A spinal thecal sac constriction model supports the theory that induced pressure gradients in the cord cause edema and cyst formation.

OBJECTIVE: Spinal cord cysts are a devastating condition that occur secondary to obstructions of the spinal canal, which may be caused by congenital malformations, trauma, spinal canal stenosis, tumors, meningitis, or arachnoiditis. A hypothesis that could explain how spinal cord cysts form in these situations has been presented recently. Therefore, a novel spinal thecal sac constriction model was implemented to test various aspects of this hypothesis. METHODS: Thecal sac constriction was achieved by subjecting rats to an extradural silk ligature at the T8 spinal cord level. Rats with complete spinal cord transection served as a second model for comparison. The animals underwent high-resolution magnetic resonance imaging and histological analysis. RESULTS: Thecal sac constriction caused edema cranial and caudal to the ligation within 3 weeks, and cysts developed after 8 to 13 weeks. In contrast, cysts in rats with spinal cord transection were located predominantly in the cranial spinal cord. Histological sections of spinal cords confirmed the magnetic resonance imaging results. CONCLUSION: Magnetic resonance imaging provided the specific advantage of enabling characterization of events as they occurred repeatedly over time in the spinal cords of individual living animals. The spinal thecal sac constriction model proved useful for investigation of features of the cerebrospinal fluid pulse pressure theory. Edema and cyst distributions were in accordance with this theory. We conclude that induced intramedullary pressure gradients originating from the cerebrospinal fluid pulse pressure may underlie cyst formation in the vicinity of spinal canal obstructions and that cysts are preceded by edema.

Functional MRI at 4.7 tesla of the rat brain during electric stimulation of forepaw, hindpaw, or tail in single- and multislice experiments.

Stimulation of peripheral nerves activates corresponding regions in sensorimotor cortex. We have applied functional magnetic resonance imaging (fMRI) techniques to monitor activated brain regions by means of measuring changes of blood oxygenation level-dependent contrast during electric stimulation of the forepaw, hindpaw, or tail in rats. During alpha-chloralose anesthesia, artificial respiration, and complete muscle relaxation, stimulations were delivered at 3 Hz via subcutaneous bipolar electrodes with 500-microseconds-current pulses of 0.2-2.0 mA. Single- or multislice gradient echo images were collected during recording sessions consisting of five alternating rest and stimulation periods. Stimulation of the right and left forepaws and hindpaws repeatedly led to robust activation of the contralateral sensorimotor cortex. There was a significant correlation (P < 0.05) between current pulse strength and amount of activation of the sensory cortex during forepaw stimulation. The center of the main cortical representation of the forepaw was situated 3.4 mm lateral to the midline and 5 mm posterior to the rhinal fissure. The main representation of the hindpaw was 2.0 mm lateral to the midline and 6 mm posterior to the rhinal fissure. Tail stimulation gave rise to a strikingly extended bilateral cortical activation, localized along the midline in medial parietal and frontal cortex 4 and 5 mm posterior to the rhinal fissure. In conclusion, the experiments provide evidence that peripheral nerve stimulation induces a fMRI signal in the respective division of the somatosensory cortex in a stimulus-related manner. The marked cortical activation elicited by tail stimulation underlines the key importance of the tail.

Magnetic resonance imaging of the membranous labyrinth during in vivo gadolinium (Gd-DTPA-BMA) uptake in the normal and lesioned cochlea.

MRI with a T1 contrast agent was used to investigate the normal and noise-damaged cochlea. The time course and distribution of the in vivo uptake of the gadodiamide chelate bound paramagnetic Gd ion (GdDTPA-BMA) throughout the membranous labyrinth of normal and impulse noise-damaged guinea pig cochleae were measured by MRI at 4.7T. Simultaneous signal enhancement of the basal, medial and apical scala tympani (ST) and scala vestibuli (SV) was observed within 10 min following i.v. injection, reaching maximum levels at around 100 min. ANOVA and post hoc paired t-tests showed statistically significant differences in the levels and rates of Gd uptake-enhancement between the scalae. The ST revealed the most rapid and extensive enhancement throughout the period of active Gd uptake, while the SV showed comparatively slower and less enhancement, and the intact scala media (SM) indicated insignificant enhancement. The in vivo Gd penetration and enhancement of the membranous SM increased significantly in the noise-damaged cochlea, suggesting lesioning of the cochlear membranes.

Magnetic resonance imaging of the cochlea, spiral ganglia and eighth nerve of the guinea pig.

The membranous labyrinth of the guinea pig cochlea and retrocochlear neural structures were investigated by magnetic resonance imaging (MRI) using an experimental system with a field strength of 4.7T and a single turn surface coil 25 mm in diameter, or standard resonators of 34 or 70 mm in diameter and gradient field strengths of 950 mTm and 200 mTm. High-resolution 2-D and 3-D images of 0.3-1.0 mm slice thickness were acquired by a rapid acquisition with relaxation enhancement (RARE) sequence and a standard multi-echo technique. Structural and dimensional aspects of the cochlea were resolved in vitro and in vivo down to <50 microm, showing the scala vestibule, scala media, scala tympani, spiral ganglia and the cochlear (eighth) nerve. In vivo perfusions with the gadodiamide (GdDTPA-BMA) chelate-bound paramagnetic gadolinium ion resulted in dynamic temporal enhancement of the scala vestibule and scala tympani, but did not penetrate the scala media.

High-resolution MRI of intact and transected rat spinal cord.

Spinal cord transection at midthoracic level leads to an immediate loss of hindlimb motor function as well as to a progressive degeneration of descending and ascending spinal cord pathways. Thoracic spinal cord in unlesioned control rats and in rats 2 to 6 months after complete midthoracic transection were imaged in vivo using an ultrahigh-field (4.7 T) magnetic resonance spectrometer. High-resolution spin-echo and inversion-recovery pulse sequences were employed. In addition, the apparent diffusion coefficients (ADCs) in longitudinal and transverse directions of the spinal cord were determined. Anatomical MRI findings were confirmed in histological spinal cord tissue preparations. In healthy spinal cord, gray and white matter were easily discerned in proton density-weighted images. An infield resolution of max. 76 micrometers per pixel was achieved. In animals with chronic spinal cord transection changes in gray-white matter structure and contrast were observed toward the cut end. The spinal cord stumps showed a tapering off. This coincided with changes in the longitudinal/transverse ADC ratio. Fluid-filled cysts were found in most cases at the distal end of the rostral stump. The gap between the stumps contained richly vascularized scar tissue. Additional pathologic changes included intramedullary microcysts, vertebral dislocations, and in one animal compression of the spinal cord. In conclusion, MRI was found to be a useful method for in vivo investigation of anatomical and physiological changes following spinal cord transection and to estimate the degree of neural degeneration. In addition, MRI allows the description of the accurate extension of fluid spaces (e.g., cysts) and of water diffusion characteristics which cannot be achieved by other means in vivo.