Transverse myelitis caused by herpes zoster following COVID-19 vaccination: A case report.

BACKGROUND: Transverse myelitis (TM) is characterized by sudden lower extremity progressive weakness and sensory impairment, and most patients have a history of advanced viral infection symptoms. A variety of disorders can cause TM in association with viral or nonviral infection, vascular, neoplasia, collagen vascular, and iatrogenic, such as vaccination. Vaccination has become common through the global implementation against coronavirus disease 2019 (COVID-19) and reported complications like herpes zoster (HZ) activation has increased. CASE SUMMARY: This is a 68-year-old woman who developed multiple pustules and scabs at the T6-T9 dermatome site 1 wk after vaccination with the COVID-19 vaccine (Oxford/AstraZeneca ([ChAdOx1S{recombinant}]). The patient had a paraplegia aggravation 3 wk after HZ symptoms started. Spinal magnetic resonance imaging (MRI) showed transverse myelitis at the T6-T9 Level. Treatment was acyclovir with steroids combined with physical therapy. Her neurological function was slowly restored by Day 17. CONCLUSION: HZ developed after COVID-19 vaccination, which may lead to more severe complications. Therefore, HZ treatment itself should not be delayed. If neurological complications worsen after appropriate management, an immediate diagnostic procedure, such as magnetic resonance imaging and laboratory tests, will start and should treat the neurological complications.

Sec-O-glucosylhamaudol mitigates inflammatory processes and autophagy via p38/JNK MAPK signaling in a rat neuropathic pain model.

BACKGROUND: This study investigated the effect of intrathecal Sec-O-glucosylhamaudol (SOG) on the p38/c-Jun N-terminal kinase (JNK) signaling pathways, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-related inflammatory responses, and autophagy in a spinal nerve ligation (SNL)-induced neuropathic pain model. METHODS: The continuous administration of intrathecal SOG via an osmotic pump was performed on male Sprague-Dawley rats (n = 50) with SNL-induced neuropathic pain. Rats were randomized into four groups after the 7th day following SNL and treated for 2 weeks as follows (each n = 10): Group S, sham-operated; Group D, 70% dimethylsulfoxide; Group SOG96, SOG at 96 µg/day; and Group SOG192, SOG at 192 µg/day. The paw withdrawal threshold (PWT) test was performed to assess neuropathic pain. Western blotting of the spinal cord (L5) was performed to measure changes in the expression of signaling pathway components, cytokines, and autophagy. Additional studies with naloxone challenge (n = 10) and cells were carried out to evaluate the potential mechanisms underlying the effects of SOG. RESULTS: Continuous intrathecal SOG administration increased the PWT with p38/JNK mitogen-activated protein kinase (MAPK) pathway and NF-κB signaling pathway inhibition, which induced a reduction in proinflammatory cytokines with the concomitant downregulation of autophagy. CONCLUSIONS: SOG alleviates mechanical allodynia, and its mechanism is thought to be related to the regulation of p38/JNK MAPK and NF-κB signaling pathways, associated with autophagy during neuroinflammatory processes after SNL.

Antinociceptive effects of intrathecal cimifugin treatment: a preliminary rat study based on formalin test.

BACKGROUND: Cimifugin is one of the components of the root of Saposhnikovia divaricata. The extract derived from S. divaricata is traditionally used as an analgesic. This study was conducted to evaluate the analgesic effect of intrathecal cimifugin in the formalin test. METHODS: Male Sprague-Dawley rats (n = 20) were randomized into four groups for intrathecal administration of 70% dimethylsulfoxide and various doses of cimifugin (100 µg, 300 µg, and 1,000 µg). The typical flinch response after the injection of 5% formalin into the hind paw was assessed in two distinct phases: phase 1 until 10 min, and phase 2 from 10 min to 60 min. ED50 values were calculated via linear regression. RESULTS: Intrathecal cimifugin significantly reduced the flinch response in both phases of the formalin test. Significant antinociceptive effects of cimifugin were found with the dose of 300 µg in phase 1 and the dose of 100 µg in phase 2. The ED50 value (95% confidence intervals) of intrathecal cimifugin was 696.1 (360.8-1,342.8) µg during phase 1 and 1,242.8 (42.0-48,292.5) µg during phase 2. CONCLUSIONS: Intrathecal cimifugin has an antinociceptive effect against formalin-induced pain. Cimifugin has an anti-inflammatory effect at low concentrations, and non-inflammatory analgesic effect at higher concentrations.

Gabexate mesilate ameliorates the neuropathic pain in a rat model by inhibition of proinflammatory cytokines and nitric oxide pathway via suppression of nuclear factor-κB.

BACKGROUND: This study examined the effects of gabexate mesilate on spinal nerve ligation (SNL)-induced neuropathic pain. To confirm the involvement of gabexate mesilate on neuroinflammation, we focused on the activation of nuclear factor-κB (NF-κB) and consequent the expression of proinflammatory cytokines and inducible nitric oxide synthase (iNOS). METHODS: Male Sprague-Dawley rats were used for the study. After randomization into three groups: the sham-operation group, vehicle-treated group (administered normal saline as a control), and the gabexate group (administered gabexate mesilate 20 mg/kg), SNL was performed. At the 3rd day, mechanical allodynia was confirmed using von Frey filaments, and drugs were administered intraperitoneally daily according to the group. The paw withdrawal threshold (PWT) was examined on the 3rd, 7th, and 14th day. The expressions of p65 subunit of NF-κB, interleukin (IL)-1, IL-6, tumor necrosis factor-α, and iNOS were evaluated on the 7th and 14th day following SNL. RESULTS: The PWT was significantly higher in the gabexate group compared with the vehicle-treated group (P < 0.05). The expressions of p65, proinflammatory cytokines, and iNOS significantly decreased in the gabexate group compared with the vehicle-treated group (P < 0.05) on the 7th day. On the 14th day, the expressions of p65 and iNOS showed lower levels, but those of the proinflammatory cytokines showed no significant differences. CONCLUSIONS: Gabexate mesilate increased PWT after SNL and attenuate the progress of mechanical allodynia. These results seem to be involved with the anti-inflammatory effect of gabexate mesilate via inhibition of NF-κB, proinflammatory cytokines, and nitric oxide.

Effect of sec-O-glucosylhamaudol on mechanical allodynia in a rat model of postoperative pain.

BACKGROUND: This study was performed in order to examine the effect of intrathecal sec-O-glucosylhamaudol (SOG), an extract from the root of the Peucedanum japonicum Thunb., on incisional pain in a rat model. METHODS: The intrathecal catheter was inserted in male Sprague-Dawley rats (n = 55). The postoperative pain model was made and paw withdrawal thresholds (PWTs) were evaluated. Rats were randomly treated with a vehicle (70% dimethyl sulfoxide) and SOG (10 µg, 30 µg, 100 µg, and 300 µg) intrathecally, and PWT was observed for four hours. Dose-responsiveness and ED50 values were calculated. Naloxone was administered 10 min prior to treatment of SOG 300 µg in order to assess the involvement of SOG with an opioid receptor. The protein levels of the δ-opioid receptor, κ-opioid receptor, and µ-opioid receptor (MOR) were analyzed by Western blotting of the spinal cord. RESULTS: Intrathecal SOG significantly increased PWT in a dose-dependent manner. Maximum effects were achieved at a dose of 300 µg at 60 min after SOG administration, and the maximal possible effect was 85.35% at that time. The medial effective dose of intrathecal SOG was 191.3 µg (95% confidence interval, 102.3-357.8). The antinociceptive effects of SOG (300 µg) were significantly reverted until 60 min by naloxone. The protein levels of MOR were decreased by administration of SOG. CONCLUSIONS: Intrathecal SOG showed a significant antinociceptive effect on the postoperative pain model and reverted by naloxone. The expression of MOR were changed by SOG. The effects of SOG seem to involve the MOR.

Nefopam downregulates autophagy and c-Jun N-terminal kinase activity in the regulation of neuropathic pain development following spinal nerve ligation.

BACKGROUND: Neurodegeneration is associated with changes in basal cellular function due to the dysregulation of autophagy. A recent study introduced the involvement of autophagy during spinal nerve ligation (SNL). Nefopam has shown potential for reducing neuropathic pain, but the underlying mechanisms are unknown. Here, we investigated the effects of nefopam on neuropathic pain development following SNL, focusing on the involvement of autophagy. METHODS: The functional role of nefopam in capsaicin-induced autophagy was assessed by human glioblastoma M059 K cells. The neuropathic pain model was used to determine whether the effect of nefopam on pain control was mediated through autophagy control. Neuropathic pain was induced by L5 and L6 SNL in male rats randomized into three groups: Group S (sham-operated), Group C (received normal saline), and Group E (received nefopam). A behavioral test using a von Frey was examined. Expression changes of autophagy in response to nefopam was analyzed in spinal cord tissues (L4-L6) by immunoblotting and immunohistochemistry. RESULTS: The paw withdrawal threshold examined on days 3, 5, 7, and 14 post-SNL was significantly higher in Group E than in Group C. SNL increased the levels of microtubule-associated protein 1 light chain 3B (LC3B-1), with concomitant reduction of sequestosome 1 (SQTSM1/p62), compared with Group S, indicating that SNL induced autophagy. These effects were reversed by nefopam injection, and the results were confirmed by immunohistochemistry for LC3-I/II. Furthermore, SNL-mediated JNK activation was markedly decreased following nefopam injection. Hematoxylin and eosin staining on Day 14 post-SNL revealed that SNL caused lymphocyte infiltration and oligodendrocyte localization in the substantia gelatinosa of the dorsal gray horn, which were reduced by nefopam injection. CONCLUSION: Collectively, the mode of action of nefopam on neuropathic pain appears to be associated with downregulation of phospho-JNK and autophagy, as well as modulation of the immune response.

Urinary trypsin inhibitor attenuates the development of neuropathic pain following spinal nerve ligation.

Following nerve injury, inflammatory and algesic mediators are released. This neuroinflammatory outbreak causes neuronal damage and chronic neuropathic pain. Urinary trypsin inhibitor (ulinastatin, UTI), which has anti-inflammatory properties and neuroprotective effects, is used to lower the levels of inflammatory factors during surgery. This study evaluated the effect of ulinastatin in a rat model of spinal nerve ligation (SNL). Neuropathic pain was induced by L5 and L6 SNL in male Sprague-Dawley rats. Rats were divided into three groups: group N (control) received normal saline through the tail vein for three days immediately following SNL, group U pre received ulinastatin (50,000 U/kg) intravenously for three days immediately following SNL, and group U post received ulinastatin (50,000 U/kg) intravenously for three days from the 3rd day following SNL. The paw withdrawal threshold was examined and the development of mechanical allodynia was confirmed with a behavioral test using a von Frey filament three days following SNL. On the 3rd, 5th, 7th, 14th, and 28th day following SNL, the paw withdrawal threshold was examined and the levels of inflammatory mediators (i.e., tumor necrosis factor alpha [TNF-α], interleukin-1ß [IL-1ß], and interleukin-6 [IL-6]) were measured by ELISA. The paw withdrawal threshold was significantly increased in the rats from group U pre compared with the rats from groups N and U post until the 7th post-SNL day (P<0.05). The levels of IL-6 also were significantly decreased in the rats from group U pre compared with the rats from group N and U post until the 7th post-SNL day (P<0.05). Ulinastatin increased the paw withdrawal threshold following SNL when it was administered before the development of neuropathic pain, and may attenuate the development of neuropathic pain.

Effect on thermoregulatory responses in patients undergoing a tympanoplasty in accordance to the anesthetic techniques during PEEP: a comparison between inhalation anesthesia with desflurane and TIVA.

BACKGROUND: It has been known that positive end-expiratory pressure (PEEP) increases the vasoconstriction threshold by baroreceptor unloading. We compared the effect on the thermoregulatory responses according to anesthetic techniques between an inhalation anesthesia with desflurane and a total intravenous anesthesia (TIVA) with propofol and reminfentanil when PEEP was applied in patients undergoing tympanoplasty. METHODS: Forty-six patients with a scheduled tympanoplasty were enrolled and the patients were divided in two study groups. Desflurane was used as an inhalation anesthetic in group 1 (n = 22), while TIVA with propofol and remifentanil was used in group 2 (n = 24). PEEP was applied by 5 cmH2O in both groups and an ambient temperature was maintained at 22-24℃ during surgery. The core temperature and the difference of skin temperature between forearm and fingertip were monitored for about 180 minutes before and after the induction of general anesthesia. RESULTS: The final core temperature was significantly higher in group 2 (35.4 ± 0.7℃) than in group 1 (34.9 ± 0.5℃). Peripheral thermoregulatory vasoconstriction was found in 5 subjects (23%) in group 1 and in 21 subjects (88%) in group 2. The time taken for reaching the thermoregulatory vasoconstriction threshold was 151.4 ± 19.7 minutes in group 1 and 88.9 ± 14.4 minutes in group 2. CONCLUSIONS: When PEEP will be applied, anesthesia with TIVA may have more advantages in core temperature preservation than an inhalation anesthesia with desflurane.

The effect of urinary trypsin inhibitor against neuropathic pain in rat models.

BACKGROUND: Nerve injury sometimes leads to chronic neuropathic pain associated with neuroinflammation in the nervous system. In the case of chronic neuropathic pain, the inflammatory and algesic mediators become predominant and result in pain hypersensitivity following nervous system damage. It is well known that urinary trypsin inhibitor (ulinastatin, UTI) has an anti-inflammatory activity. Recently, the neuroprotective action of UTI on the nervous system after ischemic injury has been reported. Thus, we evaluated the neuroprotective effect of ulinastatin in a rat model of neuropathic pain. METHODS: Neuropathic pain was induced with L5 spinal nerve ligation (SNL) in male Sprague-Dawley rats weighing 100-120 g. The rats were divided into 3 groups, with n = 8 in each group. The rats in the control group (group 1) were administered normal saline and those in group 2 were administered UTI (50,000 U/kg) intravenously through the tail vein for 3 days from the day of SNL. Rats in group 3 were administered UTI (50,000 U/kg) intravenously from the 5(th) day after SNL. The paw withdrawal threshold was measured using the von Frey test for 3 days starting from the 5(th) day after SNL. RESULTS: The paw withdrawal thresholds were significantly increased in the rats of group 2 compared to the other groups (P < 0.05). CONCLUSIONS: Ulinastatin, which was administered for 3 days after SNL, increased the paw withdrawal threshold and it could have a neuroprotective effect in the rat model of neuropathic pain.

Effects of Palonosetron, a 5-HT3 Receptor Antagonist, on Mechanical Allodynia in a Rat Model of Postoperative Pain.

BACKGROUND: 5-hydroxytryptamine 3 (5-HT3) receptors have been known to be associated with the modulation of nociceptive transmission. However, it is uncertain whether 5-HT3 plays a role in the antinociceptive or pronociceptive pathway for incisional pain. In this study, we evaluated the effects of palonosetron, a 5-HT3 receptor antagonist, on incisional pain in rats when administered intrathecally or intraplantarly. METHODS: An intrathecal catheter was implanted through the cisterna magna and placed in the intrathecal space of rats. An incision in the plantaris muscle of the right hind paw was done under anesthesia with sevoflurane. Withdrawal thresholds were evaluated with the von Frey filament after 2 hours. Palonosetron (0.5 and 0.1 µg intrathecally; 0.5 µg intraplantarly) was administered and the thresholds were observed for 4 hours. RESULTS: Mechanical hypersensitivity developed after the incision. Intrathecal palonosetron (0.5 µg and 0.1 µg) did not alter the paw withdrawal threshold. Intraplantar palonosetron (0.5 µg) also did not change the paw withdrawal threshold. CONCLUSIONS: Intrathecal and intraplantar palonosetron (0.5 µg) had no effect on modulating the mechanical hypersensitivity in the incisional pain model of rats.

The effect of low dose ketamine and priming of cisatracurium on the intubating condition and onset time of cisatracurium.

BACKGROUND: Both ketamine and priming may accelerate the onset time of neuromuscular blocking agents. We investigate the effect of low dose ketamine and cisatracurium priming on the intubating condition and onset time of cisatracurium. METHODS: After Institutional Review Board approval, 120 consecutive patients undergoing general anesthesia were randomly assigned to one of 4 groups. All patients were injected one of normal saline (group C), cisatracurium 0.01 mg/kg (group P), ketamine 0.5 mg/kg (group K) and combination of cisatracurium 0.01 mg/kg, and ketamine 0.5 mg/kg (group PK) diluted into a 5 ml solution, followed 3 minutes later by cisatracurium 0.15 mg/kg in group C and K, and 0.14 mg/kg cisatracurium in priming group. Onset time was recorded the electromyographical responses using single twitch and intubating conditions were evaluated at 60 seconds after cisatracurium administration. RESULTS: The mean onset time was most significantly accelerated in Group PK and was also significantly more accelerated in Group P and K compared with Group C (P < 0.008). It was 112.7 ± 13.2, 91.4 ± 17.9, 84.9 ± 12.7 and 76.4 ± 8.3 seconds in Group C, P, K, and PK, respectively. Intubating conditions were significantly improved in Group P, K and PK than Group C (P < 0.008). Especially, Group PK showed most significant improvement of intubating conditions. CONCLUSIONS: The combination of the low dose ketamine and cisatracurium priming accelerated the onset time and was improved the intubating conditions.

Clinical experience of symptomatic sacral perineural cyst.

Tarlov or perineural cysts are nerve root cysts found most commonly at the sacral spine level arising between covering layers of the perineurium and the endoneurium near the dorsal root ganglion and are usually asymptomatic. Symptomatic sacral perineural cysts are uncommon but sometimes require surgical treatment. A 69-year-old male presented with pain in the buttock. He was diagnosed as having a sacral cyst with magnetic resonance imaging. For the nonoperative diagnosis and treatment, caudal peridurography and block were performed. After the treatment, the patient's symptom was relieved. We suggest a caudal peridural block is effective in relieving pain from a sacral cyst.

AKAP12 regulates vascular integrity in zebrafish.

The integrity of blood vessels controls vascular permeability and extravasation of blood cells, across the endothelium. Thus, the impairment of endothelial integrity leads to hemorrhage, edema, and inflammatory infiltration. However, the molecular mechanism underlying vascular integrity has not been fully understood. Here, we demonstrate an essential role for A-kinase anchoring protein 12 (AKAP12) in the maintenance of endothelial integrity during vascular development. Zebrafish embryos depleted of akap12 (akap12 morphants) exhibited severe hemorrhages. In vivo time-lapse analyses suggested that disorganized interendothelial cell-cell adhesions in akap12 morphants might be the cause of hemorrhage. To clarify the molecular mechanism by which the cell-cell adhesions are impaired, we examined the cell-cell adhesion molecules and their regulators using cultured endothelial cells. The expression of PAK2, an actin cytoskeletal regulator, and AF6, a connector of intercellular adhesion molecules and actin cytoskeleton, was reduced in AKAP12-depleted cells. Depletion of either PAK2 or AF6 phenocopied AKAP12-depleted cells, suggesting the reduction of PAK2 and AF6 results in the loosening of intercellular junctions. Consistent with this, overexpression of PAK2 and AF6 rescued the abnormal hemorrhage in akap12 morphants. We conclude that AKAP12 is essential for integrity of endothelium by maintaining the expression of PAK2 and AF6 during vascular development.

The effects of intrathecal fentanyl for spinal anesthesia in lower extremity surgery.

BACKGROUND: Intrathecal opioids in combination with bupivacaine has been shown to provide adequate sensory blockade and early recovery from spinal anesthesia. This study was investigated the added effects of intrathecal fentanyl 10 microgram to bupivacaine for spinal anesthesia. METHODS: Sixty patients undergoing lower extremity surgery were into three groups. Group I received bupivacaine 10 mg (0.5%), gruop II received bupivacaine 5 mg with normal saline 1 ml, and group III received bupivacaine 5 mg with fentanyl 10 microg and normal saline 0.8 ml. RESULTS: There was no significant difference between group I and group III in the peak level and duration of sensory block. But the intensity of motor blockade was decreased in group III compared with group I and side effects of spinal anesthesia with local anesthetics was decreased in group III compared with group I. In Group II, 7 patients were complained the pain during surgery. CONCLUSIONS: Intrathecal fentanyl 10 microgram with bupivacaine 5 mg on spinal blockade provide reliable anesthesia for lower extremity surgery.

Effect of tramadol on bispectral index during anesthesia with desflurane.

BACKGROUND: This study is aimed to investigate the effect of tramadol on the bispectral index (BIS) during anesthesia with desflurane. METHODS: One hundred fifty adults, ASA class 1 and 2 patients, scheduled for general anesthesia for elective surgical procedures were included in this study. None of the patients were premedicated and anesthesia was induced with propofol 2 mg/kg and maintained with air-oxygen (FiO2 0.5) and desflurane, adjusted to keep the BIS between from 50 and 60. Forty minutes before completing surgery, the subjects were randomly allocated into 3 groups to receive saline (control group), tramadol 1.5 mg/kg (T1 group) or 3.0 mg/kg (T2 group) intravenously. Hemodynamics and BIS values were then recorded every 5 minutes until completion of the operation, during which time the concentrations of desflurane were not modified. RESULTS: The mean BIS values after tramadol administration weren't significantly different from the control group throughout the period of observation. No significant changes in the hemodynamics were noted, except systolic and diastolic arterial blood pressure in the T1 and T2 groups significantly increased in the first 5 minutes after the tramadol injection. CONCLUSIONS: The results indicate that the administration of tramadol while maintaining anesthesia with desflurane, adjusted to keep the BIS between 50 and 60, does not modified BIS values. So, we propose that tramadol can be safely administered as an immediate postoperative analgesia without concern about intra-operative awareness.

Protein kinase C-delta regulates the stability of hypoxia-inducible factor-1 alpha under hypoxia.

Hypoxia is a state of deficiency of available oxygen in the blood and tissues, and it occurs during several pathophysiological processes, including tumorigenesis. Under hypoxia, hypoxia-inducible factor-1 (HIF-1) plays an essential role in cellular oxygen homeostasis. In the present article protein kinase C-delta (PKC-delta) is activated by hypoxia, increases the protein stability and transcriptional activity of HIF-1alpha in human cervical adenocarcinoma cells. Moreover, the knockdown of PKC-delta inhibited vascular endothelial growth factor expression and angiogenic activity under hypoxia. These effects were completely reversed by PKC-delta overexpression following the knockdown of PKC-delta. Collectively, these findings demonstrate the role of PKC-delta as a new regulator of hypoxia-induced angiogenesis.

Thermographic assessment of inferior alveolar nerve injury in patients with dentofacial deformity.

PURPOSE: The purpose of this study was to evaluate the injury and recovery of the inferior alveolar nerve in orthognathic patients at 1 and 4 weeks after surgery using electronic thermography. MATERIALS AND METHODS: Twenty subjects with Class III dentofacial deformity were studied. All patients underwent bilateral sagittal split ramus osteotomy. To image the temperature of the face, 1 anteroposterior view and 1 lateral view were taken from both the right and left sides. Similar images were taken at 1 and 4 weeks after surgery. The control was the presurgical temperature of the 20 patients who showed unilateral or bilateral nerve damage after surgery. RESULTS: In the patients with unilateral nerve damage (n = 14), on the anteroposterior views, the temperatures of the mentum on the 2 sides differed by 0.64 degrees C at 1 week after surgery, and the difference decreased to 0.23 degrees C at 4 weeks after surgery. On the lateral images, the differences in temperature between the mentum areas were 0.10 degrees C at 1 week and 0.27 degrees C at 4 weeks after surgery. In the patients with bilateral nerve injury (n = 6), on the anteroposterior views, the temperatures of the mentum on the 2 sides differed by 0.20 degrees C at 1 week after surgery and 0.13 degrees C after 4 weeks. On the lateral views, the differences were 0.18 degrees C at 1 week and 0.34 degrees C at 4 weeks after surgery. Using the repeated measurement analysis method, the anteroposterior view showed statistically significant results in the patients with unilateral nerve damage. CONCLUSION: The infrared body temperature method is an objective method that can be applied as a supplemental diagnostic method for inferior alveolar nerve injury.

Nail-splinting technique for ingrown nails: the therapeutic effects and the proper removal time of the splint.

BACKGROUND: An ingrown nail is a common disorder that occurs most frequently in the great toe and causes much discomfort in patients. Although many therapeutic methods have been described, most of them can lead to severe damage to the nail or to frequent relapses. The nail-splinting technique is known to be a noninvasive therapeutic method for treating an ingrown nail. OBJECTIVE: Our purpose was to access the recurrence rate of the nail-splinting technique and to determine the proper removal time of the splint from the ingrown nail. METHODS: Fifty-seven patients with ingrown nail were treated with the nail-splinting technique. Subjects were randomized into two groups. For group 1 (28 patients), the splint was removed splint 3 days after treatment, whereas for group 2 (29 patients), the splint was removed splint 2 weeks after treatment. All patients underwent a follow-up examination at 1, 2, and 4 weeks after treatment and were evaluated for tissue status and level of pain. After 1 year, we evaluated the rate of recurrence by means of a telephone interview with each patient. RESULTS: A low recurrence rate (8.7%) for the nail-splinting technique was observed in both groups (7.1% in group 1 vs. 10.3% in group 2). The tissue status and level of pain were found to improve with time, with no statistical significance between the two groups (P> 0.05). CONCLUSION: This study indicates that the nail-splinting technique constitutes a very simple and effective, noninvasive therapeutic method for treating ingrown nail. We suggest that the 3-day nail-splinting technique is the most useful when the nail is intact or has only a slight defect.