Jens O. Heidenreich

MEG/EEG sources of the 170-ms response to faces are co-localized in the fusiform gyrus.

The 170-ms electrophysiological processing stage (N170 in EEG, M170 in MEG) is considered an important computational step in face processing. Hence its neuronal sources have been modelled in several studies. The current study aimed to specify the relation of the dipolar sources underlying N170 and M170. Whole head EEG and MEG were measured simultaneously during the presentation of unfamiliar faces. An Independent Component Analysis (ICA) was applied to the data prior to localization. N170 and M170 were then modelled with a pair of dipoles in a four-shell ellipse (EEG)/homogeneous sphere (MEG) arranged symmetrically across midline. The dipole locations were projected onto the individual structural MR brain images. Dipoles were localized in fusiform gyri in ten out of eleven individuals for EEG and in seven out of eleven for MEG. N170 and M170 were co-localized in the fusiform gyrus in six individuals. The ICA shifted some of the single-subject dipoles up from cerebellum to fusiform gyrus mainly due to the removal of cardiac activity. The group mean dipole locations were also found in posterior fusiform gyri, and did not differ significantly between EEG and MEG. The result was replicated in a repeated measurement 3 months later.

Reduced NAA in the thalamus and altered membrane and glial metabolism in schizophrenic patients detected by 1H-MRS and tissue segmentation.

Functional and structural abnormalities in the thalamus as well as a generalized phospholipid membrane disorder have been implicated in the pathogenesis of schizophrenic psychosis. To determine whether thalamic neuronal abnormalities and altered membrane-associated metabolites can be detected in schizophrenic patients, we used in vivo proton magnetic resonance spectroscopy (1H-MRS) in 32 acutely-ill, medicated schizophrenic patients and 17 age-matched controls. Thalamic and white matter metabolite concentrations (myo-inositol (mI), choline-containing compounds (Cho), total creatine (Cr) and N-acetylaspartate (NAA)) were estimated and corrected for atrophy (CSF) and gray and white matter contributions (GM, WM) by use of image-based voxel segmentation. Thalamic NAA was significantly reduced in schizophrenic patients, whereas Cho and mI were significantly increased in the parietal white matter. White matter Cr was significantly elevated in patients and correlated positively with the brief psychiatric rating scores (BPRS). Regional metabolite levels were inversely associated with GM and WM content reaching significance for mI and Cr in the thalamus and Cho and NAA in the white matter. Reduced NAA in the left thalamus of schizophrenic patients confirms and extends previous spectroscopic data and agrees well with histologic and imaging findings of reduced neuronal density and volume. Elevated Cho in line with 31P-MRS studies suggests increased myelin degradation thus further supporting a generalized membrane disorder in schizophrenic patients. In addition, we demonstrate the need to correct metabolite concentrations for regional tissue composition in studies employing patients with altered brain morphology.

Glutamate as a spectroscopic marker of hippocampal structural plasticity is elevated in long-term euthymic bipolar patients on chronic lithium therapy and correlates inversely with diurnal cortisol.

While an excess of glucocorticoids is associated with hippocampal pathology in mood disorders, lithium exerts robust neuroprotective and neurotrophic effects. Here, 21 stably remitted bipolar I patients who had been on chronic lithium maintenance therapy, on average, for more than a decade, and 19 carefully matched healthy controls were studied using 3 T 1H-magnetic resonance spectroscopy of left and right hippocampus. Salivary cortisol samples were obtained to assess activity of the hypothalamus–pituitary–adrenal system. Absolute concentrations of N-acetylaspartate (NAA), choline-containing compounds and total creatine were similar in euthymic bipolar patients and healthy controls. Hippocampal glutamate concentrations were significantly increased as an effect of patient status (patients>controls) and laterality (left hippocampus>right hippocampus). Hippocampal glutamate content (Glu) was strongly correlated with NAA. Across groups and within the patient group, diurnal saliva cortisol levels showed a significant inverse relationship with both Glu and NAA. Taken together, these results add to the concept of bipolar disorder as an illness involving disturbed hippocampal structural plasticity under the opposing influences of lithium and glucocorticoids.

Clinical evaluation of a new intracranial pressure monitoring device.

Summary. Background: Continuous monitoring of intracranial pressure (ICP) still plays a key role in the management of patients at risk from intracranial hypertension. Numerous ICP-measuring devices are available. The aim of the present study was to investigate the clinical characteristics and the magnetic resonance imaging (MRI) compatibility of the recently developed Neurovent-P® (REHAU AG+CO, REHAU, Germany) ICP monitoring device. Method: In a prospective two-center study, a total of 98 patients with severe head injury, subarachnoid haemorrhage, intracerebral haemorrhage, and non-traumatic brain edema underwent intraparenchymal monitoring of ICP using the Neurovent-P®. A control group comprising 50 patients underwent implantation of the Camino®-OLM-110-4B ICP monitor. The zero drift of the probes was determined before and after the ICP recording period. Technical and medical complications were documented. The MRI compatibility of the Neurovent-P® ICP probe was investigated by evaluating artifacts caused by the probe, probe function and temperature changes during MRI, and probe movement caused by the magnetic field. Findings: The mean zero drift was 0.2±0.41 mmHg (maximum 3 mmHg) for the Neurovent-P® ICP probes and 0.4±0.57 mmHg (maximum 12 mmHg) for the Camino®-OLM-110-4B ICP probes. No significant correlation was identified between the extent of zero drift following the removal of the probes and the length of monitoring. Intraparenchymal haemorrhage spatially related to the probe occurred in 1 out of 50 (2%) patients with a Camino®-OLM-110-4B probe and in 1 out of 98 (1%) with a Neurovent-P®. Damage of the probe due to kinking or overextension of the cable or glass fiber occurred in 4 of the 50 (8%) Camino®-OLM-110-4B ICP probes and in 5 of the 98 (5%) Neurovent-P® probes. On T2-weighted MR images, the Neurovent-P® ICP probe induced only small artifacts with very good discrimination of the surrounding tissue. On T1-weighted MR images, there was a good imaging quality but artifact-related local disturbances in signal occurred. There was no temperature change in the Neurovent-P® probe and in the surrounding brain tissue during MR imaging. Interpretation: The Neurovent-P® ICP measuring system is a safe and reliable tool for ICP monitoring. Handling of the Neurovent-P® system is safe when performed properly.

Assessment of 3D-TOF-MRA at 3.0 tesla in the characterization of the angioarchitecture of cerebral arteriovenous malformations: a preliminary study:

Background: The characterization of brain arteriovenous malformation (AVM) angioarchitecture remains rewarding in planning and predicting therapy. The increased signal-to-noise ratio at higher field strength has been found advantageous in vascular brain pathologies. Purpose: To evaluate whether 3.0T time-of-flight (TOF) magnetic resonance angiography (MRA) is superior to 1.5T TOF-MRA for the characterization of cerebral AVMs. Material and Methods: Fifteen patients with AVM underwent TOF-MRA at 3.0T and 1.5T and catheter angiography (DSA), which was used as the gold standard. Blinded readers scored image quality on a four-point scale, nidus size, and number of feeding arteries and draining veins. Results: Image quality of TOF-MRA at 3.0T was superior to 1.5T but still inferior to DSA. Evaluation of nidus size was equally good at 3.0T and 1.5T for all AVMs. In small AVMs, however, there was a tendency of size overestimation at 3.0T. MRA at 3.0T had increased detection rates for feeding arteries (+21%) and superficial (+13%) and deep draining veins (+33%) over 1.5T MRA. Conclusion: 3.0T TOF-MRA offers superior characterization of AVM angioarchitecture compared with 1.5T TOF-MRA. The image quality of MRA at both 3.0 and 1.5T is still far from equal to DSA, which remains the gold standard for characterization of AVM.

Magnetic resonance imaging results can affect therapy decisions in hyperacute stroke care

Background: Despite some limitations, a perfusion/diffusion mismatch can provide a working estimate of the ischemic penumbra in hyperacute stroke and has successfully been used to triage patients. Purpose: To evaluate whether the addition of magnetic resonance imaging (MRI) to clinical and non-contrast computed tomography (CT) data alters diagnosis and choice of therapy. Material and Methods: We retrospectively analyzed clinical records, and CT and MRI data fully available in 97 of 117 patients. Upon clinical examination and CT, a diagnosis and treatment path was scored and compared to treatment path after addition of MRI data. The MRI protocol included T2-weighted images, diffusion-weighted images (DWI), and perfusion-weighted images (PWI), and MR angiography (MRA). Results: MRI data were acquired in less than 15 min. In 20 of 97 patients (21%), the diagnosis changed after MRI. In 25 of 97 patients (26%), the presumptive treatment plan was changed after MRI evaluation. Thirteen patients had their treatment changed from thrombolytic to nonthrombolytic therapy. Three patients were changed from nonthrombolytic to intraarterial (IA) thrombolysis. In one patient, treatment was changed from intravenous (IV) to IA thrombolysis, and in five patients it was changed from IA to IV thrombolysis. In two patients, systemic heparin was added to antiplatelet therapy. Conclusion: The expansion of the acute stroke protocol to include MRI altered the therapy plan in 26% of our patients. The utility of MRI, shown here to improve patient stratification into best-treatment options, demonstrates the value of using MRI to optimize care in hyperacute stroke patients.

Injection therapy of lumbar facet syndrome: a prospective study

SummaryBackground. Chronic low back pain remains a major health problem. Facet joint injection therapy is an easy to perform therapeutic option. However, few prospective studies use a standardized protocol to investigate injection therapy. The aim of our study was to evaluate quantity and duration of clinical improvement after this protocol, and to identify the best time for additional repetitive injection therapy.Materials and Methods. Thirty-nine patients (21 men, 18 women; mean age 55.2 years [range, 29–87 years]) with lumbar facet syndrome were treated with injection using a standardized protocol (prednisolone acetate, lidocaine 1%, phenol 5%) under fluoroscopic control. Follow-up was based on a specially designed questionnaire. Analysis included MacNab criteria, visual analogue scale, and pain disability index.Results. Reduction of pain was found up to 6 months after treatment. The outcome was assessed excellent or good by 62% (24 patients) of the patients after 1 month, by 41% (16 patients) after 3 months, and by 36% (14 patients) after 6 months. There was no influence of age, body mass index, or previous lumbar spinal surgery on improvement after treatment. There were no severe side effects. Short-lasting self limiting mild side effects were found in 26% (increased back pain, numbness, heartburn, headache, allergy).Conclusion. Facet joint injection therapy using a standardized protocol is safe, effective, and easy to perform. The clinical effect is limited, and we recommend repetitive injection according to this protocol after 3 months.

Chronic Progressive External Ophthalmoplegia: MR Spectroscopy and MR Diffusion Studies in the Brain

OBJECTIVE The purpose of our study was to show how, despite pathognomonic signs of cerebral involvement in chronic progressive external ophthalmoplegia (CPEO), mitochondrial respiratory chain insufficiency is associated with increased lactate and reduced N-acetylaspartate. CPEO and mitochondrial myopathy are caused by mitochondrial DNA mutations leading to impaired oxidative phosphorylation. Cortical and subcortical metabolites, cerebral diffusivity, and structural MRI were assessed to characterize possible subclinical cerebral pathology in CPEO. SUBJECTS AND METHODS Ten patients with CPEO (n = 8), mitochondrial myopathy (n = 1), and Kearns-Sayre syndrome (n = 1) and 13 control group volunteers were studied by MRI, both long TE (144) proton MR spectroscopic imaging (1H MRSI), and diffusion-weighted imaging. Relative concentrations of N-acetylaspartate, choline, creatine, and lactate were estimated by Linear Combination of Model Spectra (LCModel) in healthy-appearing white matter, gray matter, and white matter hyperintensities. RESULTS Of five patients with cortical atrophy, it was moderate in three and severe in two. One patient had severe and four had moderate cerebellar atrophy. Six of 10 patients showed unspecific white matter lesions, whereas the remainder had hyperintensities in the pyramidal tract (n =2) and middle cerebellar peduncle (n = 1) despite clinical signs. No basal ganglia lesions were found. Physiologic metabolite ratios were normal and lactate was absent in supratentorial healthy-appearing cortex and subcortical white matter. Global diffusion histogram metrics revealed no abnormalities. CONCLUSION Normal spectroscopic imaging in radiologic unaffected brain and healthy global brain parenchymal diffusion findings do not support the hypothesis of a generalized cerebral energy loss in CPEO. Bilateral structural alteration of central motor pathways in two patients without clinical pyramidal signs may, however, reflect subclinical axonal injury in predilection sites in some patients.

Adult Presentation of PHACES Syndrome

A significant percentage of children with hemangiomas may have PHACES syndrome which refers to the association of posterior fossa malformations, facial hemangiomas, arterial cerebrovascular abnormalities, cardiovascular anomalies, eye abnormalities and ventral defects like sternal clefting or supraumbilical raphe. A variety of factors have led to under diagnosis of PHACES syndrome in the past including lack of awareness and limited imaging modalities. Also, patients with PHACES syndrome with arterial cerebrovascular abnormalities can present with acute ischemic stroke. However, these patients usually present before one year of age. We describe a 29-year-old woman with no history of cerebrovascular disease who initially presented with symptoms of a stroke and was subsequently diagnosed to have PHACES syndrome exhibiting an array of multiple unusual imaging findings. We also discuss the current literature and recommendations about PHACES syndrome.

Perfusion imaging of cerebral arteriovenous malformations: a study comparing quantitative continuous arterial spin labeling and dynamic contrast-enhanced magnetic resonance imaging at 3 T.

Assessment of hemodynamics in arteriovenous malformations (AVMs) is important for estimating the risk of bleeding as well as planning and monitoring therapy. In tissues with perfusion values significantly higher than cerebral cortex, continuous arterial spin labeling (CASL) permits both adequate representation and quantification of perfusion. Thirteen patients who had cerebral AVMs were examined with two magnetic resonance imaging (MRI) techniques: perfusion imaging using a CASL technique with two delay times, 800 and 1200 ms, and T(2)-weighted dynamic contrast-enhanced MRI (T(2)-DCE-MRI). The signal-to-noise ratio obtained in our study with the CASL technique at 3 T was sufficient to estimate perfusion in gray matter. Both nidal and venous perfusion turned out larger by factors of 1.71±2.01 and 2.48±1.51 in comparison to T(2)-DCE-MRI when using CASL at delay times of 800 and 1200 ms, respectively. Moreover, the venous and nidal perfusion values of the AVMs measured at T(2)-DCE-MRI did not correlate with those observed at CASL. Evaluation of average perfusion values yielded significantly different results when using a shorter versus a longer delay time. Average gray matter perfusion was 15.8% larger when measured at delay times of w=800 ms versus w=1200 ms, while nidal perfusion was 15.7% larger and venous perfusion was 34.6% larger, respectively. In conclusion, the extremely high perfusion within an AVM could be successfully quantified using CASL. A shorter postlabeling delay time of w=800 ms seems to be more appropriate than a longer time of w=1200 ms because of possible inflow of unlabeled spins at the latter.