Ascending Axon Degeneration Following Anterolateral Cordotomy. An Experimental Study in the Monkey

Mehler, William R.; Feferman, Martin E.; Nauta, Walle J. H.

doi:10.1093/brain/83.4.718

Cited by 665 publications

(106 citation statements)

References 54 publications

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“…Anatomic studies of spino-reticular projections in the cat revealed dense fiber terminations in the caudal portion of the GC (MEHLER et al, 1960). Our intracellular recordings also demonstrated synaptic connection with GC neurons from all 4 limbs as shown in Fig.…”

Section: Discussionsupporting

confidence: 75%

Ascending fibers from the gigantocellular nucleus to the centromedian nucleus of the thalamus in cats.

et al. 1986

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Centrum medianum (CM) afferent pathways, which are involved in pain sensation, were analyzed using physiological techniques. Thirty-four neurons in the gigantocellular nucleus (nucleus gigantocellularis medullae oblongatae, GC) in cats were recorded intracellularly. Of these, 5 (15%) did not respond to electrical stimulation applied to any of the 4 limbs. Twenty-nine (85%) showed spike potentials that were superimposed on excitatory post-synaptic potentials (EPSPs) with an amplitude of 7.2 mY (n =101) and a duration of 6.8 ms. The latencies from contra-and ipsilateral forelimb, contra-and ipsilateral hindlimb to the GC were 9.3 (n==25), 7.2 (n=23), 12.9 (n=28), and 10.9 ms (n=25), respectively. Of these responding neurons, 19 (66%) responded to stimuli to all 4 limbs, 7 (24%) to 3 limbs, 1(3%) to 2 limbs, and 2 (7%) to 1 limb. These afferent neurons in the GC showed spike potentials without EPSPs after stimulation of the CM in the thalamus. Extracellular activities of 37 CM neurons were also tested. Of these, 4 neurons responded to GC stimulation with a short latency of 1.6 ms. Another 33 responded with a long latency of 6.7, and 11 of them were able to follow GC stimulation of over 200 Hz with a fixed long latency; 22 responded with varying long latencies but were not able to follow stimuli over 15 Hz. Three-quarters of the CM neurons received ipsilateral inputs from the GC, and the other contralateral inputs. Three CM neurons responded to stimulation of the GC in quasi-intracellular records. These findings suggest that some ascending fibers from the GC terminate on CM neurons and play a role in pain sensation.

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Section: Discussionsupporting

confidence: 75%

Ascending fibers from the gigantocellular nucleus to the centromedian nucleus of the thalamus in cats.

et al. 1986

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“…In the other two, the lesions were located in dorsal Vc and extended posterior to Vc proper into the Vc portae and pulvinar oral nuclei, which receive STT input ("Vc-plus" lesions; patients 13 and 18) (Mehler et al, 1960;Mehler, 1962;Apkarian and Hodge, 1989).…”

Section: Radiologic Testsmentioning

confidence: 99%

Lesions Limited to the Human Thalamic Principal Somatosensory Nucleus (Ventral Caudal) Are Associated with Loss of Cold Sensations and Central Pain

et al. 2007

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Central pain is neuropathic pain resulting from a lesion of the CNS, such as a stroke [poststroke central pain (CPSP)]. Lesions involving the posterior thalamus lead to reduction or loss of sensation and to CPSP, although the responsible nuclei have not been identified. We now examine the hypotheses that thalamic lesions must extend posterior to the ventral caudal nucleus (Vc) and include ventral medial posterior nucleus (VMpo), to result in loss of cold sensibility and CPSP. Patients with small thalamic strokes associated with CPSP were evaluated by atlas-based mapping of magnetic resonance imaging scans, and by somatosensory testing. All lesions involved posterior Vc; two lesions also involved nuclei posterior to Vc, but not VMpo. All patients tested had alterations of cold pain sensation and tactile sensation, as measured by von Frey hairs. Three patients had altered cool sensation, and the patient with the least involvement of Vc had normal cool thresholds, suggesting that a critical volume of Vc must be involved before cool sensation is impaired. Perception of warm was impaired only in lesions involving nuclei posterior to Vc. Heat pain perception was never affected. In a subject with cold allodynia, a single-subject protocol PET study measured the responses to immersion of either hand in a 20°C waterbath. The scan during stimulation of the affected hand was characterized by intense activation of contralateral sensorimotor cortex. Therefore, there are modality-specific subnuclear structures in the posterior thalamus, but lesions of Vc not involving VMpo are sufficient to impair cold sensibility and to produce CPSP.

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“…In the traditional view, spinothalamic (STT) and spinal trigemino-thalamic (sVTT) tract fibers terminate in widespread patches throughout the primate ventral posterior lateral (VPL), ventral posterior medial (VPM), and other posterior and intralaminar nuclei (Getz, 1952;Mehler et al, 1960;Price et al, 1976;Craig and Burton, 1981;Honda et al, 1983;Kniffki and Mizumura, 1983;Jones, 1985;Apkarian and Hodge, 1989a,b,c;Hodge and Apkarian, 1990;Rausell and Jones, 1991a,b;Rausell et al, 1992;Ralston and Ralston, 1994;Willis and Westlund, 1997). Cells with specific responses to noxious mechanical and thermal stimuli and those that project to the thalamus via the STT are located in the marginal zone and neck of the dorsal horn (laminas I and IV-VI), and substantial numbers of lamina I cells reportedly project to VPM and VPL (Willis et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Widespread Thalamic Terminations of Fibers Arising in the Superficial Medullary Dorsal Horn of Monkeys and Their Relation to Calbindin Immunoreactivity

Graziano¹,

Jones²

2004

J. Neurosci.

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The relay of pain fibers from the spinal and medullary dorsal horn in the thalamus has become a controversial issue. This study analyzed the relationship of fibers arising in lamina I to nuclei in and around the caudal pole of the ventral posterior nuclear complex and especially to a zone of calbindin-dense immunoreactivity (VMpo) identified by some authors as the sole thalamic relay for these fibers. We show that the densest zone of calbindin immunoreactivity is part of a more extensive, calbindin-immunoreactive region that lies well within the medial tip of the ventral posterior medial nucleus (VPM), as delineated by other staining methods, and prove that the use of different anti-calbindin antibodies cannot account for differences in interpretations of the organization of the posterior thalamic region. By combining immunocytochemical staining with anterograde tracing from injections involving lamina I, we demonstrate widespread fiber terminations that are not restricted to the calbindin-rich medial tip of VPM and show that the lamina I arising fibers are not themselves calbindin immunoreactive. This study disproves the existence of VMpo as an independent thalamic pain nucleus or as a specific relay in the ascending pain system.

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Ascending Axon Degeneration Following Anterolateral Cordotomy. An Experimental Study in the Monkey

Cited by 665 publications

References 54 publications

Ascending fibers from the gigantocellular nucleus to the centromedian nucleus of the thalamus in cats.

Ascending fibers from the gigantocellular nucleus to the centromedian nucleus of the thalamus in cats.

Lesions Limited to the Human Thalamic Principal Somatosensory Nucleus (Ventral Caudal) Are Associated with Loss of Cold Sensations and Central Pain

Widespread Thalamic Terminations of Fibers Arising in the Superficial Medullary Dorsal Horn of Monkeys and Their Relation to Calbindin Immunoreactivity

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