Pathology of Peripheral Neuron Cell Bodies

Groves, Michael J.; Salvatore, Francesco

doi:10.1016/b978-0-7216-9491-7.50034-x

Cited by 17 publications

(12 citation statements)

References 480 publications

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“…The reported incidence for vacuolization of sensory neurons varies among different studies depending on the chemical or pathological condition being investigated, but previously reported morphometric data have shown that frequencies of vacuolated cells can range from relatively high (>10% of total cells, as in the case of NMDA antagonist administration [Auer and Coulter 1994]), to relatively low (1% to 2% of total cells, as in the case of nerve transection [Groves et al 1997]). The data from our current study revealed that the frequency of vacuolated neurons/neurons counted was much lower (between 0.086% and 0.7%) (Table 1) than reports of other studies that made similar vacuolar frequency calculations under different pathological conditions (Groves and Scaravilli 2005). This low incidence is similar to that reported by Groves et al (1997) under conditions of nerve-crush injuries (where vacuole frequencies were as low as 0.09%).…”

Section: Discussionsupporting

confidence: 80%

“…Cytoplasmic vacuolation of sensory neurons is a striking finding that has been reported to occur in the dorsal root ganglia following exposure to several toxic agents (Beiswanger et al 1993; Cavaletti et al 2007; Jaatinen et al 1994; Melli et al 2008), and in diabetes mellitus (Kamiya et al 2006), traumatic axonal injury (Groves et al 1997), and aging (Groves and Scaravilli 2005). They also have been seen at very low incidences in normal animals (Groves and Scaravilli 2005). In this report, we demonstrated that cytoplasmic vacuoles may also develop within neurons of the dorsal root ganglia as a result of organophosphate-induced delayed neurotoxicity (OPIDN).…”

Section: Introductionmentioning

confidence: 99%

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Vacuolation of Sensory Ganglion Neuron Cytoplasm in Rats with Long-term Exposure to Organophosphates

Rogers-Cotrone¹,

Burgess²,

Hancock³

et al. 2010

Toxicol Pathol

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Cytoplasmic vacuolation of sensory neurons has been reported to occur within the dorsal root ganglia in studies investigating various neuropathic conditions including the effects of neurotoxic chemicals. In this study, we investigated this lesion in adult (98-119 days old) male Long-Evans rats, after multiple exposures to two organophosphates (tri-ortho-tolyl phosphate [TOTP] and chlorpyrifos) and the modifying effects of concurrent corticosterone. Tri-ortho-tolyl phosphate was administered by gavage (75, 150, or 300 mg/kg) every other day between days 14 and 28 and between days 49 and 63, chlorpyrifos (60 mg/kg) was administered subcutaneously on days 7 and 42, and corticosterone was provided in the drinking water throughout the study at a concentration of 400 microg/mL. Although relatively uncommon, there was an increase in frequency of cytoplasmic vacuoles seen in treatment groups having multiple exposures to TOTP. They were characterized as peripherally located, single-limiting membrane-bound structures in the neuronal perikarya. There was no associated cell death, even when vacuoles were large. This is the initial report of an association of this change following exposure to neurotoxic organophosphates.

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Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Vacuolation of Sensory Ganglion Neuron Cytoplasm in Rats with Long-term Exposure to Organophosphates

Rogers-Cotrone¹,

Burgess²,

Hancock³

et al. 2010

Toxicol Pathol

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“…They act as signal initiators in all reflex responses, and constitute an indispensible component for the correct function of the nervous system. Multiple insults can cause damage or disease in sensory neurons, such as traumatic injury [1], infection, toxin exposure, metabolic disease, immune system disorders, cancer and chemotherapy [2] and heredity [3, 4]. The subsequent cellular dysfunction caused by such insults is associated with many disorders ranging from abnormal sensation, numbness and pain to loss of coordination in voluntary movement [2–4].…”

Section: Introductionmentioning

confidence: 99%

Derivation of sensory neurons and neural crest stem cells from human neural progenitor hNP1

et al. 2013

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Although sensory neurons constitute a critical component for the proper function of the nervous system, the in vitro differentiation of functional sensory neurons from human stem cells has not yet been reported. This study presents the differentiation of sensory neurons (SNs) from a human neural progenitor cell line, hNP1, and their functional maturation in a defined, in vitro culture system without murine cell feeder layers. The SNs were characterized by immunocytochemistry and their functional maturation was evaluated by electrophysiology. Neural crest (NC) precursors, as one of the cellular derivatives in the differentiation culture, were isolated, propagated, and tested for their ability to generate sensory neurons. The hSC-derived SNs, as well as the NC precursors provide valuable tools for developing in vitro functional systems that model sensory neuron-related neural circuits and for designing therapeutic models for related diseases.

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“…Despite widespread macrophage infiltration, sural nerve was relatively preserved, a fact accounting for the absence of electrophysiological alterations. In short, we interpret that the brunt of the pathology, combining extensive and primary de‐remyelination with secondary axonal degeneration and areas of nerve ischemia, relied on spinal nerves, such pathology implying double consequences: (1) reparative changes including dark myelinated fibers and peripheral neuron cell body chromatolysis; and (2) degenerative changes manifested as axonal degeneration in more distal nerve trunks ( Spencer and Thomas, 1974; Groves and Scaravilli, 2005 ) . Although it is well established that the pathology of GBS is heterogeneous ( Honavar et al, 1991 ) , the extreme proximal to distal variability in nerve pathology described here has been exceptionally documented ( Kanda et al, 1989; Berciano et al, 2000 ) and calls for caution in interpreting nerve pathology when sampling is limited to either proximal or distal nerve trunks.…”

Section: Discussionmentioning

confidence: 99%

Severe Guillain‐Barré syndrome: sorting out the pathological hallmark in an electrophysiological axonal case

Berciano¹,

García²,

Villagra

et al. 2009

J Peripheral Nervous Sys

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We describe a clinicopathological study of a patient presenting with severe and electrophysiological axonal Guillain-Barré syndrome (GBS). An 83-year-old man had a 2-day history of distal acroparesthesias and ascending weakness culminating in quadriplegia, the patient dying 1 month after onset. On day 3, motor conduction velocity (MCV) and distal motor latency values were normal or minimally delayed; most F waves were present with latencies normal or barely delayed. Compound muscle action potential (CMAP) amplitudes were variably reduced. On day 10, there was reduction of CMAPs with relative preservation of MCV. On histological study, the density of myelinated fibers was normal in L5 ventral and dorsal roots, where outstanding lesions included dark fibers, scattered macrophage infiltration, and occasional images of de-remyelination or axonal degeneration. In the fifth spinal nerve, there was widespread loss of myelinated fibers with focal areas showing almost complete fiber loss and variable fascicular combination of extensive de-remyelination and axonal degeneration. Wallerian-like degeneration predominated in femoral and sciatic nerves. Peripheral neuron cell bodies showed central chromatolysis. We conclude that the pathological hallmark of this electrophysiological axonal GBS case is extensive but variable de-remyelination of proximal nerve trunks with superimposed nerve ischemia and axonal degeneration.

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Pathology of Peripheral Neuron Cell Bodies

Cited by 17 publications

References 480 publications

Vacuolation of Sensory Ganglion Neuron Cytoplasm in Rats with Long-term Exposure to Organophosphates

Vacuolation of Sensory Ganglion Neuron Cytoplasm in Rats with Long-term Exposure to Organophosphates

Derivation of sensory neurons and neural crest stem cells from human neural progenitor hNP1

Severe Guillain‐Barré syndrome: sorting out the pathological hallmark in an electrophysiological axonal case

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