane and Fentanyl provided analgesia. Four functional runs were performed and the patients responses were recorded. During each one of these runs one extremity (dorsum manus or pedis) was stimulated with a brush with an operator-paced frequency of about 2 Hz. RESULTS AND CONCLUSION Clear responses were found in the somatosensory cortex contra lateral within the post central gyrus during stimulation of the left hand. Considering the other three extremities no significant responses were found. Nevertheless, we conclude that a functional Magnetic Resonance Imaging under anaesthesia is possible for patients with severe chronic disorders of consciousness and brain areas responding to stimuli can be detected.

Correspondence (letter to the editor): Additions

The diagnosis and differential diagnosis of (persistent) vegetative state, (P)VS, requires special expertise and experience (1). Recently, the term (P)VS has been substituted by the medical term Unresponsive Wakefulness Syndrome (UWS), as correctly mentioned by the authors (2). Our aim should be to reduce the unacceptably high rate of misdiagnosis in patients with (P)VS (37–43%) by improving quality management. One can only agree with the statement that above all the diagnosis of VS (UWS) is based on a qualified and standardized clinical neurological examination. Semantically, VS (UWS) and minimally conscious state (MCS) denote two functional transitory syndromes which can be clearly differentiated based on clinical findings. The reliability and validity of the German Coma Remission Scale (KRS) in identifying coma, PVS and MCS in early neurological rehabilitation has convinced specialists, health insurers and politicians (German Social Insurance Code (SGB) IX). With regard to the studies analyzed in the article, we had wished for a more adequate critical discussion on the evaluation and evidence of the way the respective neurological examination procedures were applied and what this meant for the rate of misdiagnosis. Have our recommendations of the European VS guidelines been followed in those studies (1)? Our recommendations have not been discussed in the review (2). Evidence-based, bed-side examination techniques were not mentioned. We recommended a 3-year further training program in a specialized department for VS patients. This qualification has been shown to provide medical-neurological expertise and to reduce the rate of misdiagnosis of VS by precisely allocating the typical symptoms observed with this transitory functional syndrome to the correct diagnosis. Supplementary tables on etiology, the clinical picture of full-blown VS (UWS) and clinical dynamics during the stages of regression are missing (3); these have been compiled with modifications in our guidelines (1) and continue to be valid. In UWS and MCS, not only neurotraumatologists are especially interested in the prognostic relevance of the cause, location and extent of the underlying brain damage and its functional changes over time, apart from patient age. Additional information about functional imaging is provided by Zakharova et al. (4).