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2.
Article in English | MEDLINE | ID: mdl-38602541

ABSTRACT

BACKGROUND: Traumatic spinal cord injury (SCI) is the most common preventable cause of morbidity. Despite rapid advances in medicine, effective pharmacological treatment against SCI has not yet been confirmed. This study aimed to investigate the possible anti-inflammatory, antiapoptotic, and neuroprotective effects of safinamide after SCI in a rat model. METHODS: A total of 40 male Wistar albino rats were randomly divided into four groups. Group 1 underwent only laminectomy. Group 2 underwent SCI after laminectomy. In group 3, SCI was performed after laminectomy, and immediately afterward, intraperitoneal physiological saline solution was administered. In group 4, SCI was performed after laminectomy, and 90 mg/kg of safinamide was given intraperitoneally immediately afterward. Moderate spinal cord damage was induced at the level of thoracic vertebra nine (T9). Neuromotor function tests were performed and levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1ß) were measured. In both serum and spinal cord tissue, immunohistochemistry and histopathology studies were also conducted. RESULTS: TNF-α, IL-1ß, and IL-6 levels were found to be significantly increased in group 2 and group 3. In group 4, these levels were statistically significantly decreased. Group 4 also exhibited significant improvement in neuromotor function tests compared to the other groups. Histopathologically, it was found that group 4 showed significantly reduced inflammation and apoptosis compared to the other groups. CONCLUSION: This study revealed that safinamide has neuroprotective effects against SCI due to its anti-inflammatory, antiapoptotic, and antioxidant activities.

3.
Clin Rheumatol ; 43(6): 2139-2143, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38625644

ABSTRACT

Moyamoya syndrome (MMS) is a rare, chronic, progressive cerebrovascular disorder characterized by stenosis at the apices of the intracranial internal carotid arteries, including the proximal anterior cerebral arteries and middle cerebral arteries. Cerebral angiography images are used for detection through measurement. Systemic lupus erythematosus (SLE) is an autoimmune disease that can cause multisystemic involvement. The coexistence of SLE and MMS has been rarely reported in the literature. A 46-year-old male patient with malar rash, Raynaud phenomenon presented to the hospital with a complaint of weakness in the left lower extremity, which began 3 days before the date of the visit. In the diffusion magnetic resonance imaging, multiple diffusion restrictions were observed in the right frontal region. The patient underwent MR angiography, revealing stenosis in the terminal and supraclinoid segments of the right internal carotid artery, which made us consider moyamoya disease. This patient, with a malar rash and Raynaud's, a positive antibody profile, was diagnosed as a male with SLE accompanied by MMS.


Subject(s)
Lupus Erythematosus, Systemic , Magnetic Resonance Angiography , Moyamoya Disease , Humans , Male , Moyamoya Disease/diagnostic imaging , Moyamoya Disease/complications , Middle Aged , Lupus Erythematosus, Systemic/complications , Lupus Erythematosus, Systemic/diagnostic imaging , Lupus Erythematosus, Systemic/diagnosis , Raynaud Disease/complications , Raynaud Disease/diagnosis , Cerebral Angiography , Carotid Artery, Internal/diagnostic imaging , Diffusion Magnetic Resonance Imaging
4.
Acta Radiol ; 65(1): 115-122, 2024 Jan.
Article in English | MEDLINE | ID: mdl-37872692

ABSTRACT

BACKGROUND: Neuroprotective agents are needed to reduce cerebral damage during surgical or neurointerventional procedures including stroke patients. PURPOSE: To evaluate if thiopental can be used as a neuroprotective agent when injected intra-arterially in a transient ischemia model. MATERIAL AND METHODS: In total, 24 rabbits were studied as four groups of six animals. Group 1 served as the control group. In group 2, transient ischemia was obtained by intracarotid administration of degradable starch microspheres (DSM). Group 3 was administered thiopental intra-arterially via the carotid artery. Group 4 (experimental group) received both thiopental and DSM intra-arterially. DSM and thiopental were administered through a microcatheter placed into the common carotid artery via the central ear artery access. After sacrifice, apoptotic cells in the cerebral tissues of the animals were evaluated in H&E and TUNEL stained slides. RESULTS: There was a significant increase in the number of apoptotic glial or neuronal cells in group 2 compared to the control group and group 3. The mean number of both the apoptotic neuronal cells (6.8 ± 2.1 vs. 2.5 ± 1.3, P < 0.001) and the apoptotic glial cells (9.4 ± 3.1 vs. 4.6 ± 1.6, P < 0.001) were higher in group 2 compared to group 4. In addition, a higher level of neurological improvement was observed in group 4 compared to group 2 based on neurological assessment score. CONCLUSION: The intra-arterial administration of thiopental has a protective effect on both glial and neuronal cells during temporary cerebral ischemia in low doses.


Subject(s)
Brain Ischemia , Neuroprotective Agents , Humans , Animals , Rabbits , Thiopental/therapeutic use , Injections, Intra-Arterial , Neuroprotection , Brain Ischemia/drug therapy , Cerebral Infarction , Ischemia , Neuroprotective Agents/therapeutic use
5.
World Neurosurg ; 170: e558-e567, 2023 Feb.
Article in English | MEDLINE | ID: mdl-36403936

ABSTRACT

BACKGROUND: Traumatic brain injury is still an important health problem worldwide. Traumatic brain injury not only causes direct mechanical damage to the brain but also induces biochemical changes that lead to secondary nerve cell loss. In this study, we investigated the neuroprotective effect of milrinone after traumatic brain injury (TBI) in a rat model. METHODS: Forty male Wistar albino rats, were used. Rats were divided into 4 groups: 1) sham, 2) TBI, 3) TBI + Ringers, and 4) TBI + Milrinone. In group 1 (sham), only craniotomy was performed. In group 2 (TBI), TBI was performed after craniotomy. In group 3 (TBI + Ringer), TBI was performed after craniotomy and intraperitoneal Ringers solution was given immediately afterward. Group 4 (TBI + Milrinone), TBI was performed after craniotomy, and milrinone was given 1.0 mg/kg milrinone intraperitoneally directly (0.5 mg/kg milrinone intraperitoneally again 24 hours, 48 hours, and 72 hours after trauma). Tests were performed for neurological and neurobehavioral functions. Immunohistochemistry and histopathology studies were performed. RESULTS: In group 4 compared with group 2 and group 3 groups, tests for neurological functions and neurobehavioral functions were significantly better. In the milrinone treatment used in group 4, plasma and brain tissue tumor necrosis factor, 8-OH 2-deoxyguanosine , and interleukin 6 levels were significantly decreased, and increased plasma and tissue IL-10 levels were detected. Histopathological spinal cord injury and apoptotic index increased in groups 2 and 3, while significantly decreasing in group 4. CONCLUSIONS: This study shows for the first time that the anti-inflammatory, antioxidant and antiapoptotic properties of milrinone may be neuroprotective after TBI.


Subject(s)
Brain Injuries, Traumatic , Brain Injuries , Neuroprotective Agents , Animals , Rats , Male , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Milrinone/pharmacology , Milrinone/therapeutic use , Rats, Wistar , Brain Injuries, Traumatic/drug therapy , Brain Injuries, Traumatic/pathology , Brain Injuries/pathology , Brain/pathology , Disease Models, Animal
6.
J Surg Case Rep ; 2021(4): rjaa420, 2021 Apr.
Article in English | MEDLINE | ID: mdl-33868633

ABSTRACT

Herein, we report the case of a 32-year-old man who experienced spontaneous migration of a bullet within the brain following a gunshot injury. Emergent computed tomography revealed the bullet located in the posterosuperior side of mesencephalon. During follow-up after 10 days, the neurological status of the patient had worsened. Computed tomography revealed that the bullet had migrated posteriorly and lodged in the occipital lobe. Although a few studies have reported on the spontaneous migration of a bullet within the brain, the present case is unique as the patient examination changed with migration. We recommend serial imaging and surgery in cases of bullet migration in the brain.

7.
Turk Neurosurg ; 27(5): 751-755, 2017.
Article in English | MEDLINE | ID: mdl-28481394

ABSTRACT

AIM: Cerebral vasospasm after subarachnoid hemorrhage (SAH) is an important cause of morbidity and mortality. In this study, we examined the effects of L-carnitine on the cerebral vasospasm process. MATERIAL AND METHODS: Twenty male New Zealand white rabbits were randomly divided into 4 groups. Group 1 served as control; group 2 was not subjected to SAH and received intravenous L-carnitine 3 times; group 3 was subjected to SAH and group 4 was subjected to SAH and treated with 100 mg/kg intravenous L-carnitine at 0, 24, and 48 hours after SAH. All animals were euthanized by perfusion-fixation 72 hours after SAH induction. The brains were then removed and stored in fixative +4°C overnight. The subjects" basilar arteries were sectioned from four separate zones. Basilar artery cross-sectional areas and thicknesses of vessels were measured by using the SPOT for Windows Version 4.1 computer programme. Statistical comparisons were performed by using the Kruskal-Wallis and Mann-Whitney U tests. RESULTS: Basilar artery wall thicknesses in group 4 were significantly lower than in group 3 (p=0.009). Basilar artery cross-sectional areas in group 4 were higher than in group 3 and the difference was statistically significant (p=0.008). CONCLUSION: L-carnitine was shown to be potentially beneficial on the resolution of cerebral vasospasm following SAH.


Subject(s)
Basilar Artery/drug effects , Carnitine/administration & dosage , Subarachnoid Hemorrhage/complications , Vasospasm, Intracranial/etiology , Animals , Carnitine/therapeutic use , Disease Models, Animal , Male , Rabbits , Vasospasm, Intracranial/drug therapy
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