Diffusion tensor imaging of the spinal cord at 1.5 and 3.0 Tesla.

PURPOSE: The feasibility of highly resolved diffusion tensor imaging (DTI) of the human cervical spinal cord was tested on a clinical MR unit operating at 3.0 Tesla. DTI parametrical maps and signal-to-noise ratios (SNRs) were compared to results recorded at 1.5 Tesla. MATERIALS AND METHODS: Eight healthy volunteers and one patient participated in the study. A transverse oriented single-shot ECG-triggered echo-planar imaging (EPI) sequence with double spin-echo diffusion preparation was applied for highly resolved DTI of the spinal cord. The signal yield, fractional anisotropy (FA), and mean diffusivity (MD) were compared for both field strengths. The clinical applicability of the protocol was also tested in one patient with amyotrophic lateral sclerosis (ALS) at 3.0 T. RESULTS: A mean increase in SNR of 95.7 +/- 4.6 % was found at 3.0 Tesla compared to 1.5 Tesla. Improved quality of the DTI parametrical maps was observed at higher field strength (p < 0.02). Comparable FA and MD (reported in units of 10 (-3) mm (2)/s) values were computed in the dorsal white matter at both field strengths (1.5 T: FA = 0.75 +/- 0.08, MD = 0.84 +/- 0.12, 3.0 T: FA = 0.74 +/- 0.04, MD = 0.93 +/- 0.14). The DTI images exhibited diagnostic image quality in the patient. At the site of the diseased corticospinal tract, a decrease of 46.0 +/- 3.8 % in FA (0.40 +/- 0.03) and an increase of 50.3 +/- 5.6 % in MD (1.40 +/- 0.05) were found in the ALS patient. CONCLUSION: The 3.0 Tesla field strength provides higher image quality in DTI of the spinal cord compared to 1.5 T. The proposed DTI protocol seems adequate for the assessment of spinal cord diseases.

Morphology of enkephalin-immunoreactive myenteric neurons in the human gut.

The aim of this study was the morphological and further chemical characterisation of neurons immunoreactive for leu-enkephalin (leuENK). Ten wholemounts of small and large intestinal segments from nine patients were immunohistochemically triple-stained for leuENK/neurofilament 200 (NF)/substance P (SP). Based on their simultaneous NF-reactivity and 3D reconstruction of single NF-reactive cells, 97.5% of leuENK-positive neurons displayed the appearance of stubby neurons: small somata; short, stubby dendrites and one axon. Of these leuENK-reactive stubby neurons, 91.3% did not display co-reactivity for SP whereas 8.7% were SP-co-reactive. As to their axonal projection pattern, 50.4% of the recorded leuENK stubby neurons had axons running orally whereas in 29.4% they ran anally; the directions of the remaining 20.2% could not be determined. No axons were seen to enter into secondary strands of the myenteric plexus. Somal area measurements revealed clearly smaller somata of leuENK-reactive stubby neurons (between 259+/-47 microm(2) and 487+/-113 microm(2)) than those of putative sensory type II neurons (between 700+/-217 microm(2) and 1,164+/-396 microm(2)). The ratio dendritic field area per somal area of leuENK-reactive stubby neurons was between 2.0 and 2.8 reflecting their short dendrites. Additionally, we estimated the proportion of leuENK-positive neurons in comparison to the putative whole myenteric neuron population in four leuENK/anti-Hu doublestained wholemounts. This proportion ranged between 5.9% and 8.3%. We suggest leuENK-reactive stubby neurons to be muscle motor neurons and/or ascending interneurons. Furthermore, we explain why we do not use the term "Dogiel type I neurons" for this population.