This work is aimed at the study of the innervation of sweat glands with the aim of discriminating the pathophysiology of susceptible ganglionopathies from the pathophysiology of specific neuropathies of small fibers, as a model for the study of biopsy samples of patients affected by post-herpetic neuralgia (PHN) . The study concerns the presence / absence of sympathetic nerve fibers located near the sweat glands in the skin dermis of patients affected by PHN, analyzing samples taken from dermatomeres affected by the infection, and subsequently, comparing the data obtained with the data regards the density of epidermal innervation.The results obtained demonstrate that there is a dissociation between the maintenance of the sympathetic innervation of the sweat glands and the sensitive innervation of the epidermis. This observation is compatible with the hypothesis that the damage created by the virus to the sensitive fibers has its origin mainly in the sensory ganglion of the dorsal roots, where the reactivation of the latent virus occurs. The data obtained also confirm previous studies that demonstrated that the development of dynamic mechanical allodynia is independent of the extent of the axonal damage of the afferent sensitive fibers of small caliber present in the epidermis. In anatomopathological terms, the ganglionic origin of the sensory damage allows to classify the neuropathy that occurs during an episode of HZ (and which persists in case of post-herpetic neuralgia) as a sensory neuropathy with possible cell death.
Questo lavoro è finalizzato sullo studio dell’innervazione delle ghiandole sudoripare con l’obbiettivo di discriminare la fisiopatologia delle ganglionopatie sensitive dalla fisiopatologia delle neuropatie periferiche delle piccole fibre, utilizzando come modello per lo studio campioni bioptici di pazienti affetti da nevralgia post-erpetica (PHN). Lo studio concerne nell’osservazione della presenza/assenza delle fibre nervose simpatiche situate in prossimità delle ghiandole sudoripare nel derma della cute di pazienti affetti da PHN, analizzando campioni prelevati da dermatomeri colpiti dall’infezione, e successivamente, rapportando i dati ottenuti con i dati relativi alla densità dell’innervazione epidermica. I risultati ottenuti dimostrano che esiste una dissociazione tra il mantenimento dell’innervazione simpatica delle ghiandole sudoripare e l’innervazione sensitiva dell’epidermide. Tale osservazione è compatibile con l’ipotesi che il danno creato dal virus a carico delle fibre sensitive abbia la sua origine prevalentemente nel ganglio sensitivo delle radici dorsali, dove avviene la riattivazione del virus latente. I dati ottenuti confermano inoltre studi precedenti che avevano dimostrato come lo sviluppo di allodinia meccanica dinamica sia indipendente dall’entità del danno assonale delle fibre sensitive afferenti di piccolo calibro presenti nell’epidermide. In termini anatomopatologici, l’origine gangliare del danno sensitivo permette di classificare la neuropatia che si verifica durante un episodio di HZ (e che persiste in caso di nevralgia post-herpetica) come una neuropatia sensitiva con possibile morte cellulare.
Ruolo dello studio dell’innervazione delle ghiandole sudoripare nella discriminazione tra neuropatia periferica delle piccole fibre e ganglionopatia sensitiva: l’esempio dell’herpes zoster.
MARTINO, COSTANTINO FRANCESCO
2017/2018
Abstract
This work is aimed at the study of the innervation of sweat glands with the aim of discriminating the pathophysiology of susceptible ganglionopathies from the pathophysiology of specific neuropathies of small fibers, as a model for the study of biopsy samples of patients affected by post-herpetic neuralgia (PHN) . The study concerns the presence / absence of sympathetic nerve fibers located near the sweat glands in the skin dermis of patients affected by PHN, analyzing samples taken from dermatomeres affected by the infection, and subsequently, comparing the data obtained with the data regards the density of epidermal innervation.The results obtained demonstrate that there is a dissociation between the maintenance of the sympathetic innervation of the sweat glands and the sensitive innervation of the epidermis. This observation is compatible with the hypothesis that the damage created by the virus to the sensitive fibers has its origin mainly in the sensory ganglion of the dorsal roots, where the reactivation of the latent virus occurs. The data obtained also confirm previous studies that demonstrated that the development of dynamic mechanical allodynia is independent of the extent of the axonal damage of the afferent sensitive fibers of small caliber present in the epidermis. In anatomopathological terms, the ganglionic origin of the sensory damage allows to classify the neuropathy that occurs during an episode of HZ (and which persists in case of post-herpetic neuralgia) as a sensory neuropathy with possible cell death.È consentito all'utente scaricare e condividere i documenti disponibili a testo pieno in UNITESI UNIPV nel rispetto della licenza Creative Commons del tipo CC BY NC ND.
Per maggiori informazioni e per verifiche sull'eventuale disponibilità del file scrivere a: unitesi@unipv.it.
https://hdl.handle.net/20.500.14239/25046