ABSTRACT
This case-control study primarily compared the trigeminal nociceptive function, the intraoral somatosensory profile and possible structural nerve changes between diabetic peripheral neuropathy (DPN, n = 12) patients and healthy participants (n = 12). The nociceptive blink reflex (nBR) was recorded applying an electrical stimulation over the entry zone of the right supraorbital (V1R), infraorbital (V2R) and mental (V3R) and left infraorbital (V2L) nerves. The outcomes were: individual electrical sensory (I0) and pain thresholds (IP); root mean square (RMS), area-under-the-curve (AUC) and onset latencies of R2 component of the nBR. Furthermore, a standardized full battery of quantitative sensory testing (QST) and intraepidermal nerve fibre density (IENFD) or nerve fibre length density (NFLD) assessment were performed, respectively, on the distal leg and oral mucosa. As expected, all patients had altered somatosensory sensitivity and lower IENFD in the lower limb. DPN patients presented higher I0, IP, RMS and AUC values (p < 0.050), lower warm detection thresholds (WDT) (p = 0.004), higher occurrence of paradoxical heat sensation (PHS) (p = 0.040), and a lower intraoral NFLD (p = 0.048) than the healthy participants. In addition, the presence of any abnormal intraoral somatosensory finding was more frequent in the DPN patients when compared to the reference group (p = 0.013). Early signs of trigeminal nociceptive facilitation, intraoral somatosensory abnormalities and loss of intraoral neuronal tissue can be detected in DPN patients.
Subject(s)
Diabetic Neuropathies/pathology , Nerve Fibers/pathology , Sensation , Trigeminal Nerve/pathology , Aged , Case-Control Studies , Electric Stimulation/methods , Female , Humans , Male , Middle AgedABSTRACT
Duchenne muscular dystrophy (DMD) is a recessive X-linked lethal condition which affects a boy in every 3300 births. It is caused by the absence of dystrophin, a protein occurring especially within the musculoskeletal system and in neurons in specific regions of the central nervous system (CNS). Growth hormone (GH) inhibition is believed to decrease the severity of DMD and could perhaps be used in its treatment. However, the underlying pathological mechanism is not known. The golden retriever muscular dystrophy dog (GRMD) represents an animal model in the study of DMD. In this paper we investigated the morphological aspects of the adenohypophysis as well as the total number and size of GH-granulated cells using design-based stereological methods in a limited number of dystrophic and healthy golden retrievers. GH-cells were larger (32.4%) in dystrophic dogs than in healthy animals (p=0.01) and they occupied a larger portion (62.5%) of the adenohypophysis volume (p=0.01) without changes in either adenohypophysis volume (p=0.893) or total number of GH-granulated cells (p=0.869). With regard to ultrastructure, granulated cells possessed double-layer electron-dense granules which were evenly distributed in the cytosol. Furthermore, these granules in dystrophic animals occupied a larger proportion of GH-granulated cell volume (66.9%; p=0.008) as well as of all GH-cells in the whole pars distalis of adenohypophysis (77.3%; p=0.035), albeit IGF-1 serum concentration was lower in severe cases. This suggests difficulties in the GH secretion that might possibly be associated to dystrophin absence. In contrast to earlier reports, our data suggest that a lower IGF-1 concentration may be more related to a severe, as opposed to a benign, clinical form of muscular dystrophy.