Peripheral nerve ischemia: Part 2. Accumulation of organelles

Korthals, Jan K.; Korthals, Maria A.; Wı́sniewski, Henryk M.

doi:10.1002/ana.410040603

Cited by 53 publications

(10 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In rare cases, there are a few swollen dark axons with accumulation of organelles and sometimes a central bundle of filaments. These features were first reported in experimental studies by Korthals et al . (1978 ) and then by Nukada and Dyck (1984 ; 1987 ) .…”

Section: Discussionsupporting

confidence: 64%

Combined nerve and muscle biopsy in the diagnosis of vasculitic neuropathy. A 16‐year retrospective study of 202 cases

Vital

Canron

et al. 2006

J Peripheral Nervous Sys

121

View full text Add to dashboard Cite

We reviewed 202 biopsies performed on patients with suspected vasculitic neuropathy, of which 24 Churg-Strauss cases are studied separately. Specimens from the superficial peroneal nerve and peroneus brevis muscle were taken simultaneously by one incision. Without taking into account constitutional signs, systemic involvement was present in 131 patients, whereas the remaining 47 corresponded to non-systemic patients with lesions limited to peripheral nervous system and adjoining muscles. Diagnosis of panarteritis nodosa or microscopic polyangiitis, according to the size of involved vessels, was attested by an infiltration of vessel walls by inflammatory cells associated with fibrinoid necrosis or sclerosis. Microvasculitis was diagnosed when inflammatory infiltration concerned small vessels with few or no smooth-muscle fibers and without any necrosis. Microvasculitis was present in 11 of 46 non-systemic cases, and this predominance is statistically significant. Isolated perivascular cell infiltrates in the epineurium were considered not significant but allowed the diagnosis of 'probable vasculitis' if associated with at least one of the following features: regenerating small vessels, endoneurial purpura, asymmetric nerve fiber loss, and/or asymmetric acute axonal degeneration. Necrotizing vasculitis was visible in 60 cases: in nerve (16 cases), in muscle (19 cases), and both (25 cases). Microvasculitis was present in 25 cases: in nerve (19 cases), muscle (four cases), or both (two cases). Moreover, granulomatous vasculitis was found in the nerve of one non-systemic patient presenting also sarcoid granulomas in muscle. There were 24 'probable vasculitis' and 68 negative cases. Muscle biopsy improved the yield of definite vasculitis by 27%.

show abstract

Section: Discussionsupporting

confidence: 64%

Combined nerve and muscle biopsy in the diagnosis of vasculitic neuropathy. A 16‐year retrospective study of 202 cases

Vital

Canron

et al. 2006

J Peripheral Nervous Sys

121

View full text Add to dashboard Cite

show abstract

“…We found nodal lengthening and other acute structural changes after only a few minutes of compression, which appear to explain the paranodal demyelination and axonal degeneration that are characteristic of nerve compression injury. The structural alterations that develop during acute compression are different in their time of appearance and in type from those induced by ischemia (10)(11)(12)(13)(14). We infer that the structural changes are due to stress forces rather than ischemia.…”

mentioning

confidence: 81%

Structural alterations of nerve during cuff compression.

Dyck

Lais

Giannini

et al. 1990

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

View full text Add to dashboard Cite

Whether compression nerve injury is due to ischemia, direct mechanical injury, or both remains unsettled. To assess structural changes of nerve during compression, peroneal nerves of rats were compressed at various pressures for different times, and the structural alterations were stopped by simultaneous in situ and perfusion fixation. The structural changes observed during a few minutes of compression cannot be explained by ischemic injury because the pathologic alterations characteristic of ischemia take many hours to develop and in any case are different from the ones found here. The pressure-and time-related structural changes observed in the present study under the cuffwere (i) decrease in fascicular area and increase in fiber density due to expression of endoneurial fluid; (i) compression and expression of axoplasm, sometimes to the point of fiber transection; (iii) lengthening of internodes; and (iv) obscuration of nodes of Ranvier due to cleavage and displacement of myelin and overlapping of nodes by displaced loops of myelin. At the edges of the cuff the changes were (i) increase of fascicular area probably from expressed endoneurial fluid; (ii) widening of nodal gaps, perhaps mainly from translocated axonal fluid; and (iii) disordered structure of axoplasm. We suggest that the process of paranodal demyelination and axonal transection are linked, occur during the act of compression, and are due to shear forces. The initial event is expression of endoneurial fluid, followed by compression and expression of axoplasm and cleavage and displacement oflayers of myelin. Conceivably, with prolonged cuff compression ischemic injury might be found to be superimposed on mechanical injury.In humans, nerve compression injury may follow use of a tourniquet at too high a pressure, for too long a time, or from improper application; lying in one position without moving for a long time (as may occur during anesthesia, inebriation, or coma) with a limb nerve compressed against bone by a protruding ridge or hard surface; or prolonged sitting with the legs crossed or prolonged leaning on the elbows (1, 2). Excellent recovery is expected after compression injury, whereas it is usually delayed and faulty after nerve transection. This difference in outcome is usually explained by conduction block and demyelination in the former and complete fiber degeneration and faulty regeneration in the latter (3-5).The mechanisms underlying nerve compression injury have usually been attributed to ischemia (6-8), to mechanical forces (9), or to both.In the present study the structural alterations of nerve during compression were stopped by simultaneous in situ and perfusion fixation, usually during short periods of compression. We found nodal lengthening and other acute structural changes after only a few minutes of compression, which appear to explain the paranodal demyelination and axonal degeneration that are characteristic of nerve compression injury. The structural alterations that develop during acute compression are different...

show abstract

“…Delays of up to 8 hours (and lack of oxygen during this delay) could have rendered the terminals ischemic or dystrophic. As noted above, axons in dystrophic conditions have an increased number of MVBs, presumably in response to such insults (Altick et al ., 2009; Schroer et al ., 1992), in addition to an increase in the number of other organelles, such as autophagosomes and mitochondria (Dixon, 1967; Einheber et al ., 2006; Korthals et al ., 1978; Marty and Peschanski, 1994; Matthews and Raisman, 1972; Wang et al ., 2006). In support of this notion, MVBs can rapidly form de novo (Chu-Wang and Oppenheim, 1980), apparently within minutes (Birks et al ., 1972; Piper and Luzio, 2001; Weldon, 1975), and the number of MVBs can increase significantly within hours of a mechanical insult or drug treatment (Altick et al ., 2009; Bresnahan, 1978; Claude et al ., 1982b).…”

Section: Distribution Of Mvbs In Neuronal Compartmentsmentioning

confidence: 99%

Multivesicular bodies in neurons: Distribution, protein content, and trafficking functions

Bartheld

Altick

2011

Progress in Neurobiology

176

157

View full text Add to dashboard Cite

SummaryMultivesicular bodies (MVBs) are intracellular endosomal organelles characterized by multiple internal vesicles that are enclosed within a single outer membrane. MVBs were initially regarded as purely prelysosomal structures along the degradative endosomal pathway of internalized proteins. MVBs are now known to be involved in numerous endocytic and trafficking functions, including protein sorting, recycling, transport, storage, and release. This review of neuronal MVBs summarizes their research history, morphology, distribution, accumulation of cargo and constitutive proteins, transport, and theories of functions of MVBs in neurons and glia. Due to their complex morphologies, neurons have expanded trafficking and signaling needs, beyond those of "geometrically simpler" cells, but it is not known whether neuronal MVBs perform additional transport and signaling functions. This review examines the concept of compartment-specific MVB functions in endosomal protein trafficking and signaling within synapses, axons, dendrites and cell bodies. We critically evaluate reports of the accumulation of neuronal MVBs based on evidence of stress-induced MVB formation. Furthermore, we discuss potential functions of neuronal and glial MVBs in development, in dystrophic neuritic syndromes, injury, disease, and aging. MVBs may play a role in Alzheimer's, Huntington's, and Niemann-Pick diseases, some types of frontotemporal dementia, prion and virus trafficking, as well as in adaptive responses of neurons to trauma and toxin or drug exposure. Functions of MVBs in neurons have been much neglected, and major gaps in knowledge currently exist. Developing truly MVB-specific markers would help to elucidate the roles of neuronal MVBs in intra-and intercellular signaling of normal and diseased neurons. KeywordsEndosome; Trafficking; Axonal Transport; Sorting; Release; Endocytosis; Degradation Definition of MVBs and scope of this reviewBased on their original discovery and historical tradition, MVBs are defined -as their name implies -by morphological criteria at the ultrastructural level. MVBs appear in ultrathin sections as spherical organelles characterized by a single outer ("limiting") membrane that Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Cooney et al., 2002). The small vesicles as well as the matrix, the lumenal space between the internal vesicles, are typically clear, but they can be of varying electron densities (Roizin et al., 1967). The internal vesicles can have heterogeneous sizes with a diameter of 50-100 nm, although they frequently are uniform in size, about 60-70 nm in...

show abstract

Peripheral nerve ischemia: Part 2. Accumulation of organelles

Cited by 53 publications

References 33 publications

Combined nerve and muscle biopsy in the diagnosis of vasculitic neuropathy. A 16‐year retrospective study of 202 cases

Combined nerve and muscle biopsy in the diagnosis of vasculitic neuropathy. A 16‐year retrospective study of 202 cases

Structural alterations of nerve during cuff compression.

Multivesicular bodies in neurons: Distribution, protein content, and trafficking functions

Contact Info

Product

Resources

About