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Spinothalamic Tract (spinothalamic + tract)

Distribution by Scientific Domains

Life Sciences	66%
Medical Sciences	33%

Selected Abstracts

Correlation of anatomy and function in medulla oblongata infarction

EUROPEAN JOURNAL OF NEUROLOGY, Issue 2 2009
C. Eggers
Background:, A presentation of all aspects of the dorsolateral medulla oblongata syndrome is clinically very rare to find. In most cases patients present with fragmentary symptoms, e.g. ipsilateral axial lateropulsion, nystagmus, dysarthria, dysphagia or hemiataxia. However, the clinical presentation and lesion anatomy at the level of the medulla oblongata is still unsatisfactory. The aim of this study was to correlate the functional deficit with structural MRI-data. Methods:, We included thirteen patients (eight male, five female, mean age 65.5) with medulla oblongata infarction with clinically predominant ipsilateral axial lateropulsion and correlated clinical with structural deficits. Results:, Magnetic resonance imaging lesion mapping demonstrated ipsilateral axial lateropulsion to result from lesions of the spinocerebellar tract, the inferior cerebellar peduncle or the inferior vestibular nucleus. Nystagmus was associated with lesions of the inferior vestibular nucleus, dissociated sensory loss with the spinothalamic tract and hemiataxia with the spinocerebellar tract. Conclusions:, Correlating dysfunction and lesion anatomy is a promising approach to enhance our knowledge on medulla oblongata topography. [source]

Neuropathic pain in spinal cord injury: significance of clinical and electrophysiological measures

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2009
Susanne Wydenkeller
Abstract A large percentage of spinal cord-injured subjects suffer from neuropathic pain below the level of the lesion (bNP). The neural mechanisms underlying this condition are not clear. The aim of this study was to elucidate the general effects of spinal deafferentiation and of bNP on electroencephalographic (EEG) activity. In addition, the relationship between the presence of bNP and impaired function of the spinothalamic tract was studied. Measurements were performed in complete and incomplete spinal cord-injured subjects with and without bNP as well as in a healthy control group. Spinothalamic tract function, assessed by contact heat evoked potentials, did not differ between subjects with and without bNP; nevertheless, it was impaired in 94% of subjects suffering from bNP. In the EEG recordings, the degree of deafferentiation was reflected in a slowing of EEG peak frequency in the 6,12-Hz band. Taking into account this unspecific effect, spinal cord-injured subjects with bNP showed significantly slower EEG activity than subjects without bNP. A discrimination analysis in the subjects with spinothalamic tract dysfunction correctly classified 84% of subjects as belonging to either the group with bNP or the group without bNP, according to their EEG peak frequency. These findings could be helpful for both the development of an objective diagnosis of bNP and for testing the effectiveness of new therapeutic agents. [source]

Nociceptive spinothalamic tract and postsynaptic dorsal column neurons are modulated by paraventricular hypothalamic activation

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2008
Gerardo Rojas-Piloni
Abstract Previously, we demonstrated that stimulation of the paraventricular hypothalamic nucleus diminishes the nociceptive dorsal horn neuronal responses, and this decrease was mediated by oxytocin in the rat. In addition, we have proposed that oxytocin indirectly inhibits sensory transmission in dorsal horn neurons by exciting spinal inhibitory GABAergic interneurons. The main purpose of the present study was to identify which of the neurons projecting to supraspinal structures to transmit somatic information are modulated by the hypothalamic-spinal descending activation. In anaesthetized rats, single-unit extracellular and juxtacellular recordings were made from dorsal horn lumbar segments, which receive afferent input from the toe and hind-paw regions. The projecting spinothalamic tract and postsynaptic dorsal column system were identified antidromically. Additionally, in order to label the projecting dorsal horn neurons, we injected fluorescent retrograde neuronal tracers into the ipsilateral gracilis nucleus and contralateral ventroposterolateral thalamic nucleus. Hence, juxtacellular recordings were made to iontophoretically label the recorded neurons with a fluorescent dye and identify the recorded projecting cells. We found that only nociceptive evoked responses in spinothalamic tract and postsynaptic dorsal column neurons were significantly inhibited (48.1 ± 4.6 and 47.7 ± 8.2%, respectively) and non-nociceptive responses were not affected by paraventricular hypothalamic nucleus stimulation. We conclude that the hypothalamic-spinal system selectively affects the transmission of nociceptive information of projecting spinal cord cells. [source]

Neurotoxins in the Neurobiology of Pain

HEADACHE, Issue 2003
Stephen D. Silberstein MD
Migraine is a common, chronic, incapacitating, neurovascular disorder that affects an estimated 12% of the population. Understanding the basic mechanisms of pain is important when treating patients with chronic pain disorders. Pain, an unpleasant sensory and emotional experience, is usually triggered by stimulation of peripheral nerves and often associated with actual or potential tissue damage. Peripheral nerve fibers transmit pain signals from the periphery toward the spinal cord or brain stem. The different diameter pain fibers (A and C) vary in the speed of conduction and the type of pain transmitted (eg, sharp versus dull). When stimulated, peripheral pain fibers carrying sensory input from the body enter at different layers of the dorsal horn, which is then propagated toward the thalamus via the spinothalamic tract within the spinal cord. Conversely, sensory input from the face does not enter the spinal cord but enters the brain stem via the trigeminal nerve. This review describes in detail the neurobiological mechanisms and pathways for pain sensation, with a focus on migraine pain. [source]

Asynchrony of the early maturation of white matter bundles in healthy infants: Quantitative landmarks revealed noninvasively by diffusion tensor imaging

HUMAN BRAIN MAPPING, Issue 1 2008
Jessica Dubois
Abstract Normal cognitive development in infants follows a well-known temporal sequence, which is assumed to be correlated with the structural maturation of underlying functional networks. Postmortem studies and, more recently, structural MR imaging studies have described qualitatively the heterogeneous spatiotemporal progression of white matter myelination. However, in vivo quantification of the maturation phases of fiber bundles is still lacking. We used noninvasive diffusion tensor MR imaging and tractography in twenty-three 1,4-month-old healthy infants to quantify the early maturation of the main cerebral fascicles. A specific maturation model, based on the respective roles of different maturational processes on the diffusion phenomena, was designed to highlight asynchronous maturation across bundles by evaluating the time-course of mean diffusivity and anisotropy changes over the considered developmental period. Using an original approach, a progression of maturation in four relative stages was determined in each tract by estimating the maturation state and speed, from the diffusion indices over the infants group compared with an adults group on one hand, and in each tract compared with the average over bundles on the other hand. Results were coherent with, and extended previous findings in 8 of 11 bundles, showing the anterior limb of the internal capsule and cingulum as the most immature, followed by the optic radiations, arcuate and inferior longitudinal fascicles, then the spinothalamic tract and fornix, and finally the corticospinal tract as the most mature bundle. Thus, this approach provides new quantitative landmarks for further noninvasive research on brain-behavior relationships during normal and abnormal development. Hum Brain Mapp, 2008. © 2007 Wiley-Liss, Inc. [source]