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

Kim, Jong H.; Greenspan, Joel D.; Coghill, Robert C.; Ohara, Shuichi; Lenz, Frederick A.

doi:10.1523/jneurosci.0716-07.2007

Cited by 109 publications

(86 citation statements)

References 72 publications

(106 reference statements)

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“…Direct evidence for what specific regions of the human thalamus are involved in conveying thermosensory information has been provided by studies endorsing thalamic micro-stimulation during stereotactic surgery in patients with pain and movement disorders (80,194,195), as well as by studies assessing thermo-sensory abnormalities and central pain in stroke patients with constrained thalamic lesions (179). Micro-stimulation of the posterior and inferior ventral caudal nucleus (a portion of the ventral posterior lateral nucleus; VPL) of the human thalamus has been shown to evoke non painful thermal sensations (194,195).…”

Section: Thalamic Integrationmentioning

confidence: 99%

Neurophysiology of Skin Thermal Sensations

Filingeri

2016

Comprehensive Physiology

105

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Undoubtedly, adjusting our thermoregulatory behavior represents the most effective mechanism to maintain thermal homeostasis and ensure survival in the diverse thermal environments that we face on this planet. Remarkably, our thermal behavior is entirely dependent on the ability to detect variations in our internal (i.e. body) and external environment, via sensing changes in skin temperature and wetness. In the past 30 years, we have seen a significant expansion of our understanding of the molecular, neuroanatomical and neurophysiological mechanisms that allow humans to sense temperature and humidity. The discovery of temperature-activated ion channels which gate the generation of action potentials in thermosensitive neurons, along with the characterization of the spino-thalamo-cortical thermosensory pathway, and the development of neural models for the perception of skin wetness, are only some of the recent advances which have provided incredible insights on how biophysical changes in skin temperature and wetness are transduced into those neural signals which constitute the physiological substrate of skin thermal and wetness sensations. Understanding how afferent thermal inputs are integrated and how these contribute to behavioral and autonomic thermoregulatory responses under normal brain function is critical to determine how these mechanisms are disrupted in those neurological conditions which see the concurrent presence of afferent thermosensory abnormalities and efferent thermoregulatory dysfunctions. Furthermore, advancing the knowledge on skin thermal and wetness sensations is crucial to support the development of neuro-prosthetics. In light of the above, this review will focus on the peripheral and central neurophysiological mechanisms underpinning skin thermal and wetness sensations in humans.

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Section: Thalamic Integrationmentioning

confidence: 99%

Neurophysiology of Skin Thermal Sensations

Filingeri

2016

Comprehensive Physiology

105

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“…CPSP often results from VP thalamic lesions (Kim, 1992;Kim et al, 2007) and is associated with increased VP thalamic bursting (Lenz et al, 1989;Wang and Thompson, 2008). For the main part, the proposed models underlying CPSP involve reduced activity or inhibition of the medial and/or lateral thalamus by the ascending spinothalamic tracts (Klit et al, 2009).…”

Section: Neuropathic Pain and The Thalamusmentioning

confidence: 99%

“…Although many neuropathic pain conditions are initiated by peripheral nerve injury, neuropathic pain can occur after a centrally located stroke, i.e., central post-stroke pain (CPSP), which usually involves damage to the spinothalamic tract or thalamic ventroposterior nucleus (VP) (Kim, 1992;Kim et al, 2007). The development of CPSP highlights the fact that neuropathic pain can result from changes restricted to the brain, without the need for "peripheral" changes.…”

Section: Introductionmentioning

confidence: 99%

Different Pain, Different Brain: Thalamic Anatomy in Neuropathic and Non-Neuropathic Chronic Pain Syndromes

Gustin¹,

Peck²,

Wilcox³

et al. 2011

J. Neurosci.

207

180

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Trigeminal neuropathic pain (TNP) and temporomandibular disorders (TMD) are thought to have fundamentally different etiologies. It has been proposed that TNP arises through damage to, or pressure on, somatosensory afferents in the trigeminal nerve, whereas TMD results primarily from peripheral nociceptor activation. Because some reports suggest that neuropathic pain is associated with changes in brain anatomy, it is possible that TNP is maintained by changes in higher brain structures, whereas TMD is not. The aim of this investigation is to determine whether changes in regional brain anatomy and biochemistry occur in both conditions. Twenty-one TNP subjects, 20 TMD subjects, and 36 healthy controls were recruited. Voxel-based morphometry of T1-weighted anatomical images revealed no significant regional gray matter volume change in TMD patients. In contrast, gray matter volume of TNP patients was reduced in the primary somatosensory cortex, anterior insula, putamen, nucleus accumbens, and the thalamus, whereas gray matter volume was increased in the posterior insula. The thalamic volume decrease was only seen in the TNP patients classified as having trigeminal neuropathy but not those with trigeminal neuralgia. Furthermore, in trigeminal neuropathy patients, magnetic resonance spectroscopy revealed a significant reduction in the N-acetylaspartate/creatine ratio, a biochemical marker of neural viability, in the region of thalamic volume loss. The data suggest that the pathogenesis underlying neuropathic and non-neuropathic pain conditions are fundamentally different and that neuropathic pain conditions that result from peripheral injuries may be generated and/or maintained by structural changes in regions such as the thalamus.

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“…Indeed, multiple lines of evidence suggest a critical role for the thalamus in chronic pain processing. In humans, thalamic activation can evoke painful sensations (Lenz et al, 1993;Davis et al, 1996); lesions encompassing the somatosensory thalamus [ventroposterior nucleus (VP)] can result in persistent neuropathic pain (Kim et al, 2007;Klit et al, 2009;Hong et al, 2010); and individuals with neuropathic pain have reduced thalamic volumes and biochemical changes indicative of neuronal loss (Pattany et al, 2002;Apkarian et al, 2004;Gustin et al, 2011) and display more frequent bursting activity of VP thalamic neurons (Hirayama et al, 1989;Lenz et al, 1989Lenz et al, , 1998Gerke et al, 2003). These thalamic alterations may result in the development of thalamocortical dysrhythmia.…”

Section: Introductionmentioning

confidence: 99%

Chronic Pain: Lost Inhibition?

Henderson¹,

et al. 2013

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Human brain imaging has revealed that acute pain results from activation of a network of brain regions, including the somatosensory, insular, prefrontal, and cingulate cortices. In contrast, many investigations report little or no alteration in brain activity associated with chronic pain, particularly neuropathic pain. It has been hypothesized that neuropathic pain results from misinterpretation of thalamocortical activity, and recent evidence has revealed altered thalamocortical rhythm in individuals with neuropathic pain. Indeed, it was suggested nearly four decades ago that neuropathic pain may be maintained by a discrete central generator, possibly within the thalamus. In this investigation, we used multiple brain imaging techniques to explore central changes in subjects with neuropathic pain of the trigeminal nerve resulting in most cases (20 of 23) from a surgical event. Individuals with chronic neuropathic pain displayed significant somatosensory thalamus volume loss (voxel-based morphometry) which was associated with decreased thalamic reticular nucleus and primary somatosensory cortex activity (quantitative arterial spin labeling). Furthermore, thalamic inhibitory neurotransmitter content was significantly reduced (magnetic resonance spectroscopy), which was significantly correlated to the degree of functional connectivity between the somatosensory thalamus and cortical regions including the primary and secondary somatosensory cortices, anterior insula, and cerebellar cortex. These data suggest that chronic neuropathic pain is associated with altered thalamic anatomy and activity, which may result in disturbed thalamocortical circuits. This disturbed thalamocortical activity may result in the constant perception of pain.

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

Cited by 109 publications

References 72 publications

Neurophysiology of Skin Thermal Sensations

Neurophysiology of Skin Thermal Sensations

Different Pain, Different Brain: Thalamic Anatomy in Neuropathic and Non-Neuropathic Chronic Pain Syndromes

Chronic Pain: Lost Inhibition?

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