I have for some time now, been reading articles textbooks, and research papers by Dr. Serge Marchand, PhD. Some of these quotes are from articles, textbooks and others are from research papers. Dr. Marchand is one of the lesser known pain experts, but in my opinion he deserves a lot more attention, for the great work that he does.
Dr. Serge Marchand PhD is Professor of Medicine at the Univ. de Sherbrooke, directing the pain research labs at the Research Center of the Sherbrooke University hospital. He received his PhD in Neuroscience from the Université de Montréal in 1992 and then after completed his post-doctoral training in neuroanatomy at the University of California, San Francisco in 1994.
He is the author of several articles and books in the field of pain mechanisms and treatment, and is the author of the book “The Phenomenon of Pain” from IASP press and co-author of the book “Mental Health and Pain” from Springer Press 2014.
His projects aim at better understanding the role of factors such as sex hormones, the autonomic, spinal and cortical activity related to pain perception in healthy subjects during their development, from infants to elderly and in different population of patients suffering from chronic pain.
Without further ado, here are 20 something quotes from Dr. Serge Marchand PhD:
“Pain is a complex phenomenon that includes sensory, cognitive and affective components. The painful experience is the resultant of the interaction between these components. Dr. Serge Marchand PhD
“Pain is more then the mere representation of the nociceptive signal. From the periphery to the brain, the nociceptive signal will be modulated at all the levels of the central nervous system. The perception of pain is the finality of a complex series of endogenous mechanisms that will either emphasize the signal (excitatory mechanisms) or reduce the signal (inhibitory mechanisms). A chronic pain condition can produce changes that will affect these mechanisms in different ways. It is then not surprising that two patients presenting apparently similar pain problems may respond quite differently to the same treatment, since the physiopathology behind the pain is totally different.” Dr. Serge Marchand PhD
“Hyperalgesia is defined as an exaggerated response to a normally painful stimulation. In the 1950s, Hardy proposed that two kinds of hyperalgesia could affect the skin: primary hyperalgesia, occurring directly at the site of injury, and secondary hyperalgesia, with its origins in the central nervous system (CNS)” Dr. Serge Marchand PhD
“Since the publication of the gate control theory by Melzack and Wall in 1965, which states that pain information does not circulate in a linear manner, but is rather modulated upon its arrival at the spinal cord, several studies have confirmed that nociceptive information is modulated at all levels of the CNS. This modulation can be excitatory, increasing the nociceptive response, or inhibitory, producing analgesia” Dr. Serge Marchand PhD
“We have known for a long time that pain is a complex sensory and emotional experience demanding the participation of the higher centers of the CNS. It is only once the nociceptive information is sent to the cortex that we can really speak of pain, since pain is a perception.” Dr. Serge Marchand PhD
“It was at the end of the 1970s that the concept of diffuse noxious inhibitory control (DNIC) was proposed. This model reveals how a localized nociceptive stimulation can produce a generalized hypoalgesia of nociceptive afferents.” Dr. Serge Marchand PhD
“According to the DNIC theory, nociceptive stimulation activates the pool of nociceptive neurons corresponding to the spinal segment that they innervate while inhibiting the other nociceptive neurons of the spinal cord serving the rest of the body. By reducing the activity of multireceptive neurons, DNIC lessens the back- ground noise and highlights the activity of specific neurons recruited by nociceptive stimulation. According to this hypothesis, pain is not solely triggered by excitatory processes, but by the perception of a contrast between the activities of the excitatory and inhibitory neurons.” Dr. Serge Marchand PhD
“Changes in the activity of the nociceptive system from the periphery to the cortex can be responsible for the development and maintenance of a chronic pain condition. However, they will implicate several different mechanisms that will respond differently to a treatment. Recent scientific data using brain imaging are supporting a cortical reorganization of white and gray matter in patients suffering from chronic pain” Dr. Serge Marchand PhD
“It is now well known that from nociceptive stimulation to perception, there is a wide range of endogenous mechanisms that influence our experience of pain. These endogenous excitatory and inhibitory mechanisms increase or decrease the nociceptive signal, which results in more or less pain. A purely linear view is no longer adequate to understand pain or how pain can persist or even appear without apparent injury. To understand the neurophysiology of pain, we must look at the afferent nociceptive impulses from the periphery to higher centers, but we must also pay attention to endogenous pain modulation mechanisms at all levels of the central nervous system.” Dr. Serge Marchand PhD
“On the other hand, a nociceptive stimulation can recruit descending inhibitory mechanisms that will reduce the nociceptive signal all over the body. The same is also true for the higher centers. Cognitive information, such as expectations related to a treatment, can enhance or reduce the efficacy of endogenous pain modulations such as DNIC (Diffuse Noxious Inhibitory Control). The initial nociceptive stimulus is therefore not the only factor contributing to pain perception. Between these two events are four steps marked by a series of chemical and electrical reactions: transduction, transmission, modulation, and perception.” Dr. Serge Marchand PhD
“The differences in conduction velocity between the Aδ and C fibers can be appreciated when isolating the sensation of first and second pain. Following a brief nociceptive stimulation, the Aδ fibers will rapidly transmit a brief and acute pinprick-like sensation perceived to be precisely located at the point of stimulation. It is this precision and fast conduction that will result in the nociceptive withdrawal reflex. Following this activity, C fibers will transmit their information, with a relatively long delay (hundred of milliseconds to a second depending on the location of the stimulus). This second sensory input results in a more diffuse deep pain sensation.” Dr. Serge Marchand PhD
“As previously mentioned, the nociceptive information that reaches the higher centers have undergone many excitatory and inhibitory influences at all levels of the central nervous system. The fourth step, the perception of pain, is the translation from a noxious stimulus to pain perception. However, pain perception can be present without peripheral nociceptive inputs and will be colored by emotions and the sum of the subject’s past experiences.” Dr. Serge Marchand PhD
“Afferent fibers originating in the periphery fall into three groups, namely Aβ, C and Aδ fibers. The Aβ fibers are large myelinated fibers that conduct at high speed and usually transmit non- nociceptive signals. They do however also participate in pain modulation as will be later explained. The other two classes of fibers, the larger myelinated Aδ fibers and the thin unmyelinated C fibers mainly transmit nociceptive signals. It is important to underline that Aβ fibers can also play a role in pain, be responsible for static mechanical allodynia and even central sensitization” Dr. Serge Marchand PhD
“Primary hyperalgesia can be explained by the release of different inflammatory factors in the periphery, which leads to the recruitment of nociceptors near the site of the injury. After an injury, several pronociceptive substances are released in the periphery (potassium, prostaglandins, bradykinin, histamine, substance P, and serotonin), which has the effect of recruiting nociceptors and producing sensitization. The injury site as well as the neighboring tissues will thus have lower pain thresholds.Secondary hyperalgesia, on the other hand, can be explained by a central phenomenon that is known by the general term ‘central sensitization’” Dr. Serge Marchand PhD
“On the clinical side, the phenomenon of central sensitization allows us to better understand the importance of relieving pain as early as possible in order to avoid chronification.” Dr. Serge Marchand PhD
“It is interesting to note that pharmacological treatment that targets some mental health problems are also useful in the treatment of certain pain. For example, antidepressants used in the context of mood disorders are also helpful in relieving some type of pain. This combined effect on mood and pain is due to the involvement of certain neurotransmitters, such as serotonin and noradrenaline, both acting on mood and in the modulation of endogenous mechanisms of pain control. The initial nociceptive stimulus is therefore not the only factor contributing to pain perception.” Dr. Serge Marchand PhD
“Another interesting example is the demonstration that manipulating the expectation related to an analgesic procedure can completely reverse the analgesic effect of endogenous pain modulation and the related pain experience. By suggesting that a procedure that is normally analgesic would produce more pain, subjects indeed reported more pain.” Dr. Serge Marchand PhD
“As scary as brain changes with chronic pain can sound, it is important to underline that studies are also reporting that this loss of brain matter can be reversed after an adequate treatment” Dr. Serge Marchand PhD
“Physiological responses to pain treatments are strongly colored by past painful conditions, treatment history and other individual characteristics that can initiate endogenous excitatory or inhibitory mechanisms. Thus, the emotional state of the patient actively participates in pain development, persistency and responses to treatment.” Dr. Serge Marchand PhD
“Based on the understanding of pain neurophysiology, we may devise treatment plans for pain management in the clinical setting. Treatments could be aimed towards either reducing excitatory mechanisms or enhancing inhibitory activity. The first goal is to identify as best as possible the mechanisms implicated.” Dr. Serge Marchand PhD
