Cortical hyperexcitability has been found in early Amyotrophic Lateral Sclerosis (ALS) and is hypothesized to be a key factor in pathogenesis. The current pilot study aimed to investigate cortical inhibitory/excitatory balance in ALS using short-echo Magnetic Resonance Spectroscopy (MRS). Patients suffering from ALS were scanned on a 3 T Trio Siemens MR scanner using Spin Echo Full Intensity Acquired Localized (SPECIAL) Magnetic Resonance Spectroscopy in primary motor cortex and the occipital lobe. Data was compared to a group of healthy subjects. Nine patients completed the scan. MRS data was of an excellent quality allowing for quantification of a range of metabolites of interest in ALS. In motor cortex, patients had Glutamate/GABA and GABA/Cr- ratios comparable to healthy subjects. However, Glutamate/Cr (p = 0.002) and the neuronal marker N-acetyl-aspartate (NAA/Cr) (p = 0.034) were low, possibly due to grey-matter atrophy, whereas Glutathione/Cr (p = 0.04) was elevated. In patients, NAA levels correlated significantly with both hand strength (p = 0.027) and disease severity (p = 0.016). In summary SPECIAL MRS at 3 T allows of reliable quantification of a range of metabolites of interest in ALS, including both excitatory and inhibitory neurotransmitters. The method is a promising new technique as a biomarker for future studies on ALS pathophysiology and monitoring of disease progression.

ObjectiveThe aim of this cross-sectional study was to investigate the cortical metabolite concentrations in patients suffering from migraine with aura (MWA). We hypothesized that occipital γ-aminobutyric acid (GABA) levels are lower in MWA patients.BackgroundRecent studies have indicated that a disturbance in the inhibitory GABA is involved in triggering the migraine aura. We aimed to explore this using a novel magnetic resonance spectroscopy sequence.MethodsUsing spin echo full intensity acquired localized spectroscopy on a Siemens 3 Tesla magnetic resonance scanner, we obtained occipital and parietal metabolite concentrations in 14 patients suffering from migraine with aura and a group of 16 matched healthy subjects.All scans were performed at Aarhus University Hospital, at the Center for Functionally Integrative Neuroscience (CFIN).ResultsNo difference was found in GABA/(Total creatine) levels in either the occipital cortex (p = 0.744) or in the somatosensory cortex (p = 0.305).ConclusionThese findings indicate that cortical GABA levels are normal in patients suffering from relatively few migraine attacks. Previous studies have reported that cortical GABA in patients with more frequent migraines is reduced; further investigation of the inhibitory system in migraine patients is warranted to determine the underlying mechanisms.

Transient ischemic attack (TIA) is an ischemic episode of neurologic dysfunction characterized by a spontaneous clinical resolution of symptoms within 24 hours. Mechanisms of this remarkable recovery are not yet well understood. In patients with permanent brain injury caused by a stroke cortical levels of γ-Aminobutyric acid (GABA) are decreased. In this study, we aimed to investigate, whether similar alterations of cortical GABA are also present in patients with TIA. Ten first-time TIA patients with temporary unilateral motor symptoms from upper limb and 10 control subjects underwent Magnetic Resonance Spectroscopy (MRS) with SPECIAL technique. GABA:creatine (GABA:CR) ratios were measured in the hand area of the primary motor cortex in both hemispheres. GABA:CR ratios were significantly lower in the symptomatic hemisphere of TIA patients when compared with healthy subjects. Whether reduced GABA is induced directly by transient ischemia or is a secondary compensatory mechanism, which facilitate re-establishment of normal function remains to be elucidated. Further research investigating our findings in larger samples will aid in understanding of the clinical significance of GABA alterations in TIA patients. GABA MRS may provide vital information about mechanisms involved in recovery after transient ischemia, which may have crucial importance for development of new neuroprotective strategies in stroke.

Background: Movement related cortical beta (13-30 Hz) modulation is fundamental in the preparation and execution of movement. This oscillatory modulation is altered in amyotrophic lateral sclerosis (ALS) during active movement, with reports of both decreased and increased beta band power. These beta band changes have never been examined in a proprioceptive paradigm in ALS. Methods: Using magnetoencephalography (MEG) we examined 11 ALS patients and 12 healthy participants. We recorded beta band activity during a session of active movement of the dominant hand index finger, using a visual cue. We also recorded activity during a passive movement of the same finger using a MEG compatible pneumatically activated device. All ALS patients underwent a clinical examination including an estimation of the muscle strength of the arm used for the experiment. Results: Using an analysis of variance (ANOVA), we find that movement related beta band power is modified by ALS and the amplitude of beta power is decreased, both for the active and passive movements. We also find that the beta band power modulation depends on the muscle strength of the arm used, with movement related power amplitude being decrease in patients with arm weakness. This was observed for both active and passive movement. Conclusion: ALS patients show decreased movement related beta band amplitude compared to the healthy control group. The decrease seems to depend on disease severity. These results show that ALS affects the motor outputs and sensory inputs of the sensorimotor cortex and that the modulation differs depending on disease severity. Severity dependent modulation of beta power could be related to disturbance in excitatory/inhibitory intracortical circuitry.