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K Hamandi

Publications and source records attributed to K Hamandi.

5 recordsLinked to original sources

Modelling cardiac signal as a confound in EEG-fMRI and its application in focal epilepsy studies.

Cardiac noise has been shown to reduce the sensitivity of functional Magnetic Resonance Imaging (fMRI) to an experimental effect due to its confounding presence in the blood oxygenation level-dependent (BOLD) signal. Its effect is most severe in particular regions of the brain and a method is yet to take it into account in routine fMRI analysis. This paper reports the development of a general and robust technique to improve the reliability of EEG-fMRI studies to BOLD signal correlated with interictal epileptiform discharges (IEDs). In these studies, ECG is routinely recorded, enabling cardiac effects to be modelled, as effects of no interest. Our model is based on an over-complete basis set covering a linear relationship between cardiac-related MR signal and the phase of the cardiac cycle or time after pulse (TAP). This method showed that, on average, 24.6 +/- 10.9% of grey matter voxels contained significant cardiac effects and 22.3 +/- 24.1% of those voxels exhibiting significantly IED-correlated BOLD signal also contained significant cardiac effects. We quantified the improvement of the TAP model over the original model, without cardiac effects, by evaluating changes in efficiency, with respect to estimating the contrast of the effects of interest. Over voxels containing significant, cardiac-related signal, efficiency was improved by 18.5 +/- 4.8%. Over the remaining voxels, no improvement was demonstrated. This suggests that, while improving sensitivity in particular regions of the brain, there is no risk that the TAP model will reduce sensitivity elsewhere.

Electroencephalography↗

fMRI temporal clustering analysis in patients with frequent interictal epileptiform discharges: comparison with EEG-driven analysis.

Temporal clustering analysis (TCA) is an exploratory data-driven technique that has been proposed for the analysis of resting fMRI to localise epileptiform activity without need for simultaneous EEG. Conventionally, fMRI of epileptic activity has been limited to those patients with subtle clinical events or frequent interictal epileptiform EEG discharges, requiring simultaneous EEG recording, from which a linear model is derived to make valid statistical inferences from the fMRI data. We sought to evaluate TCA by comparing the results with those of EEG correlated fMRI in eight selected cases. Cases were selected with clear epileptogenic localisation or lateralisation on the basis of concordant EEG and structural MRI findings, in addition to concordant activations seen on EEG-derived fMRI analyses. In three, areas of activation were seen with TCA but none corresponding to the electro-clinical localisation or activations obtained with EEG driven analysis. Temporal clusters were closely coincident with times of maximal head motion. We feel this is a serious confound to this approach and recommend that interpretation of TCA that does not address motion and physiological noise be treated with caution. New techniques to localise epileptogenic activity with fMRI alone require validation with an appropriate independent measure. In the investigation of interictal epileptiform activity, this is best done with simultaneous EEG recording.

Cluster Analysis↗

Irreversible damage to the spinal cord following spinal anesthesia.

The authors report five patients with damage to the distal spinal cord following spinal anesthesia. The patients developed leg weakness and sensory disturbance. MRI of the lumbosacral spine showed an abnormal area of high signal within the conus medullaris in all patients. Symptoms and signs persisted at 1- to 2.5-year follow-ups. Incorrect needle placement and type of needle used are possible factors leading to spinal cord injury.

Adult↗

Screening for the beta-amyloid precursor protein mutation (APP717: Val----Ile) in extended pedigrees with early onset Alzheimer's disease.

Screening for the APP717 mutation in 5 further families with early onset Alzheimer's disease failed to reveal further cases with this variant. Screening a further 100 normal individuals for this mutation also failed to reveal further occurrences of this variant in the general population. Sequencing of exons 16 and 17 of the beta-amyloid precursor protein gene (the exons which encode the beta-amyloid fragment) in pedigree FAD4 revealed them to be of normal sequence. The significance of these observations to the genetics of Alzheimer's disease is discussed.

Alzheimer Disease↗