Adolescent lumbar disc herniation: Impact, diagnosis, and treatment.

BACKGROUND: Symptomatic lumbar intervertebral disc herniation (LDH) is rare in children and adolescents. To date, the treatments available for child and adolescent LDH, and the effect of each treatment, have not been fully reviewed. OBJECTIVE: The purpose of this retrospective study is to report the etiology, familial history, presenting symptoms, level of herniation, duration of symptoms, radiological findings, as well as treatment methods and outcome. METHODS: We retrospectively reviewed medical records of all patients with inclusion criteria of being younger than 20 years. (10-19 years); we used magnetic resonance imaging (MRI) to confirm lumbar disc herniations between 2013 and 2016. All patients were followed up for a minimum of 12 months and discharged if they remained almost asymptomatic for 6 months. All patients were treated conservatively and 6 patients they have progressive neurological deficit and persistent back pain, were treated with surgical procedures. The Visual Analogue Scale (VAS), as well as the Oswestry Disability Scale (ODS) and the modified Ashworth Scale (AS) were used to analyze physical examination findings both before and after treatment. To detect lumbar disc degeneration, we used the modified Pfirrmann grading system with MRI. All statistical analyses were performed with commercially available SPSS 15.0 software, while p ≤ 0.05 was considered statistically significant. RESULTS: A total of 70 cases with lumbar disc herniation have been treated. The mean age was 17.14 ± 2.15 years (range 9-19 years). The male to female ratio was 35:35. The mean duration of symptoms was 7.21 ± 1.69 months. The follow-up duration was 17.31 ± 4.17 months. The most common level was L4-5 in 38 (54%) patients and the second was L5-S1 in 24 (34%) patients. Subligamentous protruded discs were found in 42 (60%), extruded in 6 (9%), and disc bulge with intact annulus in 22 (31%) cases. VAS before treatment was 6.05 ± 0.83, while at 6 months after treatment it was 3.1 ± 0.6. However, at the first-year examination, VAS was 2.17 ± 0.76. The ODS was indexed before treatment 42.03 ± 3.75, at 6 months being 25.01 ± 2.75 and at the first year 9.92 ± 2.67. VAS and the OSD were both significantly decreased after treatment (p < 0.05). CONCLUSIONS: Either conservative or surgical methods can be performed comfortably for adolescent lumbar disc herniations. We proposed surgical treatment for patients with incapacitating persistent low back pain or radicular pain that lasted more than 6 weeks, despite rest and medication. We also pursued the development of neurological deficits, including recurrent pain that disturbed routine life activities.

Acute Paraplegia due to Thoracic Hematomyelia.

Spontaneous intraspinal intramedullary hemorrhage is a rare entity with the acute onset of neurologic symptoms. The etiology of idiopathic spontaneous hematomyelia (ISH) is unknown, and there are few published case reports. Hematomyelia is mostly associated with trauma, but the other nontraumatic etiologies are vascular malformations, tumors, bleeding disorders, syphilis, syrinx, and myelitis. MRI is a good choice for early diagnosis. Hematomyelia usually causes acute spinal cord syndrome due to the compression and destruction of the spinal cord. A high-dose steroid treatment and surgical decompression and evacuation of hematoma are the urgent solution methods. We present idiopathic spontaneous hematomyelia of a previously healthy 80-year-old male with a sudden onset of back pain and paraplegia.

The antioxidant and antiapoptotic effects of crocin pretreatment on global cerebral ischemia reperfusion injury induced by four vessels occlusion in rats.

AIMS: Cerebral ischemia reperfusion (IR) injury is a process in which oxidative and apoptotic mechanisms play a part. Neuroprotective agents to be found could work out well for the efficient and safe minimization of cerebral IR injury. Crocin is a strong antioxidant agent; however the influence of this agent on the experimental cerebral ischemia model has not been studied extensively and thus it is not well-known. The objective of our study was to investigate the antioxidant, antiapoptotic and protective effects of crocin on the global cerebral IR induced by four-vessel occlusion. MAIN METHODS: A total of 30 adult female Sprague-Dawley rats were equally and randomly separated into three groups as follows: sham, IR and IR+crocin (40mg/kg/day orally for 10days). 24h after electrocauterization of bilateral vertebral arteries, bilateral common carotid arteries were occluded for 30min and reperfused for 30min. Oxidative stress parameters (TAS, TOS, OSI), haematoxylin and eosin staining, caspase-3 and hypoxia-inducible factor-1 alpha (HIF-1α) expressions and TUNEL methods were investigated. KEY FINDINGS: There was a significant difference between the IR and sham groups by means of OSI level, histopathological scoring, caspase-3, HIF-1α and TUNEL-positive cell parameters. We have also observed that pre-treatment with crocin reduced these parameter levels back to the baseline. SIGNIFICANCE: The data obtained from the present study suggest that crocin may exert antiapoptotic, antioxidant and protective effects in IR-mediated brain injury induced by four-vessel occlusion. To the best of our knowledge, this would be the first study to be conducted in this field.

Ligamentum flavum thickening at lumbar spine is associated with facet joint degeneration: An MRI study.

OBJECTIVE: Degenerative changes in posterior elements of the spine such as thickening or hypertrophy of the ligamentum flavum (LF) may result in spinal stenosis. In the present study, we aimed to investigate the potential factors including age, intervertebral disc degeneration (IDD), facet joint degeneration (FJD), end plate degeneration (EPD), which may affect LF thickening and to reveal the relationship among those factors at each level of lumbar spine by evaluating the magnetic resonance images (MRI). METHODS: A total of 200 individuals with low back and/or leg pain complaints who had undergone lumbar MRI were included in this study. The thickness of LF, FJD, IDD and EPD were assessed at all lumbar levels. RESULTS: Totally 1000 end plates, 1000 intervertebral discs and 2000 facet joints were evaluated and the thicknesses of 2000 LFs were measured from MRI images of 200 patients (100 males and 100 females). The mean age was 46.87 ± 12.47 years. LF thickness was strongly associated with FJD especially on the ipsilateral side. Age and IDD were correlated at whole vertebral levels. The age related changes (LF thickness, FJD, IDD and EPD) were more prominent at L4-L5 vertebral level. However, gender had no effect on LF thickness. CONCLUSION: The results of this study suggest that LF thickening may occur independently or could be associated with FJD especially on the ipsilateral side and this relationship is due to the vertebral level. The degree of disc degeneration increases with age and age related changes may be predominantly observed at L4-L5 vertebral level.

Cabazitaxel causes a dose-dependent central nervous system toxicity in rats.

BACKGROUND: Chemotherapeutic agents may lead to serious neurological side effects, which in turn can deteriorate the quality of life and cause dose limiting. Direct toxic effect or metabolic derangement of chemotherapeutic agents may cause these complications. Cabazitaxel is a next generation semi-synthetic taxane derivative, which is effective in both preclinical models of human tumors sensitive or resistant to chemotherapy and in patients with progressive prostate cancer despite docetaxel treatment. AIM: The primary aim of this study was to investigate the central nervous system toxicity of Cabazitaxel. Secondary aim was to investigate the safety dose of Cabazitaxel for the central nervous system. METHODS: A total of 24 adult male Wistar-Albino rats were equally and randomly divided into four groups as follows: group 1 (Controls), group 2 (Cabazitaxel 0.5mg/kg), group 3 (Cabazitaxel 1.0mg/kg) and group 4 (Cabazitaxel 1.5mg/kg). Cabazitaxel (Jevtana, Sanofi-Aventis USA) was intraperitoneally administered to groups 2, 3 and 4 at 0.5, 1.0 and 1.5mg/kg (body-weight/week) doses, respectively for four consecutive weeks. Beside this, group 1 received only i.p. saline at the same volume and time. At the end of the study, animals were sacrificed and bilateral brain hemispheres were removed for biochemical, histopathological and immunohistochemical examinations. RESULTS: Intraperitoneal administration of Cabazitaxel has exerted neurotoxic effect on rat brain. We have observed that biochemical and immunohistochemical results became worse in a dose dependent manner. CONCLUSION: Our findings have suggested that Cabazitaxel may be a neurotoxic agent and can trigger apoptosis in neuron cells especially at high doses.

Selenium protects cerebral cells by cisplatin induced neurotoxicity.

PURPOSE: To evaluate the central nervous system toxicity of cisplatin and neuroprotective effect of selenium. METHODS: Twenty-one male Wistar albino rats were divided into three groups: control (C), cisplatin (CS), cisplatin and selenium (CSE, n=7 in each group). Cisplatin (12 mg/kg/day, i.p.) was administered to CS and CSE groups for three days. Furthermore, CSE group received 3mg/kg/day (twice-a-day as 1.5 mg/kg) selenium via oral gavage five days before cisplatin injection and continued for 11 consecutive days. The same volumes of saline were administered to C group intraperitoneally and orally at same time. RESULTS: Heterochromatic and vacuolated neurons and dilated capillary vessels in the brain were observed in the histochemical examinations of cisplatin treated group. Rats that were given a dose of 3mg/kg/day selenium decreased the cisplatin induced histopathological changes in the brain, indicating a protective effect. In addition, cytoplasmic staining of the cell for bcl-2, both cytoplasmic and nuclear staining for bax were determined to be positive in the all groups. Bax positive cells were increased in the CS group compared to C group, in contrast to decreased bcl-2 positivity. CONCLUSION: Selenium limited apototic activity and histological changes due to the cisplatin related central neurotoxicity.

The Effect of Coumaric Acid on Ischemia-Reperfusion Injury of Sciatic Nerve in Rats.

The aim of the study was to determine the effect of coumaric acid on sciatic nerve ischemia/reperfusion (SNI) injury in rats. The rats were randomly divided into four groups: control group (no medication or surgical procedure), SNI group, SNI + coumaric acid (CA) group, and SNI + methylprednisolone (MP) group. Ischemia was achieved by abdominal aorta clamping, and all animals were sacrificed 24 h after ischemia. Harvested sciatic nerve segments were investigated histopathologically and for tissue biochemistry. A significant decrease in MDA, an increase in NRF1 levels, and increase in SOD activity were observed in the groups which received coumaric acid and methylprednisolone when compared to the corresponding untreated group (p < 0.05). Ischemic fiber degeneration significantly reduced in the SNI + CA and SNI + MP groups, especially in the SNI + MP group, compared to the SNI group (p < 0.05). Beta amyloid protein expressions were significantly decreased in the SNI + CA group compared to the SNI group (p < 0.05). Our study revealed that coumaric acid treatment after ischemia/reperfusion in rat sciatic nerves reduced oxidative stress and axonal degeneration. Therefore, coumaric acid may play a role in the treatment of peripheral nerve injuries due to ischemia/reperfusion.

Selenium protects cerebral cells by cisplatin induced neurotoxicity

PURPOSE: To evaluate the central nervous system toxicity of cisplatin and neuroprotective effect of selenium. METHODS: Twenty-one male Wistar albino rats were divided into three groups: control (C), cisplatin (CS), cisplatin and selenium (CSE, n=7 in each group). Cisplatin (12 mg/kg/day, i.p.) was administered to CS and CSE groups for three days. Furthermore, CSE group received 3mg/kg/day (twice-a-day as 1.5 mg/kg) selenium via oral gavage five days before cisplatin injection and continued for 11 consecutive days. The same volumes of saline were administered to C group intraperitoneally and orally at same time. RESULTS: Heterochromatic and vacuolated neurons and dilated capillary vessels in the brain were observed in the histochemical examinations of cisplatin treated group. Rats that were given a dose of 3mg/kg/day selenium decreased the cisplatin induced histopathological changes in the brain, indicating a protective effect. In addition, cytoplasmic staining of the cell for bcl-2, both cytoplasmic and nuclear staining for bax were determined to be positive in the all groups. Bax positive cells were increased in the CS group compared to C group, in contrast to decreased bcl-2 positivity. CONCLUSION: Selenium limited apototic activity and histological changes due to the cisplatin related central neurotoxicity. .

The Neuroprotective Effect of Coumaric Acid on Spinal Cord Ischemia/Reperfusion Injury in Rats.

The main causes of spinal cord ischemia are a variety of vascular pathologies causing acute arterial occlusions. We investigated neuroprotective effects of coumaric acid on spinal cord ischemia injury in rats. Rats were divided randomly into four groups of eight animals as follows: control, ischemia, ischemia + coumaric acid, and ischemia + methylprednisolone. In the control group, only a laparotomy was performed. In all other groups, the spinal cord ischemia was performed by the infrarenal aorta cross-clamping model. Levels of malondialdehyde and nuclear respiratory factor 1 were analyzed, as were the activity of superoxide dismutase. Histopathological and immunohistochemical evaluations were performed. Neurological evaluation was performed with the Tarlov scoring system. The ischemia + coumaric acid group was compared with the ischemia group, and a significant decrease in malondialdehyde and levels was observed. Nuclear respiratory factor 1 level and superoxide dismutase activity of the ischemia + coumaric acid group were significantly higher than in the ischemia group. In histopathological samples, the ischemia + coumaric acid group is compared with the ischemia group, and there was a significant increase in numbers of normal neurons. In immunohistochemical staining, hypoxia-inducible factor-1α and NF-kappa B immunopositive neurons were significantly decreased in the ischemia + coumaric acid group compared with that in the ischemia group. The neurological deficit scores of the ischemia + coumaric acid group were significantly higher than the ischemia group at 24 h. Our results revealed for the first time that coumaric acid exhibits meaningful neuroprotective activity following ischemia-reperfusion injury of the spinal cord.

Neuroprotective effect of alpha-lipoic acid and methylprednisolone on the spinal cord ischemia/reperfusion injury in rabbits.

OBJECTIVE: The aim of this study is to investigate the putative neuroprotective effect of alpha-lipoic acid (LA) on spinal ischemia/reperfusion (I/R) injury in rabbits. METHODS: Thirty-five adult female New Zeland rabbits, weighing 2,000-3,500 g (mean: 2,800), were divided randomly into five groups of seven rabbits each (n: 7) as Group 1: sham, only laparotomy; Group 2 (I/R): I/R; Group 3 (LA): I/R and 100 mg/kg of LA; Group 4 (MP): I/R and 30 mg/kg of methylprednisolone (MP); and Group 5 (LA + MP): I/R and 100 mg/kg of LA plus 30 mg/kg of MP. RESULTS: A statically significant effect of LA, MP, and LA plus MP on lowering malondialdehyde levels both in the blood and in the cerebrospinal fluid (CSF) has been observed. Nitric oxide is significantly decreased in the blood and spinal cord tissues, and also in the CSF but it is not significant. Superoxide dismutase, catalase, and glutathione levels were increased by LA administration. CONCLUSION: LA exhibits antioxidant efficacy in spinal cord I/R injury, but it cannot decrease the oxidative stress. The histopathological result of the present study also demonstrated that LA has neuroprotective effect in spinal cord injury.

Attenuation of cerebral vasospasm and secondary injury by testosterone following experimental subarachnoid hemorrhage in rabbit.

BACKGROUND: The vasodilatator effects of testosterone have been widely studied and demonstrated. Based on previous studies of these vasodilatatory activities, we hypothesized that testosterone might have potential effects on subarachnoid hemorrhage-induced cerebral vasospasm. METHODS: Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits in each group: group 1 (control); group 2 (subarachnoid hemorrhage); group 3 (subarachnoid hemorrhage + vehicle); and group 4 (subarachnoid hemorrhage + testosterone). Testosterone (15 mg/kg, intraperitoneally) was administered 5 min after the intracisternal blood injection and continued for 72 h once per day in the same dose for group 4. Animals were killed 72 h after subarachnoid hemorrhage. Basilar artery cross-sectional areas, arterial wall thicknesses, and hippocampal degeneration scores were evaluated in all groups. RESULTS: Intraperitoneal administration of testosterone was found to attenuate cerebral vasospasm and provide neuroprotection after subarachnoid hemorrhage in rabbits. Testosterone treatment was determined to be effective at increasing the luminal area and reducing the wall thickness of the basilar artery. CONCLUSIONS: Our findings show that testosterone has some preventive effects on SAH-induced vasospasm and secondary neuronal injury in rabbits. We propose that the vasodilatatory activity of testosterone is due to its effects on inhibiting calcium channels, activating potassium channels, augmenting nitric oxide synthesis, and inhibiting oxidant stress and inflammation.

Anti-inflammatory and antiapoptotic effect of interleukine-18 binding protein on the spinal cord ischemia-reperfusion injury.

We investigated the anti-inflammatory and antiapoptotic effects of interleukin-18 binding protein (IL-18BP) on spinal cord ischemia/reperfusion (I/R) injury in rats. Twenty-one adult male rats were divided into three groups: sham, I/R, and I/R+IL-18BP. Proinflammatory cytokines were determined in rat blood samples by using ELISA, while apoptosis was immunohistochemically evaluated in spinal cord tissue using caspase 3. Both IL-18 and TNF-α were significantly decreased in the IL-18BP group compared to that in the sham group. The highest caspase 3 levels were observed in the I/R group, while the lowest levels were found in the sham group. The mean Tarlov score of the I/R group was significantly lower than that of the sham group. However, the mean Tarlov score of the IL-18BP group was significantly higher than that of the I/R group. The results of the current study demonstrate that IL-18BP plays both anti-inflammatory and antiapoptotic roles in spinal cord I/R injury.

Pneumocephalus and pneumorrhachis after spinal surgery: case report and review of the literature.

Trauma is a common cause of pneumocephalus, or air in the cranial cavity, and of pneumorrhachis, or the presence of intraspinal air. After spinal surgery, occurrence of pneumocephalus, especially with pneumorrhachis, is extremely rare. We report the case of a patient who developed pneumocephalus and pneumorrhachis after lumbar disc surgery and pedicle screw fixation. There was no cerebrospinal fluid leakage during surgery. On postoperative day 1, the patient complained of headache, nausea, and dizziness. Brain and lumbar computed tomography scans revealed pneumocephalus and pneumorrhachis. With conservative treatment, the patient's complaints resolved within 10 days.

The effect of electromagnetic radiation on the rat brain: an experimental study.

AIM: The aim of this study is to determine the structural changes of electromagnetic waves in the frontal cortex, brain stem and cerebellum. MATERIAL AND METHODS: 24 Wistar Albino adult male rats were randomly divided into four groups: group I consisted of control rats, and groups II-IV comprised electromagnetically irradiated (EMR) with 900, 1800 and 2450 MHz. The heads of the rats were exposed to 900, 1800 and 2450 MHz microwaves irradiation for 1h per day for 2 months. RESULTS: While the histopathological changes in the frontal cortex and brain stem were normal in the control group, there were severe degenerative changes, shrunken cytoplasm and extensively dark pyknotic nuclei in the EMR groups. Biochemical analysis demonstrated that the Total Antioxidative Capacity level was significantly decreased in the EMR groups and also Total Oxidative Capacity and Oxidative Stress Index levels were significantly increased in the frontal cortex, brain stem and cerebellum. IL-1ß level was significantly increased in the EMR groups in the brain stem. CONCLUSION: EMR causes to structural changes in the frontal cortex, brain stem and cerebellum and impair the oxidative stress and inflammatory cytokine system. This deterioration can cause to disease including loss of these areas function and cancer development.