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In this inaugural period, both in GBS and its animal model, experimental autoimmune neuritis, the outstanding pathological feature is inflammatory edema predominating in proximal nerve trunks, particularly spinal nerves, and possibly in preterminal nerve segments. Nerve trunks external to the subarachnoid angle possess epi\u2010 perineurium that is relatively inelastic and of low compliance. Here such edema can increase endoneurial fluid pressure that, when sufficiently critical, may stretch the perineurium and constrict transperineurial microcirculation, compromising blood flow and producing the potential for ischemic nerve injury, whose consequence is rapid partial or complete loss of nerve excitability. These histopathological features correlate well with electrophysiological and imaging findings reported in early GBS stages. Spinal nerve edema and ischemia help to understand the pattern of Wallerian\u2010like degeneration observed in the axonal form of GBS, predominating in motor spinal roots at their exit from the dura matter (spinal nerves) with centrifugal distribution in more distant motor nerve trunks, and centripetal extension to the distal portion of intrathecal roots. The similarity of initial pathogenic mechanisms between demyelinating and axonal forms of GBS explains why an early increase of serum biomarkers of axonal damage is detected in both forms. In conclusion, knowledge of the microscopic anatomy of the peripheral nervous system is an essential step for a reliable understanding of pathophysiological mechanisms operating in the early phase of any classic GBS subtype.<\/jats:p>","DOI":"10.1111\/neup.13006","type":"journal-article","created":{"date-parts":[[2024,10,1]],"date-time":"2024-10-01T06:14:56Z","timestamp":1727763296000},"page":"85-99","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Microscopical anatomy of the peripheral nervous system: An essential notion for understanding the pathophysiology of very early classic <scp>Guillain\u2010Barr\u00e9<\/scp> syndrome"],"prefix":"10.1111","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9261-9748","authenticated-orcid":false,"given":"Jos\u00e9","family":"Berciano","sequence":"first","affiliation":[{"name":"University of Cantabria, Service of Neurology, University Hospital \u201cMarqu\u00e9s de Valdecilla (IDIVAL)\u201d, and \u201cCentro de Investigaci\u00f3n Biom\u00e9dica en Red de Enfermedades Neurodegenerativas (CIBERNED)\u201d  Santander Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2024,9,30]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(08)70215-1"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(16)00339-1"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrneurol.2014.138"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1093\/ilar\/ilt054"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1529-8027.2011.00338.x"},{"key":"e_1_2_8_7_1","first-page":"1","article-title":"Very early Guillain\u2010Barr\u00e9 syndrome: A clinical\u2010electrophysiological and ultrasonographic study","volume":"5","author":"Berciano J","year":"2019","journal-title":"Clin Neurophysiol Pract"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1007\/s13760-021-01603-7"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00415-016-8204-2"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00415-020-10034-y"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.clineuro.2024.108131"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.1097\/00005792-194902010-00003"},{"key":"e_1_2_8_13_1","volume-title":"Handbuch der speziallen pathologischen Anatomie und Histologie. 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