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Central nervous system lesions
Published in Ibrahim Natalwala, Ammar Natalwala, E Glucksman, MCQs in Neurology and Neurosurgery for Medical Students, 2022
Ibrahim Natalwala, Ammar Natalwala, E Glucksman
TRUE – Pain and temperature sensation is lost in a shawl-like pattern. Pain and temperature sensation is carried in the spinothalamic tract. Typically, the dorsal columns are spared and thus the patient retains vibration, proprioception, touch and pressure sense.
Spinal Cord and Reflexes
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Positioned closely to the lateral spinothalamic tract, and similarly having its neurons of origin in the dorsal horn of the spinal cord, is the spinoreticular tract. The axons of this tract decussate to the other side of the spinal cord and ascend the spinal cord to terminate on third-order neurons in the medullary-pontine reticular formation. The third-order neurons project to intralaminar nuclei of the thalamus, which in turn project diffusely to many parts of the cerebral cortex. In this way, pain reaches consciousness and results in behavioral arousal and a memory of the pain. In fact, this pathway through the reticular formation is considered part of the ascending reticular arousal system (ARAS), which is responsible for regulating states of consciousness, alertness, and sleep-wake transitions.
Central Modulation of Pain
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The spinothalamic tract has a central role in pain perception and transmits information regarding pain, cold, warmth and touch. The majority of the projection neurons that travel in the STT originate in the superficial laminae I and II and deeper lamina V of the spinal dorsal horn, with some in lamina X and the ventral horn. Before ascending, the STT neurons decussate (cross midline) through the ventral white commissure (junction between two parts) to the opposite ventrolateral quadrant of the spinal cord white matter, where they ascend in the ventrolateral funiculus (VLF – bundle of nerve fibres) to the contralateral thalamus.
Chameleons, red herrings, and false localizing signs in neurocritical care
Published in British Journal of Neurosurgery, 2022
Boyi Li, Tolga Sursal, Christian Bowers, Chad Cole, Chirag Gandhi, Meic Schmidt, Stephan Mayer, Fawaz Al-Mufti
Cervical disc herniation (CDH) typically results in ipsilateral neck and arm pain corresponding to the level of the lesion.73 However, false localizing CDH can present with contralaterally radiating neck pain and contralateral upper and lower extremity pain. Diagnosis can be confirmed on MRI. It is hypothesized that this FLS results from cord compression of the lateral spinothalamic tract.73 The symptoms can be completely resolved by surgical discectomy and fusion, further confirming the false localizing nature of the condition.73 CDH as a FLS can also present as hemifacial hyperhidrosis with no facial flushing, anisocoria or blepharoptosis, compensating for anhidrosis/hypohydrosis on the ipsilateral side below the lesion.74 Useful diagnostic tools include the Minor test, quantitative sudomotor function tests, and microneurography of sudomotor nerve activity.74 Tests showing no intramedullary signal abnormalities on MRI suggest that the pathophysiology may be impairment of premotor neuron from the hypothalamus to the intermediolateral nucleus by the disc herniation.74 The ipsilateral anhidrosis or hypohydrosis can directly be attributed to the disc herniation myelopathy.74 Of note, crossed hypohydrosis can occur ipisilateral but above the hyperhidrosis.74 Thus, when patients present with hemihydrosis, the Minor test should be done to determine the anhidrotic and hyperhidrotic areas, and thermography to determine the localization of the potential CDH to be investigated further.74
How Does Our Brain Generate Sexual Pleasure?
Published in International Journal of Sexual Health, 2021
Barry R. Komisaruk, Maria Cruz Rodriguez del Cerro
There is an intriguing parallelism between two processes that are antithetical – pain and orgasm. Both systems share the same neural pathways through the spinal cord and into the brain, where at some (still undiscovered) point they diverge. Both pain and genital afference utilize the spinothalamic system. In cases of intractable abdominal pain from cancer, as a desperate procedure, the spinothalamic tract was surgically severed. The pain disappeared, but so did the ability to experience orgasms. When months later the pain started to recur, so did the orgasmic capacity (Elliott, 1969). The spinothalamic system activates the reticular system and the pathways project to the insular cortex and the anterior cingulate cortex. Both these cortical regions are activated not only by pain, but also by orgasm (Komisaruk & Cerro, 2015). Perhaps they both control facial expressions, which could account for the similarity of facial grimaces during pain and orgasm. Alternatively, perhaps the genital input actively inhibits the pain input, but the fMRI methodology is not able to distinguish between active excitation and active inhibition, or that the neurons in anterior cingulate and insular cortices that respond to orgasm and pain are not identical. The sympathetic division of the autonomic system is activated by both pain and orgasm…the heart rate and blood pressure increase dramatically during both. But obviously, as pain feels different from orgasmic pleasure, the neural pathways for the two phenomena must diverge at some point in the brain (Komisaruk et al., 2006).
Safety considerations for the management of cholestatic itch
Published in Expert Opinion on Drug Safety, 2021
The pathophysiology of cholestasis-induced pruritus has not been completely elucidated. It seems that a common first step for all cholestatic disorders is the activation of nerve endings and skin receptors by pruritogens. This signal is then transduced to secondary neurons in the dorsal horn of the spinal cord crossing to the contralateral side to project through the spinothalamic tract to the ventromedial nucleus of the thalamus and end at the primary sensory cortex, supplementary motor area, anterior cingulate cortex and parietal lobe [10]. Although this pathway and the involved anatomic structures are well defined, many questions regarding its activation, function and regulation are yet to be answered. Bile salts/acids, endogenous opioids, histamine, serotonin, substance P and even nitric oxide have been proposed as inducers of the itch stimuli but extensive research has failed to show a linear and consistent correlation between their concentration and the intensity of symptoms [11,12].