Landmarks for the Location of the Subthalamic Nucleus Using Magnetic Resonance Imaging

Deep brain stimulation has become an option for advanced Parkinson's disease treatment since the 1990s, but the first reports are from Benabid's team, a French neurosurgeon, in the 1980s. The subthalamic nucleus (STN), more specifically its dorsolateral portion, is the most commonly stimulated brain area. One of the major aspects for a good surgical result is the accurate location of this target. Therefore, the present article aimed to identify landmarks that facilitate and refine the location of the STN using nuclear magnetic resonance imaging (NMRI) of the skull. In order to achieve this goal, a search for articles was performed using the PubMed and Science Direct online databases, and articles regarding the use of NMRI to target STN were included. The precise location of the dorsolateral portion of the STN is fundamental to achieve the best possible effect on motor symptoms and to minimize side effects. One of the most used location methods is the NMRI, associated or not with tomography or ventriculography. The location strategies can be classified as direct and indirect. Landmarks are among the indirect strategies, and the most important ones (red nucleus, Sukeroku sign, dent internal capsule sign, supramammillary commissure, mammillothalamic tract, and interpeduncular cistern) are described in the present article. The various landmarks can be combined to locate with more accuracy the dorsolateral portion of the STN and the ideal position of the electrodes to achieve the best possible clinical result.

Loss of neuronal projections in the dystrophin-deficient mdx mouse is not progressive.

Lack of dystrophin is known to reduce several cerebral fiber systems. To investigate if the loss of fibers is progressive, we analyzed projections of the trigeminal sensory system to the red nucleus in 3, 6, and 12 month old dystrophin-deficient mdx mice. The retrograde tracer fluorogold was injected in the magnocellular part of the red nucleus, and the number of labeled neurons in the oral part of the spinal trigeminal nucleus (Sp5O) was counted. We found that the number of labeled Sp5O neurons was reduced by 50% in mdx mice compared to age-matched control mice. The number of labeled Sp5O neurons did not change significantly between 3 and 12 months neither in mdx nor in control mice. In addition, the number of labeled neurons in the interstitial system of the trigeminal nerve was reduced by 43% in mdx mice. We conclude that fiber loss did not continue beyond the age of 3 months. Our data suggest that lack of full-length dystrophin impairs neuronal migration or axonal outgrowth, or increases neuronal death during fetal or early life.

Projections from the anterior interposed nucleus to the red nucleus diminish with age in the mouse.

To analyse the effect of ageing on the projection of the anterior interposed nucleus to the red nucleus, we injected the retrograde tracer fluorogold in the red nucleus of 3-, 6- and 12-month-old mice. The number of labelled neurones in the anterior interposed nucleus fell by 9% between 3 and 6 months and by another 9% between 6 and 12 months (all P < 0.001). This suggests that loss of neurones from the cerebellar nuclei starts well before old age.

The interstitial system of the trigeminal spinal tract projects to the red nucleus in mice.

We studied projections from the interstitial system of the spinal trigeminal tract (InSy-S5T) to the red nucleus of the mouse with retrograde tracers (fluorogold and latex microbeads impregnated with rhodamine and fluorescein). Injections in the magnocellular part of the red nucleus caused labeling of cells in the rostral, intermediate, and caudal paratrigeminal nucleus (Pa5), dorsal paramarginal nucleus (PaMD), insular trigemeo-lateral cuneate nucleus (I5CuL), and the trigeminal extension of the parvocellular reticular formation (5RPC). All projections were bilateral, but contralateral projections were stronger. The number of retrogradely labeled cells in the InSy-S5T in 3-, 6-, and 12-month-old mice was similar. Injections restricted to the parvocellular red nucleus did not label the nuclei of the InSy-S5T. This projection from the InSy-S5T to the red nucleus may mediate modulation of the facial muscles by pain and other sensory information.

Morphological changes in the trigemino-rubral pathway in dystrophic (mdx) mice.

The lack of dystrophin that causes Duchenne muscle disease affects not only the muscles but also the central nervous system. Dystrophin-deficient mdx mice present changes in several brain fiber systems. We compared the projections from the trigeminal sensory nuclear complex to the red nucleus in control and mdx mice using retrograde tracers. Injection of 200 nL 2% fluorogold into the red nucleus caused labeling in the mesencephalic trigeminal nucleus, the principal sensory nucleus and the oral, interpolar, and caudal subnuclei of the spinal trigeminal nucleus in both control and mdx mice. Injection of latex microbeads labeled with rhodamine and fluorescein gave results similar to those seen with fluorogold. The number of labeled neurons in the trigeminal sensory nuclear complex was significantly reduced in mdx mice. In the oral subnucleus of the spinal trigeminal nucleus this reduction was 50%. These results indicate that the trigemino-rubral pathway is reduced in dystrophin-deficient mice.

Glutathione monoethyl ester improves functional recovery, enhances neuron survival, and stabilizes spinal cord blood flow after spinal cord injury in rats.

Secondary damage after spinal cord (SC) injury remains without a clinically effective drug treatment. To explore the neuroprotective effects of cell-permeable reduced glutathione monoethyl ester (GSHE), rats subjected to SC contusion using the New York University impactor were randomly assigned to receive intraperitoneally GSHE (total dose of 12 mg/kg), methylprednisolone sodium succinate (total dose of 120 mg/kg), or saline solution as vehicle. Motor function, assessed using the Basso-Beattie-Bresnahan scale for 8 weeks, was significantly better in GSHE (11.2+/-0.6, mean+/-S.E.M., n=8, at 8 weeks) than methylprednisolone (9.3+/-0.6) and vehicle (9.4+/-0.7) groups. The number of neurons in the red nuclei labeled with FluoroRuby placed caudally to the injury site was significantly higher in GSHE (158+/-9.3 mean+/-S.E.M., n=4) compared with methylprednisolone (53+/-14.7) and vehicle (46+/-16.4) groups. Differences in the amount of spared SC tissue at the epicenter and neighboring areas were not significant among experimental groups. In a second series of experiments, using similar treatment groups (n=6), regional changes in microvascular SC blood flow were evaluated for 100 min by laser-Doppler flowmetry after clip compression injury. SC blood flow fell in vehicle-treated rats 20% below baseline and increased significantly with methylprednisolone approximately 12% above baseline; changes were not greater than 5% in rats given GSHE. In conclusion, GSHE given to rats early after moderate SC contusion/compression improves functional outcome and red nuclei neuron survival significantly better than methylprednisolone and vehicle, and stabilizes SC blood flow. These results support further investigation of reduced glutathione supplementation after acute SC injury for future clinical application.

Errores neurorradiológicos frecuentes en TC y RM / Frequent neuroradiological misinterpretations in CT and MR

Se presenta una revisión de las variantes anatómicas normales más frecuentes de ver en cráneo, cerebro y espacios de líquido cefalorraquídeo, que pueden ser malinterpretradas como hallazgos patológicos llevando a la realización de estudios más complejos e innecesarios. En la mayoría de los ejemplos, las variantes anatómicas son solo visibles en TC y en otros casos son exclusivas de RM. El propósito de esta revisión es conocer las variantes más frecuentemente observadas en imágenes de RM y TC con el fin de obtener un diagnóstico acertado evitando la realización de estudios posteriores innecesarios que solo llevan a aumentar los costos en salud de nuestros pacientes.

Fluoxetine-induced tremor: clinical features in 21 patients.

We report a cohort of 21 patients (12 females and nine males), with a mean age of 42.4 years, who developed tremor after receiving fluoxetine at a mean dose of 25.7 mg per day. The mean latency period for tremor appearance was 54.3 days. Severity was found to be mild. In all patients, tremor was postural, with P<0.0005, compared to patients with rest tremor and P<0.05 compared to action/intention-tremor patients. The frequency range was 6-12 Hz/s. After fluoxetine was discontinued, tremor disappeared in 10 patients after a mean latency period of 35.5 days. In the remaining 11 patients, tremor persisted up to the end of the observation period (a mean of 449 days). We believe that this tremor phenomenon is due to the involvement of the red nucleus and the inferior olivary nucleus through their projections to the thalamus and the spinal cord.

Histopathology of the brain-stem nuclei of horses with "Mal seco", an equine dysautonomia.

"Mal seco" is a disease of unknown aetiology affecting horses in Argentina. It is similar to grass sickness, a primary dysautonomia of horses in Europe. A histopathological study of the brain stem nuclei of three horses with "mal seco" was performed. Changes were found that consisted of chromatolysis, cytoplasmic vacuoles, eosinophilic sphaeroids, and pyknotic and eccentric nuclei. These changes were most severe at the oculomotor, vestibular and abducent nuclei. The results provide further evidence to suggest that "mal seco" and grass sickness may be the same disease.

Red nucleus lesions delay the evolution of amygdala kindling in cats.

There are some papers which claim that the red nucleus (RN) is related to epileptic manifestations. Though the lesion or electrographic recording of the RN include many paths which assemble into it, the possibility that its cells are implicated in epilepsy is deduced. This paper compares the evolution of amygdaloid kindling in cats with bilateral RN lesions, with the epileptic disturbances provoked by lesion or stimulation of approach cells. Due to the intrinsic error of the stereotaxic method, only 7 of 13 cats show lesions in the RN with a diameter extending down to 150 micron. Only these show a shortening of the afterdischarge duration, a delay in the appearance of the consecutive clinical stages, and a lengthening in the appearance of generalized tonic-clonic seizures. In comparison, the 6 other cats show lesions mainly in the adjacent central tegmental field, and their kindling evolution was similar to that of a control group with intact mesencephalon. We conclude that the RN lesions interfere with the kindling generation, presumably by lesioning the cerebello-cerebral paths which produce a depression of cortical activity, during the consolidation of clinical and electrographic manifestations.