We sought an optimal method for targeted delivery into dorsal root ganglia (DRGs) for experimental studies, in terms of precision of delivery and avoidance of behavioral disturbances. We examined three approaches for injection into rat DRGs: percutaneous injection without surgical exposure, injection after deep exposure, and injection following deep exposure and partial laminectomy. Coomassie blue and Fast Blue were injected into DRGs for validation. At necropsy, the spread of Coomassie blue and Fast Blue was investigated under stereomicroscope and fluorescent microscope, respectively. We found that percutaneous approach did not provide any successful DRG injections. Deep exposure prior to intraganglionic injection provided variable results, but intraganglionic injection after deep exposure plus partial laminectomy was successful in 100% of attempts. Our subsequent skeletal analysis showed that the anatomical location of DRG is not compatible with successful DRG injection without surgical exposure. Neither of the methods using surgical exposure caused behavioral disturbances. Based on these results we conclude that partial laminectomy offers the most precise method of injecting DRG and does not produce behavioral evidence of nerve damage. Intraganglionic injection after deep exposure alone is less predictable, while percutaneous approaches only allow injection in the peripheral nerve.
BACKGROUND Injury of a spinal nerve or dorsal root ganglion (DRG) during selective spinal nerve blocks is a potentially serious complication that has not been adequately investigated. Our hypothesis was that local anesthetic injection into these structures may result in an inflammatory response and hyperalgesia. METHODS We evaluated inflammatory and behavioral responses after injection of 4 μL lidocaine or saline into the L5 spinal nerve or DRG of rats after partial laminectomy. Behavioral testing was performed before and after surgery to examine hyperalgesia in response to nociceptive mechanical stimulation of the foot. DRGs were harvested and stained, and rings of immunoreactive glial cells around neurons were counted. RESULTS Animals demonstrated hyperalgesia on the ipsilateral paw up to 4 days after lidocaine injection into the DRG but not after injection into the spinal nerve. The number of glial fibrillary acid protein immunopositive glial cell rings, which represent activation of satellite cells, significantly increased in DRGs after injection of lidocaine into either the DRG or the spinal nerve. The number of glial fibrillary acid protein-positive cells in the lidocaine-injected group was significantly larger than in the saline-injected group. Sporadic OX-42 immunopositive cells, which represent activated microglia, were also seen in lidocaine-injected DRGs. Testing for Pan-T expression, which labels activated T lymphocytes, showed no positive cells. CONCLUSIONS Lidocaine injection into the DRG may produce hyperalgesia, possibly due to activation of resident satellite glial cells. In a clinical setting, local anesthetic injection into the DRG should be avoided during selective spinal nerve blocks.
The enzyme calcium/calmodulin-dependent protein kinase II (CaMKII) is associated with memory and its α isoform is critical for development of activity-induced synaptic changes. Therefore, we hypothesized that CaMKII is involved in altered function of dorsal root ganglion (DRG) neurons after neuronal injury. To test this hypothesis, Sprague–Dawley rats were made hyperalgesic by L5 and L6 spinal nerve ligation (SNL), and changes in total phosphorylated and unphosphorylated CaMKII (tCaMKII) and phosphorylated form of its α isoform (pCaMKIIα) were analyzed using immunochemistry in different subpopulations of DRG. SNL did not induce any changes in tCaMKII between experimental groups, while the overall percentage of pCaMKIIα-positive neurons in injured L5 DRG SNL (24.8%) decreased significantly when compared to control (41.7%). SNL did not change the percentage of pCaMKIIα/N52 colabeled neurons but decreased the percentage of N52-negative nonmyelinated neurons that expressed pCaMKIIα from 27% in control animals to 11% after axotomy. We also observed a significant decrease in the percentage of small nonpeptidergic neurons labeled with IB4 (37.6% in control vs. 4.0% in L5 SNL DRG), as well as a decrease in the percentage of pCaMKIIα/IB4 colabeled neurons in injured L5 DRGs (27% in control vs. 1% in L5 DRG of SNL group). Our results show that reduction in pCaMKIIα levels following peripheral injury is due to the loss of IB4-positive neurons. These results indicate that diminished afferent activity after axotomy may lead to decreased phosphorylation of CaMKIIα.
The sodium leak channel, a Na+‐permeable, nonselective cation channel, is widely expressed in the nervous system, contributing a basal Na+‐leak conductance and regulating neuronal excitability. A 3‐year‐old girl, heterozygous for a de novo missense mutation in NALCN (c.956C>T; p.Ala319Val) predicted to be deleterious, presented from birth with: stimulus‐induced, episodic contractures of the limbs and face with associated respiratory distress; distal arthrogryposis; severe axial hypotonia; and severe global developmental delay (CLIFAHDD syndrome). In infancy, she manifested a reversed sleep‐wake rhythm, nocturnal life‐threatening respiratory rhythm disturbances with central apnea. Sevoflurane sensitivity caused respiratory depression and cardiac arrest.
More women are applying, enrolling and graduating from the University of Split School of Medicine. Women also perform statistically better on entrance exam and have better graduation grades, yet they remain a minority in faculty and leadership positions. A review of county-wise employment statistics revealed that women were more frequently unemployed and less likely to specialize in this study.
One of the unresolved questions in neuropathic pain research is whether we can prevent or reverse mechanical hyperalgesia by rhizotomy or ganglionectomy. However, one of the obstacles in answering that question is lack of a standardized surgical procedure used in experimental ganglionectomy. We tested the hypothesis that laminectomy performed during ganglionectomy induces lumbar column deformity. We further examined whether spinal deformity is a source of pain-related behavior. Five conditions were studied. Fifth and sixth lumbar (L5 and L6) ganglionectomy were performed in rats using either minimal or extensive laminectomy technique. Two other groups had minimal and extensive laminectomy without ganglionectomies. A final control group had no surgery. Sensory responsiveness of the plantar aspect of the hind paw was repeatedly tested, and a plain radiograph in anteroposterior projection was made to assess the extent of deformity by measurement of deformity angles. Hyperalgesia resulted in groups with extensive laminectomy regardless of performance or absence of ganglionectomy, while in groups with minimal laminectomy there was no increase in pain-related behavior. Lateral deformity of the spine was observed in rats with or without ganglionectomy, confirming that laminectomy can produce deformity. The extent of deformity was more pronounced in rats exposed to the extensive laminectomy. Our results indicate that laminectomy can produce spine deformity and that there is a direct relationship between the extent of laminectomy and the development of mechanical hypersensitivity. The data presented suggest that there is a need for standardization of laminectomy procedure in rat experimental pain models.
From the beginning of SARS-CoV-2 virus pandemic, it was clear that respiratory symptoms are often accompanied with neurological symptoms. Neurological manifestations can occur even after mild forms of respiratory disease, and neurological symptoms are very often associated with worsening of the patient’s condition. The aim of this study was to show abnormal brain neuroimaging findings evaluated by MRI in patients after SARS-CoV-2 infection and neurological symptoms. Methods: Sixteen patients after mild forms of SARS-CoV-2 infection, twenty-three patients after moderate forms of SARS-CoV-2 infection as well as sixteen healthy participants in the control group underwent MRI 3T brain scan. All subjects in the SARS-CoV-2 group had small, punctuate, strategically located and newly formed hyperintense lesions on T2 and FLAIR sequences. New lesions were formed more often in the bilateral frontal subcortical and bilateral periventricular, correlated with the severity of the clinical picture. These changes indicate an example of silent cerebrovascular disease related to SARS-CoV-2 and once again emphasize the neurotropism of the virus.
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