Pain as the presenting symptom of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)

Boukhris, S.; Magy, Laurent; Mohamed, Khalil; Sindou, Philippe; Vallat, Jean‐Michel

doi:10.1016/j.jns.2006.12.012

Cited by 43 publications

(27 citation statements)

References 20 publications

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“…Although having a length-dependent, sensory painful neuropathy pattern in the initial period of the disease, the presence of an important proximal weakness in the lower limbs in the absence of a significant distal weakness in the upper limbs, and the non-uniform demyelinating pattern observed on NCS suggested this patient had a non length-dependent demyelinating neuropathy, compatible to CIDP 4 , that may occasionally be heralded by pain 5 . CSF is highly abnormal in patients with CIDP when several punctures are carried out, but one normal examination does not rule out this disease As there was no improvement with steroid treatment, a sural nerve biopsy was carried out, revealing an amyloid infiltrate.…”

Section: Discussionmentioning

confidence: 84%

Clinical and electrophysiological correlates of TTRala71 amyloid neuropathy

Marques¹,

Borgetti²,

Marques³

et al. 2010

Arq. Neuro-Psiquiatr.

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Section: Discussionmentioning

confidence: 84%

Clinical and electrophysiological correlates of TTRala71 amyloid neuropathy

Marques¹,

Borgetti²,

Marques³

et al. 2010

Arq. Neuro-Psiquiatr.

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“…Although pain is typically regarded as a secondary sign of CIDP, Boukhris et al [21] described the characteristics of 5 patients in whom pain was the main cause of referral and the most prominent symptom. Patients presented initially with pain in the lower limbs associated with modest motor impairment (1 case), distal paresthesia (4 cases), cramps (1 case) and fatigue (2 cases).…”

Section: Pain In Immune-mediated Neuropathiesmentioning

confidence: 99%

Fatigue, Pain, Anxiety and Depression in Guillain-Barré Syndrome and Chronic Inflammatory Demyelinating Polyradiculoneuropathy

Merkies

Kieseier²

2016

Eur Neurol

602

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Background: In the clinical evaluation of patients with Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), scant attention is paid to symptoms such as fatigue, pain and anxiety/depression. We aimed at addressing seminal studies that focused on the burden of these symptoms and their impact on quality of life (QoL) in these conditions. Summary: Fatigue, pain, and anxiety/depression are increasingly being recognized in patients with GBS and CIDP, although their pathophysiological provenance remains unknown. Fatigue and pain are significant in terms of prevalence and intensity, may be a presenting symptom, and can persist for years after apparent functional recovery, suggesting residual injury. Anxiety/depression has also been examined although studies are limited. Despite their negative impact on QoL, the long-term dynamics of these symptoms in patients with GBS and particularly CIDP receiving therapy in routine clinical practice have not been systematically evaluated. Such observations formed the basis for the ongoing (GAMEDIS) studies evaluating the effect of Gamunex® on fatigue and depression in patients with CIDP, of which some preliminary data are presented. Key Messages: Strength and sensory deficits are the main areas of focus in patients with GBS and CIDP, but they do not explain the total reduction in QoL, suggesting the possible role of other complaints. A more comprehensive approach to patient care demands that factors such as pain, fatigue and anxiety/depression receive greater attention. The non-interventional GAMEDIS studies are expected to provide valuable insight into the long-term effectiveness of Gamunex® in everyday practice.

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“…As an example of the role of chemokine signaling in chronic pain one might consider PNS and CNS inflammatory demyelinating diseases such as GuillainBarré syndrome, Charcot-Marie-Tooth disease types 1 and 4, and multiple sclerosis, which are frequently accompanied by a neuropathic pain syndrome (76,77). Epidemiological studies suggest that chronic pain syndromes afflict 50-80% of patients with multiple sclerosis and 70-90% of individuals with Guillain-Barré syndrome (78).…”

Section: Chemokines and Their Receptors In Acute And Chronic Painmentioning

confidence: 99%

Chemokines and the pathophysiology of neuropathic pain

White

Jung²,

Miller

2007

Proc. Natl. Acad. Sci. U.S.A.

318

265

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Chemokines and chemokine receptors are widely expressed by cells of the immune and nervous systems. This review focuses on our current knowledge concerning the role of chemokines in the pathophysiology of chronic pain syndromes. Injury-or disease-induced changes in the expression of diverse chemokines and their receptors have been demonstrated in the neural and nonneural elements of pain pathways. Under these circumstances, chemokines have been shown to modulate the electrical activity of neurons by multiple regulatory pathways including increases in neurotransmitter release through Ca-dependent mechanisms and transactivation of transient receptor channels. Either of these mechanisms alone, or in combination, may contribute to sustained excitability of primary afferent and secondary neurons within spinal pain pathways. Another manner in which chemokines may influence sustained neuronal excitability may be their ability to function as excitatory neurotransmitters within the peripheral and central nervous system. As is the case for traditional neurotransmitters, injury-induced up-regulated chemokines are found within synaptic vesicles. Chemokines released after depolarization of the cell membrane can then act on other chemokine receptor-bearing neurons, glia, or immune cells. Because up-regulation of chemokines and their receptors may be one of the mechanisms that directly or indirectly contribute to the development and maintenance of chronic pain, these molecules may then represent novel targets for therapeutic intervention in chronic pain states. In his landmark treatise Sir Charles Scott Sherrington proposed the concept that pain is the evolved response to a potentially harmful, noxious stimulus (1). An example would be placing your hand on a hot iron and the resulting sensation of pain, which produces almost immediate withdrawal, thereby preventing tissue damage. This conscious perception of pain is the result of activity in a set of well defined neural pathways that start with the primary afferent neurons. These pseudounipolar neurons are responsible for the transmission of pain (''nociceptors'') and have unmyelinated or lightly myelinated axons. The cell bodies of nociceptors are found in the dorsal root ganglia (DRG). Nociceptors have both a peripheral connection that innervates potentially diseased or traumatized nerves, muscles, tendons, organs, and epithelia, and a centrally projecting axon that enters the central nervous system. This central axon conveys ''nociceptive'' information to second-order neurons in the dorsal horn of the spinal cord. Neural connections from the dorsal horn to the thalamus, and from there to the cortex, relay this noxious information to higher centers of conscious experience (Fig. 1). The central axons of primary afferent nociceptive neurons also provide information to polysynaptic spinal cord interneurons, which are essential for the initiation of the nociceptive withdrawal reflex. These neurons trigger motor reflexes that are important in the avoidance of potentially harmful ...

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Pain as the presenting symptom of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)

Cited by 43 publications

References 20 publications

Clinical and electrophysiological correlates of TTRala71 amyloid neuropathy

Clinical and electrophysiological correlates of TTRala71 amyloid neuropathy

Fatigue, Pain, Anxiety and Depression in Guillain-Barré Syndrome and Chronic Inflammatory Demyelinating Polyradiculoneuropathy

Chemokines and the pathophysiology of neuropathic pain

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