3T external phased-array magnetic resonance imaging in detection of obstetric anal sphincter lesions: a pilot study.

BACKGROUND: Three-dimensional endoanal ultrasound (3D EAUS) has been the gold standard for detecting anal sphincter lesions in patients with a history of obstetric anal sphincter injury (OASI). Advances in imaging technologies have facilitated the detection of these lesions with external phased-array magnetic resonance imaging (MRI), which could offer an alternative imaging modality for the diagnosis of residual OASI (ROASI) in centers where 3D EAUS imaging is not available. PURPOSE: To compare two diagnostic modalities: the 3D EAUS and 3T external phased-array MRI in the detection of residual anal sphincter lesions. MATERIAL AND METHODS: A total of 24 women with a history of OASI were imaged with both 3D EAUS and 3T external phased-array MRI after primary repair of the injury. Intraclass correlation (ICC) and interrater reliability (IRR) values were calculated for the grade and circumference of the sphincter lesion. Sphincter lesions were graded according to the Sultan classification. RESULTS: There was an almost perfect agreement between 3D EAUS and 3T external phased-array MRI in determining the extent of the sphincter lesions according to the Sultan classification (κ = 0.881; P < 0.001) and the circumference of the external anal sphincter defects, measured in degrees (κ = 0.896; P < 0.001). CONCLUSION: The results of this study indicate that 3T external phased-array MRI and 3D EAUS yield comparable results in the diagnosis of ROASI. These findings suggest that 3T external phased-array MRI could serve as an alternative diagnostic modality to 3D EAUS in the diagnosis of ROASI.

Comparison of 3D endoanal ultrasound and external phased array magnetic resonance imaging in the diagnosis of obstetric anal sphincter injuries.

OBJECTIVES: The gold standard of postpartum anal sphincter imaging has been the 3D endoanal ultrasound (EAUS). Development of magnetic resonance imaging (MRI) has allowed anal sphincter evaluation without the use of endoanal coils. The aim of this study is to compare these two modalities in diagnosing residual sphincter lesions post obstetric anal sphincter injury (OASI). METHODS: Forty women were followed up after primary repair of OASI with both 3D EAUS and external phased array MRI. Details of the anal sphincter injury and sphincter musculature were gathered and analysed. RESULTS: There was a moderate interrater reliability (κ = 0.510) between the two imaging modalities in detecting sphincter lesions, with more lesions detected by MRI. There was a moderate intraclass correlation (ICC) between the circumference of the tear (κ = 0.506) and a fair ICC between the external anal sphincter thickness measurements at locations 3 and 9 on the proctologic clock face (κ = 0.320) and (κ = 0.336). CONCLUSIONS: The results of our study indicate that the use of external phased array MRI is feasible for detecting obstetric anal sphincter lesions postpartum. This allows for imaging of the sphincter defects in centres where EAUS imaging is not available. KEY POINTS: • A two centre prospective study that showed external phased array MRI to be a valid imaging modality for diagnosing obstetric anal sphincter injuries.

Critical neural targets for (the level of) human consciousness: Arousal arrest and unconsciousness after sumatriptan administration.

BACKGROUND: Insufficient understanding of the mechanisms of consciousness can make unconsciousness a diagnostic challenge, directly effecting the treatment and the outcome of the patient. Consciousness is a product of brainstem arousal (wakefulness, the level of consciousness) and cortical information integration (awareness, the contents of consciousness). The thalamus serves as a critical hub in the arousal pathway. The nuclei within the internal medullary lamina, together with the associated thalamocortical connections, have been implicated as being especially important for human consciousness. CASE STUDY: A 17-year old male migraineur developed a sudden episode of unconsciousness after receiving a single dose of intranasal sumatriptan for the treatment of prolonged migraine-associated symptoms. Diffusion-weighted magnetic resonance imaging revealed a small bilateral thalamic infarction affecting the centromedian and parafascicular nuclei and the associated non-specific thalamocortical connections as the likely reason for the impairment of consciousness. With the exception of occasional fatigue due to a persistent lesion on the left thalamus, the patient experienced full recovery. Corresponding to the injury, diffusion tensor tractography imaging revealed a distinctive defect on the thalamocortical fibres originating from the left centromedian/parafascicular nuclei complex. CONCLUSIONS: The presented case offers an outstanding example of the importance of the arousal system and non-specific thalamocortical connectivity for normal waking consciousness.

A characteristic time sequence of epileptic activity in EEG during dynamic penicillin-induced focal epilepsy--a preliminary study.

Penicillin-induced focal epilepsy is a well-known model in experimental epilepsy. However, the dynamic evolution of waveforms, DC-level changes, spectral content and coherence are rarely reported. Stimulated by earlier fMRI findings, we also seek for the early signs preceding spiking activity from frequency domain of EEG signal. In this study, EEG data is taken from previous EEG/fMRI series (six pigs, 20-24kg) of an experimental focal epilepsy model, which includes dynamic induction of epileptic activity with penicillin (6000IU) injection into the somatosensory cortex during deep isoflurane anaesthesia. No ictal discharges were recorded with this dose. Spike waveforms, DC-level, time-frequency content and coherence of EEG were analysed. Development of penicillin induced focal epileptic activity was not preceded with specific spectral changes. The beginning of interictal spiking was related to power increase in the frequencies below 6Hz or 20Hz, and continued to a widespread spectral increase. DC-level and coherence changes were clear in one animal. Morphological evolution of epileptic activity was a collection of the low-amplitude monophasic, bipolar, triple or double spike-wave forms, with an increase in amplitude, up to large monophasic spiking. In conclusion, in the time sequence of induced epileptic activity, immediate shifts in DC-level EEG are plausible, followed by the spike activity-related widespread increase in spectral content. Morphological evolution does not appear to follow a clear continuum; rather, intermingled and variable spike or multispike waveforms generally lead to stabilised activity of high-amplitude monophasic spikes.

Association between visual degeneration of intervertebral discs and the apparent diffusion coefficient.

The value of apparent diffusion coefficient (ADC) measurements in intervertebral disc has been studied because ADC provides an estimate of free diffusion of unbound water and could be used as a quantitative tool to estimate degenerative changes. However, the challenging nature of diffusion imaging of spine and limited numbers of subjects in earlier studies has produced contradictory findings. We aimed to determine the relation between ADC and visual degenerative changes in lumbar intervertebral discs in a sufficiently large homogeneous study group. Lumbar spines of 228 volunteer middle-aged men were MR imaged at 1.5 T including anatomic and diffusion-weighted imaging. ADC values, T2 signal intensity and height, and width of the three lowest lumbar intervertebral discs were measured and disc degeneration visually graded. The calculated average ADC of 530 measured discs was 2.01 x 10(-3) mm(2)/s+/-0.29 (+/-S.D.). The reduction in ADC between visually normal and moderately degenerated discs was 4%. Severely degenerated discs showed 5% larger ADC values than normal discs, presumably due to free water in cracks and fissures of those discs. T2 signal intensity of the disc was significantly correlated with the ADC values, whereas other measured parameters did not show correlation. There was no evident difference in ADC between the studied anatomic lumbar levels. Because there is considerable overlap between ADC values of normal and degenerated discs, we conclude that ADC measurements of intervertebral discs, at least with current technology, have limited clinical value.

In vivo quantification of delayed gadolinium enhancement in the nucleus pulposus of human intervertebral disc.

PURPOSE: To quantify the delayed contrast agent enhancement in the nucleus pulposus of the intervertebral disc by means by T1 relaxation time measurements, and to correlate the enhancement with visual grading of disc degeneration. Diffusion of nutrients through the endplate is a key factor in tissue viability in the intervertebral disc. It can be simulated in vivo using magnetic resonance imaging (MRI) by measuring delayed gadolinium (Gd) enhancement of the disc. MATERIALS AND METHODS: Twenty male volunteers underwent a lumbar spine examination at 1.5T. T2-weighted sagittal images were used to score disc degeneration. T1 relaxation times were measured before and 90 minutes after intravenous administration of Gd-DTPA-BMA by applying a series of sagittal single-slice inversion-recovery fast spin-echo (IR-FSE) scans. RESULTS: A total of 93 discs were analyzed. A statistically significant decrease in the T1 relaxation time of the nucleus pulposus was observed as a result of contrast-agent intake. The percentage change in the T1 relaxation rate for individual discs was up to 126%. A positive trend was observed between the change in the T1 relaxation rate and the grading of disc degeneration. CONCLUSION: Quantification of delayed enhancement of the intervertebral disc may provide a new means of studying alterations in degenerative disc disease (DDD) that explain the variation in diffusion into the intervertebral disc.

BOLD signal increase preceeds EEG spike activity--a dynamic penicillin induced focal epilepsy in deep anesthesia.

In 40-60% of cases with interictal activity in EEG, fMRI cannot locate any focus or foci with simultaneous EEG/fMRI. In experimental focal epilepsy, a priori knowledge exists of the location of the epileptogenic area. This study aimed to develop and to test an experimental focal epilepsy model, which includes dynamic induction of epileptic activity, simultaneous EEG/fMRI, and deep anesthesia. Reported results are from seven pigs (23 +/- 2 kg) studied under isoflurane anesthesia (1.2-1.6 MAC, burst-suppression EEG) and muscle relaxant. Hypo- and hypercapnia were tested in one pig. Penicillin (6000 IU) was injected via a plastic catheter (inserted into the somatosensory cortex) during fMRI (GRE-EPI, TE = 40 ms, 300 ms/two slices, acquisition delay 1700 ms) in 1.5 T (N = 6). Epileptic spikes between acquisition artifacts were reviewed and EEG total power calculated. Cross-correlation between voxel time series and three model functions resembling induced spike activity were tested. Activation map averages were calculated. Development of penicillin induced focal epileptic activity was associated with linear increase and saturation up to approximately 10-20%, in BOLD activation map average. Its initial linear increase reached 2.5-10% at the appearance of the first distinguished spike in ipsilateral EEG in all six animals. Correlated voxels were located mainly in the vicinity of the penicillin injection site and midline, but few in the thalamus. In conclusion, development of focal epileptic activity can be detected as a BOLD signal change, even preceding the spike activity in scalp EEG. This experimental model contains potential for development and testing different localization methods and revealing the characteristic time sequence of epileptic activity with fMRI during deep anesthesia.

Separation of physiological very low frequency fluctuation from aliasing by switched sampling interval fMRI scans.

Anesthetized children have dominant blood-oxygen-level-dependent (BOLD) signal sources presenting high-power fluctuations at very low frequencies (VLF <0.05 Hz). Aliasing of frequencies higher than critically sampled has been regarded as one probable origin of the VLF fluctuations. Aliased signal frequencies change when the sampling rate of the data is altered. In this study, the aliasing of VLF BOLD signal fluctuation was analysed by switching the repetition time (TR) of magnetic resonance (MR) images. Eleven anesthetized children were imaged at 1.5 T using TRs of 500 and 1200 ms. The BOLD signal sources were separated with independent component analysis (ICA). Occipital cortex signal sources had nonaliased VLF fluctuation ( approximately 0.03 Hz) in 9 of 11 subjects. Arterial signal sources failed to present stable power peaks at frequencies lower than 0.42 Hz presumably due to aliasing. Cerebrospinal fluid (CSF)-related signal sources showed nonaliased VLF in four subjects. In conclusion, the VLF BOLD signal fluctuation in the occipital cortex is a true physiological fluctuation, not a result of signal aliasing.

BOLD-contrast functional MRI signal changes related to intermittent rhythmic delta activity in EEG during voluntary hyperventilation-simultaneous EEG and fMRI study.

Differences in the blood oxygen level dependent (BOLD) signal changes were studied during voluntary hyperventilation (HV) between young healthy volunteer groups, (1) with intermittent rhythmic delta activity (IRDA) (N = 4) and (2) controls (N = 4) with only diffuse arrhythmic slowing in EEG (normal response). Subjects hyperventilated (3 min) during an 8-min functional MRI in a 1.5-T scanner, with simultaneous recording of EEG (successful with N = 3 in both groups) and physiological parameters. IRDA power and average BOLD signal intensities (of selected brain regions) were calculated. Hypocapnia showed a tendency to be slightly lighter in the controls than in the IRDA group. IRDA power increased during the last minute of HV and ended 10-15 s after HV. The BOLD signal decreased in white and gray matter after the onset of HV and returned to the baseline within 2 min after HV. The BOLD signal in gray matter decreased approximately 30% more in subjects with IRDA than in controls, during the first 2 min of HV. This difference disappeared (in three subjects out of four) during IRDA in EEG. BOLD signal changes seem to depict changes, which precede IRDA. IRDA due to HV in healthy volunteers represent a model with a clearly defined EEG pattern and an observable BOLD signal change.