Detection of atrophy of dorsal root ganglion with 3‐T magnetic resonance neurography in sensory ataxic neuropathy associated with Sjögren's syndrome

Yoshida, Takeshi; Sueyoshi, Takeshi; Suwazono, Shugo; Kinjo, Mitsuyo; Nodera, Hiroyuki

doi:10.1111/ene.13647

Cited by 3 publications

(8 citation statements)

References 4 publications

(5 reference statements)

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“…The spectrum of the disease may be caused by environmental agents that lead to epigenetic phenomena working on diverse and complex mechanisms of organ injuries, such as vasculitis and lymphocytic infiltration [90,91,92]. In addition, the changes in SS patients in the CNS and PNS (such as in the dorsal spinal cord and the dorsal ganglion roots), including autonomic dysfunction, diffuse decreases in white matter, and loss of gray matter in the hippocampal area, may influence peripheral organ function and induce neurological symptoms [93,94,95].…”

Section: Autoimmunity Neuropathy and Chronic Painmentioning

confidence: 99%

“…It is interesting to note that structures that are altered in the CNS, PNS, exocrine glands, and cornea (based on image exams) of SS patients are also sensitive to changes in the KP caused by trauma or ischemic damage (Table 1). These observations suggest that common inflammatory events are shared in autoimmune and non-immune inflammatory diseases, such as the synapses of the sensorial fibers, in the dorsal ganglion root, hippocampus, thalamus, and LFU [2,12,13,20,29,40,53,93,105,106,107,108] (Table 1). Those locations must be investigated in future studies addressing the anatomic correlations of clinical and biochemical changes in SS.…”

Section: Autoimmunity Neuropathy and Chronic Painmentioning

confidence: 99%

“…A loss or damage of nerve fibers, dorsal root ganglionitis, nerve vasculitis, and reduction of the CNS matter can be observed in imaging exams, such as magnetic resonance images (MRIs) or skin biopsies of SS patients; they are implicated in the underlying mechanisms and they could potentially function as diagnostic markers of neurological manifestations of SS [38,93,94,109]. For example, cognitive impairment in SS patients is associated with antibodies against the subtype 2 of the N-methyl aspartate receptor (NR2) (anti-NR2 antibodies) in the cerebrospinal fluid (CSF) mediating hippocampal gray matter atrophy, as observed by MRI [40].…”

Section: Autoimmunity Neuropathy and Chronic Painmentioning

confidence: 99%

“…The NR2 subtype NMDA receptor is ubiquitously distributed throughout the brain, with an unusually high density in the hippocampus [185]. The hippocampus is a brain structure that is linked to the autonomous nervous system, with critical importance for memory formation and learning, and it is also affected in mood disorders and in SS [93,94,186,187]. Likewise, the N-methyl aspartate receptor 2B (NR2B) subunit of the NMDA receptor is widespread in the dorsal root ganglion and it may mediate peripheral sensitization and visceral pain [188].…”

Section: Kp and Neurological Manifestationsmentioning

confidence: 99%

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Neurological and Inflammatory Manifestations in Sjögren’s Syndrome: The Role of the Kynurenine Metabolic Pathway

Oliveira

Fantucci

Adriano

et al. 2018

IJMS

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For decades, neurological, psychological, and cognitive alterations, as well as other glandular manifestations (EGM), have been described and are being considered to be part of Sjögren’s syndrome (SS). Dry eye and dry mouth are major findings in SS. The lacrimal glands (LG), ocular surface (OS), and salivary glands (SG) are linked to the central nervous system (CNS) at the brainstem and hippocampus. Once compromised, these CNS sites may be responsible for autonomic and functional disturbances that are related to major and EGM in SS. Recent studies have confirmed that the kynurenine metabolic pathway (KP) can be stimulated by interferon-γ (IFN-γ) and other cytokines, activating indoleamine 2,3-dioxygenase (IDO) in SS. This pathway interferes with serotonergic and glutamatergic neurotransmission, mostly in the hippocampus and other structures of the CNS. Therefore, it is plausible that KP induces neurological manifestations and contributes to the discrepancy between symptoms and signs, including manifestations of hyperalgesia and depression in SS patients with weaker signs of sicca, for example. Observations from clinical studies in acquired immune deficiency syndrome (AIDS), graft-versus-host disease, and lupus, as well as from experimental studies, support this hypothesis. However, the obtained results for SS are controversial, as discussed in this study. Therapeutic strategies have been reexamined and new options designed and tested to regulate the KP. In the future, the confirmation and application of this concept may help to elucidate the mosaic of SS manifestations.

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Section: Autoimmunity Neuropathy and Chronic Painmentioning

confidence: 99%

Section: Autoimmunity Neuropathy and Chronic Painmentioning

confidence: 99%

Section: Autoimmunity Neuropathy and Chronic Painmentioning

confidence: 99%

Section: Kp and Neurological Manifestationsmentioning

confidence: 99%

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Neurological and Inflammatory Manifestations in Sjögren’s Syndrome: The Role of the Kynurenine Metabolic Pathway

Oliveira

Fantucci

Adriano

et al. 2018

IJMS

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“…It is interesting to notice that the same structures that are altered in image exams of SS patients compared to control individuals are those where the TKP has shown to be more sensitive to handle in experimental studies, as synapses of the sensorial fibers, at the dorsal ganglion root, hippocampus, thalamus and LFU [2,12,13,27,39,77,[90][91][92][93][94][95] (Table 2). [94,98] Increase in kynurenine in salivary gland after ductal ligation, LG atrophy due to tryptophan deprivation [90,99] The concept implicit in the neuroimmunendocrine network predicts that cellular and molecular communication among those three systems are responsible for the homeostasis of the body organs; and a disruption in this network take part in the mechanism of the diseases [100][101][102][103].…”

Section: B Ss and The Mechanisms Of Neurological Manifestationsmentioning

confidence: 99%

Neurologic and Inflammatory Manifestations in Sjögren’s Syndrome: The Role of Tryptophan/kynurenine Pathway

Oliveira¹,

Fantucci²,

Adriano³

et al. 2018

Preprint

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For decades, neurologic and other extra glandular manifestations have been described in Sjögren’s syndrome (SS). More recently, neuropathic, psychological and cognitive alterations are being considered part of the disease. The lacrimal glands (LG), the ocular surface (OS), salivary glands (SG) and the central nervous system (CNS) are integrated to modulate the autonomic functions and, not just those organs, but also the hippocampus, which is linked to the autonomic nervous system, and modulate behavior responses appears to be compromised in the SS. Recent studies confirm that the tryptophan/kynurenine pathway (TKP) can be stimulated by interferon-γ (IFN-γ) and other cytokines, activating the indoleamine-pyrrole 2,3-dioxygenase (IDO) in SS. This pathway interferes on serotonergic and glutamatergic neurotransmission, mostly in the hippocampus, and other structures of the CNS. Although not demonstrated, it is plausible that this constant interference induces clinical signs of SS, and contributes to the discrepancy between symptoms and signs, towards manifestations of hyperalgesia and depression in patients with SS. Therapeutic strategies are being reexamined and new options designed and tested to regulate the involved steps of the TKP. In the future, the application of this concept may offer a clue to the mosaic of manifestations of SS.

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Practical diagnostic tips for the Sjögren Clinic: pearls, myths and mistakes

Brito-Zerón

Retamozo

Flores-Chávez³

et al. 2022

Clinical and Experimental Rheumatology

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More than 90 years have passed since Hendrik Sjögren began to consider that behind the dryness that several of his patients presented, there could be a systemic disease potentially linked to abnormal immune responses. For many years, the disease was mostly considered a minor syndrome compared with other systemic autoimmune diseases such as systemic lupus erythematosus (SLE), systemic sclerosis (SSc) and vasculitis, and advances in its understanding were slow and little recognised. The irruption of new technologies at the end of the 20th century rapidly promoted the development of international projects with a wide impact and diffusion. In the last 20 years, a significant improvement has been achieved in epidemiological determinants, pathogenic mechanisms, diagnostic accuracy, and a standardised therapeutic approach for patients with Sjögren's syndrome (SS). These developments have provided the tools for an early diagnosis and personalised management for most patients. However, a significant number of early myths and ongoing controversies are still making the appropriate management of SS difficult in daily clinical practice. This review provides a selection of pearls, myths, and mistakes that may serve as practical diagnostic tips for the Sjögren Clinic in four specific scenarios: defining the appropriate epidemiological background, enabling the earliest diagnostic suspicion as possible, improving the systemic characterisation of the disease, and designing an optimal follow-up of patients.

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Detection of atrophy of dorsal root ganglion with 3‐T magnetic resonance neurography in sensory ataxic neuropathy associated with Sjögren's syndrome

Cited by 3 publications

References 4 publications

Neurological and Inflammatory Manifestations in Sjögren’s Syndrome: The Role of the Kynurenine Metabolic Pathway

Neurological and Inflammatory Manifestations in Sjögren’s Syndrome: The Role of the Kynurenine Metabolic Pathway

Neurologic and Inflammatory Manifestations in Sjögren’s Syndrome: The Role of Tryptophan/kynurenine Pathway

Practical diagnostic tips for the Sjögren Clinic: pearls, myths and mistakes

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Detection of atrophy of dorsal root ganglion with 3‐T magnetic resonance neurography in sensory ataxic neuropathy associated with Sjögren's syndrome

Cited by 3 publications

References 4 publications

Neurological and Inflammatory Manifestations in Sjögren’s Syndrome: The Role of the Kynurenine Metabolic Pathway

Neurological and Inflammatory Manifestations in Sjögren’s Syndrome: The Role of the Kynurenine Metabolic Pathway

Neurologic and Inflammatory Manifestations in Sj&ouml;gren&rsquo;s Syndrome: The Role of Tryptophan/kynurenine Pathway

Practical diagnostic tips for the Sjögren Clinic: pearls, myths and mistakes

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Product

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Neurologic and Inflammatory Manifestations in Sjögren’s Syndrome: The Role of Tryptophan/kynurenine Pathway