Possible anti-inflammatory, antioxidant, and neuroprotective effects of apigenin in the setting of mild traumatic brain injury: an investigation.

OBJECTIVE: Apigenin is a plant flavone proven with biological properties such as anti-inflammatory, antioxidant, and antimicrobial effects. This study, it was aimed to examine the possible anti-inflammatory, antioxidant, and neuroprotective effects of apigenin in the setting of the mild traumatic brain injury (TBI) model. METHODS: Wistar albino male rats were randomly assigned to groups: control (n = 9), TBI (n = 9), TBI + vehicle (n = 8), and TBI + apigenin (20 and 40 mg/kg, immediately after trauma; n = 6 and n = 7). TBI was performed by dropping a 300 g weight from a height of 1 m onto the skull under anesthesia. Neurological examination and tail suspension tests were applied before and 24 h after trauma, as well as Y-maze and object recognition tests, after that rats were decapitated. In brain tissue, luminol- and lucigenin-enhanced chemiluminescence levels and cytokine ELISA levels were measured. Histological damage was scored. Data were analyzed with one-way ANOVA. RESULTS: After TBI, luminol (p < .001) and lucigenin (p < .001) levels increased, and luminol and lucigenin levels decreased with apigenin treatments (p < .01-.001). The tail suspension test score increased with trauma (p < .01). According to the pre-traumatic values, the number of entrances to the arms (p < .01) in the Y-maze decreased after trauma (p < .01). In the object recognition test, discrimination (p < .05) and recognition indexes (p < .05) decreased with trauma. There was no significant difference among trauma apigenin groups in behavioral tests. Interleukin (IL)-10 levels, one of the anti-inflammatory cytokines, decreased with trauma (p < .05), and increased with 20 and 40 mg apigenin treatment (p < .001 and p < .01, respectively). The histological damage score in the cortex was decreased in the apigenin 20 mg treatment group significantly (p < .05), but the decrease observed in the apigenin 40 mg group was not significant. CONCLUSION: The results of this study revealed that apigenin 20 and 40 mg treatment may have neuroprotective effects in mild TBI via decreasing the level of luminol and lucigenin and increasing the IL-10 levels. Additionally, apigenin 20 mg treatment ameliorated the trauma-induced cortical tissue damage.

Cingulate sulcus morphology and paracingulate sulcus variations: Anatomical and radiological studies.

The sulci and gyri found across the cerebrum differ in morphology between individuals. The cingulate sulcus is an important landmark for deciding the surgical approach for neighboring pathological lesions. Identifying the anatomical variations of anterior cingulate cortex morphology would help to determine the safe-entry route through neighboring lesions. In this study, magnetic resonance imaging data acquired from 149 healthy volunteers were investigated retrospectively for anatomical variations of the paracingulate sulcus. Also, human cadaveric brain hemispheres were investigated for cingulate and paracingulate sulcus anatomy. All participants had cingulate sulci in both hemispheres (n = 149, 100%). Three types of paracingulate sulcus patterns were identified: "prominent," "present," and "absent." Hemispheric comparisons indicated that the paracingulate sulcus is commonly "prominent" in the left hemisphere (n = 48, 32.21%) and more commonly "absent" in the right hemisphere (n = 73, 48.99%). Ten (6.71%) people had a prominent paracingulate sulcus in both the right and left hemispheres. Seven (4.70%) of them were male, and 3 (2.01%) of them were female. Paracingulate sulci were present in both hemispheres in 19 people (12.75%), of which 9 (6.04%) were male and 10 (6.71%) were female. There were 35 (23.49%) participants without paracingulate sulci in both hemispheres. Eleven (7.38%) were male and 24 (16.11%) were female. There were 73 (48.99%) participants without right paracingulate sulcus and 57 (38.26%) participants without left paracingulate sulcus (p = 0.019). In the examinations of the cadaver hemispheres, the paracingulate sulcus was present and prominent in 25%, and the intralimbic sulcus was present in 15%. It has been observed that the paracingulate sulcus is more prominent in the normal male brain compared to females. In females, there were more participants without paracingulate sulcus. This study shows that there are both hemispheric and sex differences in the anatomy of the paracingulate sulcus. Understanding the cingulate sulcus anatomy and considering the variations in the anterior cingulate cortex morphology during surgery will help surgeons to orient this elegant and complex area.

The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits.

The neuroprotective and vasodilatory effects of cinnamaldehyde have been widely studied and documented. On the basis of these findings, we hypothesized that cinnamaldehyde exhibits therapeutic effects on subarachnoid hemorrhage-induced early brain injury and cerebral vasospasm. Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits: control, subarachnoid hemorrhage, subarachnoid hemorrhage + vehicle, and subarachnoid hemorrhage + cinnamaldehyde. An intraperitoneal dose of 50 mg/kg cinnamaldehyde was administered 5 min following an intracisternal blood injection, followed by three further daily injections at identical doses. The animals were sacrificed 72 h after subarachnoid hemorrhage was induced. The cross-sectional areas and arterial wall thicknesses of the basilar artery were measured and hippocampal degeneration scores were evaluated. Treatment with cinnamaldehyde was effective in providing neuroprotection and attenuating cerebral vasospasm after subarachnoid hemorrhage in rabbits. It effectively increased the cross-sectional areas of the basilar artery and reduced the arterial wall thickness; in addition, hippocampal degeneration scores were lower in the cinnamaldehyde group. The findings of this study showed, for the first time to our knowledge, that cinnamaldehyde exhibits neuroprotective activity against subarachnoid hemorrhage-induced early brain injury and that it can prevent vasospasm. Potential mechanisms underlying the neuroprotection and vasodilation were discussed. Cinnamaldehyde could play a role in subarachnoid hemorrhage treatment.

Central liponeurocytoma as a clinical entity.

INTRODUCTION: Liponeurocytomas are mostly localized in cerebellar hemispheres and the second most common location is the vermis. It is rarely observed within the intracranial ventricles. Here, we present a case of liponeurocytoma located in the right lateral ventricle and the systematic review of the literature. STATE OF THE ART: We searched PubMed with keyword 'central liponeurocytoma' and the references of the related articles. There were no language or year restrictions. We included articles focusing on liponeurocytomas located in the central nervous system leaving a total of 17 articles and 21 reported cases. CLINICAL IMPLICATIONS: A 62-year-old female presented with confusion and mental disorientation without any other neurological deficit. Her magnetic resonance imaging (MRI) revealed a lateral ventricle located mass lesion which was hypointense on T1-weighted images (WI) and heterogeneously hyperintense on T2-WI with cystic component. Via craniotomy, yellow-beige colored, soft and moderately vascularized mass lesion was gross totally resected. Despite postoperative MRI revealed total resection, patient had left-sided hemiparesis. The patient recovered well in her postoperative period and there was no recurrence on her 6th month follow-up MRI. FUTURE DIRECTIONS: Intraventricular liponeurocytoma has a favorable clinical course, and radiological features may be useful in the diagnosis of this rare tumor before surgery. Supratentorial intraventricular location should be kept in mind in the differential diagnosis of the lateral ventricular tumors.

Surgical Management Thoracolumbar Fractures in Patients with Ankylosing Spondylitis: Technical Note with Case Series.

OBJECTIVE: Ankylosing spondylitis (AS) is a chronic inflammatory joint disease. Complications such as traumatic spinal fractures are mostly caused by hyperextension and are unstable. We report the cases of 5 patients with AS surgically treated for thoracolumbar fractures. METHODS AND RESULTS: We shared our experience of posterior stabilization surgery performed for the treatment of thoracolumbar fractures after traumas such as fall-accident in patients with AS. Patients were all men, and their ages were between 52 and 77 years. The first 3 patients woke up with neurologic deficits and were managed surgically under general anesthesia. We managed the last 2 patients with unilateral short-level stabilization under local anesthesia followed by bilateral long-level stabilization under general anesthesia. No neurologic deterioration was found in the postoperative examination of these 2 patients. We assume that the reason for neurologic deterioration after general anesthesia is the relaxation of muscles. All 3 columns of the spine are affected in patients with AS and the stability is provided by the tone of the muscles around the spine. CONCLUSIONS: To prevent postoperative neurologic complications after the surgical treatment of traumatic hyperextension thoracic and lumbar fractures in patients with AS, we recommend securing the fracture level with unilateral short-level stabilization under local anesthesia and then completing the operation with general anesthesia.

Antioxidant and neuroprotective effects of dexpanthenol in rats induced with traumatic brain injury.

Trauma-induced primary damage is followed by secondary damage, exacerbating traumatic brain injury (TBI). Dexpanthenol has been shown to protect tissues against oxidative damage in various inflammation models. This study aimed to investigate possible antioxidant and neuroprotective effects of dexpanthenol in TBI. Wistar albino male rats were randomly assigned to control (n = 16), trauma (n = 16) and dexpanthenol (500 mg/kg; n = 14) groups. TBI was induced under anesthesia by dropping a 300 g weight from 70-cm height onto the skulls of the rats. Twenty-four hours after the trauma, the rats were decapitated and myeloperoxidase (MPO) levels, luminol- and lucigenin-enhanced chemiluminescence (CL), malondialdehyde (MDA) levels, superoxide dismutase (SOD) levels, and catalase (CAT) and caspase-3 activities were measured in brain tissues. Following transcardiac paraformaldehyde perfusion, histopathological damage was graded on hematoxylin-eosin-stained brain tissues. In the trauma group, MPO level, caspase-3 activity and luminol-lucigenin CL levels were elevated (p < 0.05-0.001) when compared to controls; meanwhile in the dexpanthenol group these increases were not seen (p < 0.05-0.001) and MDA levels were decreased (p < 0.05). Decreased SOD and CAT activities (p < 0.01) in the vehicle-treated TBI group were increased above control levels in the dexpanthenol group (p < 0.05-0.001). in the dexpanthenol group there was relatively less neuronal damage observed microscopically in the cortices after TBI. Dexpanthenol reduced oxidative damage, suppressed apoptosis by stimulating antioxidant systems and alleviated brain damage caused by TBI. Further experimental and clinical investigations are needed to confirm that dexpanthenol can be administered in the early stages of TBI.

Mildronate Has Ameliorative Effects on the Experimental Ischemia/Reperfusion Injury Model in the Rabbit Spinal Cord.

BACKGROUND: Mildronate is a useful anti-ischemic agent and has antiinflammatory, antioxidant, and neuroprotective activities. The aim of this study is to investigate the potential neuroprotective effects of mildronate in the experimental rabbit spinal cord ischemia/reperfusion injury (SCIRI) model. METHODS: Rabbits were randomized into 5 groups of 8 animals as groups 1 (control), 2 (ischemia), 3 (vehicle), 4 (30 mg/kg methylprednisolone [MP]), and 5 (100 mg/kg mildronate). The control group underwent only laparotomy. The other groups have the spinal cord ischemia model by a 20-minute aortic occlusion just caudal to the renal artery. The malondialdehyde and catalase levels and caspase-3, myeloperoxidase, and xanthine oxidase activities were investigated. Neurologic, histopathologic, and ultrastructural evaluations were also performed. RESULTS: The serum and tissue myeloperoxidase, malondialdehyde, and caspase-3 values of the ischemia and vehicle groups were statistically significantly higher than those of the MP and mildronate groups (P < 0.001). Serum and tissue catalase values of the ischemia and vehicle groups were statistically significantly lower than those of the control, MP, and mildronate groups (P < 0.001). The histopathologic evaluation showed a statistically significantly lower score in the mildronate and MP groups than in the ischemia and vehicle groups (P < 0.001). The modified Tarlov scores of the ischemia and vehicle groups were statistically significantly lower than those of the control, MP, and mildronate groups (P < 0.001). CONCLUSIONS: This study presented the antiinflammatory, antioxidant, antiapoptotic, and neuroprotective effects of mildronate on SCIRI. Future studies will elucidate its possible use in clinical settings in SCIRI.

Primary Hydatid Cyst of Lumbar Paravertebral Muscle.

Hydatid cyst disease as a zoonosis usually infests the liver and lungs, and it rarely affects muscles. Here, we presented a 36-year-old female patient with low back pain. Radiological evaluation revealed a soft tissue lesion located at the left paravertebral region without vertebral invasion. Surgical exploration and removal of the cyst were performed. The pathological diagnosis was hydatid cyst. After the surgery, the patient was treated with albendazole which is used to decrease the consequences of spillage and the possibility of recurrence. Hydatid cyst disease is rarely seen in paravertebral muscle tissue and needs to be correctly managed. Primary muscle involvement of hydatid cyst must be kept in mind for differential diagnosis of paravertebral cystic mass lesions.

Neuroprotective Effects of Dexpanthenol on Rabbit Spinal Cord Ischemia/Reperfusion Injury Model.

OBJECTIVE: Dexpanthenol (DXP) reportedly protects tissues against oxidative damage in various inflammation models. This study aimed to evaluate its effects on oxidative stress, inflammation, apoptosis, and neurological recovery in an experimental rabbit spinal cord ischemia/reperfusion injury (SCIRI) model. METHODS: Rabbits were randomized into 5 groups of 8 animals each: group 1 (control), group 2 (ischemia), group 3 (vehicle), group 4 (methylprednisolone, 30 mg/kg), and group 5 (DXP, 500 mg/kg). The control group underwent laparotomy only, whereas other groups were subjected to spinal cord ischemia by aortic occlusion (just caudal to the 2 renal arteries) for 20 min. After 24 h, a modified Tarlov scale was employed to record neurological examination results. Malondialdehyde and caspase-3 levels and catalase and myeloperoxidase activities were analyzed in tissue and serum samples. Xanthine oxidase activity was measured in the serum. Histopathological and ultrastructural evaluations were also performed in the spinal cord. RESULTS: After SCIRI, serum and tissue malondialdehyde and caspase-3 levels and myeloperoxidase and serum xanthine oxidase activities were increased (P < 0.05-0.001). However, serum and tissue catalase activity decreased significantly (P < 0.001). DXP treatment was associated with lower malondialdehyde and caspase-3 levels and reduced myeloperoxidase and xanthine oxidase activities but increased catalase activity (P < 0.05-0.001). Furthermore, DXP was associated with better histopathological, ultrastructural, and neurological outcome scores. CONCLUSIONS: This study was the first to evaluate antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective effects of DXP on SCIRI. Further experimental and clinical investigations are warranted to confirm that DXP can be administered to treat SCIRI.

Neuroprotective Effect of Plasminogen Activator Inhibitor-1 Antagonist in the Rat Model of Mild Traumatic Brain Injury.

Plasminogen activator inhibitor-1 (PAI-1) antagonists are known for their neuroprotective effects. In this study, it was aimed to investigate the possible protective effects of PAI-1 antagonists in a rat mild traumatic brain injury (TBI) model. Sprague-Dawley male rats were grouped as sham (n = 7), TBI (n = 9), and TBI + PAI-1 antagonist (5 and 10 mg/kg TM5441 and TM5484; n = 6-7). Under anesthesia, TBI was induced by dropping a metal 300-g weight from a height of 1 m on the skull. Before and 24-h after trauma neurological examination, tail suspension, Y-maze, and novel object recognition tests were performed. Twenty-four hours after TBI, the rats were decapitated and activities of myeloperoxidase, nitric oxide release, luminol-, and lucigenin-enhanced chemiluminescence were measured. Also, interleukin-1ß, interleukin-6, tumor necrosis factor, interleukin-10, tumor growth factor-ß, caspase-3, cleaved caspase-3, and PAI levels were measured with the ELISA method in the brain tissue. Brain injury was graded histopathologically following hematoxylin-eosin staining. Western blot and immunohistochemical investigation for low-density lipoprotein receptor, matrix metalloproteinase-3, and nuclear factor-κB were also performed. Data were analyzed using GraphPad Prism 8.0 (GraphPad Software, San Diego, CA, USA) and expressed as means ± SEM. Values of p < 0.05 were considered to be statistically significant. Higher levels of myeloperoxidase activity in the TBI group (p < 0.05) were found to be suppressed in 5 and 10 mg/kg TM5441 treatment groups (p < 0.05-p < 0.01). The tail suspension test score was increased in the TBI group (p < 0.001) and decreased in all treatment groups (p < 0.05-0.001). The histologic damage score was increased statistically significantly in the cortex, dentate gyrus, and CA3 regions in the TBI group (p < 0.01-0.001), decreased in the treatment groups in the cortex and dentate gyrus (p < 0.05-0.001). PAI antagonists, especially TM5441, have antioxidant and anti-inflammatory properties against mild TBI in the acute period. Behavioral test results were also improved after PAI antagonist treatment after mild TBI.

Neuroprotective Effect of Cinnamaldehyde on Secondary Brain Injury After Traumatic Brain Injury in a Rat Model.

OBJECTIVE: The aim of this study was to investigate the possible neuroprotective effects of cinnamaldehyde (CA) on secondary brain injury after traumatic brain injury (TBI) in a rat model. METHODS: Rats were randomly divided into 4 groups: control (n = 9), TBI (n = 9), vehicle (0.1% Tween 80; n = 8), and CA (100 mg/kg) (n = 9). TBI was induced by the weight-drop model. In brain tissues, myeloperoxidase activity and the levels of luminol-enhanced and lucigenin-enhanced chemiluminescence were measured. Interleukin 1ß, interleukin 6, tumor necrosis factor α, tumor growth factor ß, caspase-3, and cleaved caspase-3 were evaluated with an enzyme-linked immunosorbent assay method. Brain injury was histopathologically graded after hematoxylin-eosin staining. Y-maze and novel object recognition tests were performed before TBI and within 24 hours of TBI. RESULTS: Higher myeloperoxidase activity levels in the TBI group (P < 0.001) were suppressed in the CA group (P < 0.05). Luminol-enhanced and lucigenin-enhanced chemiluminescence, which were increased in the TBI group (P < 0.001, for both), were decreased in the group that received CA treatment (P < 0.001 for both). Compared with the increased histologic damage scores in the cerebral cortex and dentate gyrus of the TBI group (P < 0.001), scores of the CA group were lower (P < 0.001). Decreased number of entries and spontaneous alternation percentage in the Y-maze test of the TBI group (P < 0.05 and P < 0.01, respectively) were not evident in the CA group. CONCLUSIONS: CA has shown neuroprotective effects by limiting neutrophil recruitment, suppressing reactive oxygen species and reducing histologic damage and acute hippocampal dysfunction.

Amelioration of Cerebral Vasospasm and Secondary Injury by Vigabatrin After Experimental Subarachnoid Hemorrhage in the Rabbit.

BACKGROUND: Vigabatrin, an antiepileptic drug, increases the level of gamma aminobutyric acid in the brain by inhibiting its catabolism. Because gamma aminobutyric acid has been proved to have vasodilatory effects, in the present study, we investigated the effect of vigabatrin to treat experimental subarachnoid hemorrhage (SAH)-induced vasospasm. METHODS: A total of 30 New Zealand white rabbits were divided into 3 groups of 10 each: the control group, SAH group, and vigabatrin group. Experimental SAH was established by injection of autologous arterial blood into the cisterna magna. In the vigabatrin group, the rabbits were administered vigabatrin for 3 days after induction of the SAH. The first dose of vigabatrin was given 2 hours after SAH induction. A daily dose of 500 mg/kg vigabatrin was administered intraperitoneally. After 3 days, the rabbits were sacrificed, and the brains were removed, together with the cerebellum and brainstem. The basilar artery wall thickness and lumen areas were measured. The neuronal degeneration in the hippocampus (CA1, CA3, and dentate gyrus) was also evaluated. RESULTS: The arterial wall thickness of the vigabatrin group was less than that in the SAH group (P < 0.001), and the mean luminal area of the vigabatrin group was greater than that in the SAH group (P < 0.001). Additionally, the hippocampal neuronal degeneration score of the vigabatrin group was lower than that of the SAH group (P < 0.001). CONCLUSION: These findings have indicated that vigabatrin has a vasodilatory effect in an experimental SAH model in the rabbit. Moreover, it showed a neuroprotective effect in the hippocampal neurons against secondary injury induced by SAH.

Neuroprotective effects of mildronate in a rat model of traumatic brain injury.

OBJECTIVE: Traumatic brain injury (TBI) is one of the most common preventable causes of mortality and morbidity. Inflammation, apoptosis, oxidative stress, and ischemia are some of the important pathophysiological mechanisms underlying neuronal loss after TBI. Mildronate is demonstrated to be beneficial in various experimental models of ischemic diseases via anti-inflammatory, antioxidant, and neuroprotective mechanisms. This study aimed to investigate possible antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective effects of mildronate in a rat model of TBI. METHODS: A total of 46 male rats were divided into three groups of control, saline-treated TBI, and mildronate-treated TBI. Both TBI groups were subjected to closed-head contusive weight-drop injuries followed by treatment with saline or mildronate (100 mg/kg) administered intraperitoneally. The forebrain was removed 24 h after trauma induction, the activities of myeloperoxidase (MPO) and caspase-3, levels of superoxide dismutase (SOD), luminol- and lucigenin-enhanced chemiluminescence were measured, and histomorphological evaluation of cerebral tissues was performed. RESULTS: Increased MPO and caspase-3 activities in the vehicle-treated TBI group (p < 0.001) were suppressed in the mildronate-treated TBI group (p < 0.001). Similarly, increase in luminol and lucigenin levels (p < 0.001 and p < 0.01, respectively) in the vehicle-treated TBI group were decreased in the mildronate-treated TBI group (p < 0.001). Concomitantly, in the vehicle-treated TBI group, TBI-induced decrease in SOD activity (p < 0.01) was reversed with mildronate treatment (p < 0.05). On histopathological examination, TBI-induced damage in the cerebral cortex was lesser in the mildronate-treated TBI group than that in other groups. CONCLUSION: This study revealed for the first time that mildronate, exhibits neuroprotective effects against TBI because of its anti-inflammatory, antiapoptotic, and antioxidant activities.

Antifibrotic Effect of Boric Acid in Rats with Epidural Fibrosis.

BACKGROUND: Epidural fibrosis is a major problem after spine surgery, with some patients having recurrent symptoms secondary to excessive formation of scar tissue resulting in neurologic compression. We used a rat laminectomy model to determine if topical application of boric acid could be helpful in the prevention of epidural fibrosis. METHODS: Rats were randomly assigned to 2 control and 2 experimental groups (n = 8 for each group). The negative control group received no surgery, and the positive control group underwent laminectomy only. Experimental groups were classified according to the study agents applied onto the dura mater after laminectomy at the L3 level: 2.5% boric acid solution and 5% boric acid solution. The extent of epidural fibrosis was assessed 4 weeks later macroscopically and histopathologically. RESULTS: Boric acid reduced epidural fibrosis in rats after laminectomy. The effect of 5% boric acid solution was more pronounced (P < 0.05) compared with the 2.5% solution. CONCLUSIONS: The antifibrotic effect of boric acid solution for the prevention of epidural fibrosis suggests that boric acid should be further evaluated in future studies for the prevention of epidural fibrosis.

Acute Bilateral Foot Drop as Presenting Symptom of Hemorrhagic Synovial Cyst of Lumbar Spine.

BACKGROUND: Acute bilateral foot drop is a rare clinical presentation. CASE DESCRIPTION: A 77-year-old male presented with acute bilateral weakness of the foot and ankle dorsiflexion. Magnetic resonance imaging of the lumbar spine revealed ligamentum flavum hypertrophy, as well as a mass lesion that appeared hyperintense on T1-weighted images and hypointense on T2-weighted images. Emergent decompressive laminectomy and hemorrhagic synovial cyst excision were performed. Histopathologic examination of the tissue revealed a synovial cyst with hemorrhage. CONCLUSION: Here, we describe a unique case of a hemorrhagic synovial cyst with a presenting symptom of acute bilateral foot drop.

The effect of vitamin D supplementation on pain, quality of life, and nerve conduction studies in women with chronic widespread pain.

The aim of this study was to investigate the effects of vitamin D supplementation on pain, quality of life, and nerve conduction studies (NCSs) in women with chronic widespread pain (CWP) diagnosed with Vitamin D insufficiency. Thirty-three female participants with CWP and vitamin D insufficiency were included in this open-label trial. They were evaluated by routine NCSs in upper and lower limbs, pain scales, and the Nottingham Health Profile before and 8 weeks after starting vitamin D supplementation therapy. The P-value was adjusted to account for the number of comparisons performed in each assessment. After 8 weeks of treatment, participants reported significantly lower pain scores (P=0.000). The total Nottingham Health Profile score and subscores for pain, emotional reactions, and physical activity domains were significantly lower (0.000≤P≤0.008). However, no statistically significant changes in NCSs were detected, except trends toward increases in the amplitudes of left median and ulnar sensory nerve potentials and a decrease in the distal latency of the right median sensory potential (0.01≤P≤0.04). Vitamin D supplementation therapy decreased pain and increased quality of life without significantly affecting nerve conduction in patients with CWP.

Psychosocial functioning in pediatric patients with pectus excavatum and pectus carinatum.

BACKGROUND/AIM: Pectus excavatum and pectus carinatum are the most commonly seen anterior chest wall deformities. Recent studies reveal that minimal invasive repair of pectus deformities improves the quality of life. Our aim is to assess the psychosocial functioning and sociodemographic characteristics of pediatric patients with pectus deformities and evaluate the differences between patients operated on with minimal invasive repair techniques and nonoperated patients. MATERIALS AND METHODS:  Thirty-two patients with pectus deformities who were operated on 6 months or more before and 31 nonoperated patients participated in the study. The Children's Depression Inventory, Piers-Harris Children's Self-Concept Scale, Capa Social Phobia Scale for Children and Adolescents, Strengths and Difficulties Questionnaire - Self-Report Version (SDQ-SR), and State-Trait Anxiety Inventory for Children - Trait Version were completed by the patients. The SDQ-Parent Report Version (SDQ-PR) was completed by their parents. RESULTS:  There were no statistically significant differences between operated and nonoperated patient groups in terms of total scores on the psychiatric rating scales. Prosocial behavior subscale scores in SDQ-SR (P = 0.013) and SDQ-PR (P = 0.019) were lower in the operated group. CONCLUSION: Prosocial behavior levels were lower in the operated group. Further exploration of the psychosocial profile of pediatric patients with pectus deformities would better elucidate their needs in the course of their socioemotional development.