Learning and memory deficits in rats induced by chronic thinner exposure are reversed by melatonin.

Thinner is a neurotoxic mixture which is widely used as an aromatic industrial solvent. This product has been shown to cause functional and structural changes in the central nervous system. We investigated the effect of exposure to high concentrations (3000 p.p.m.) of thinner for 45 days (1 hr/day) on cognitive functions and the levels of neural cell adhesion molecules (NCAM) and lipid peroxidation products (LPO) in the hippocampus, cortex and cerebellum of rats. The actions of melatonin on the effects produced by thinner exposure were also tested. Thinner exposure caused a significant increase in LPO (malondialdehyde and 4-hydroxyalkenals) in all brain regions. Melatonin administration significantly reduced LPO and elevated glutathione levels in the brain regions. NCAM (180 kDa) was significantly decreased in hippocampus and cortex of thinner-exposed rats. Furthermore, thinner-exposed rats showed cognitive deficits in passive avoidance and Morris water maze tasks, whereas in the rats chronically treated with melatonin these effects were reversed. This study indicates that treatment with melatonin prevents learning and memory deficits caused by thinner exposure possibly by reducing oxidative stress and regulating neural plasticity.

Skull metastasis from thyroid follicular carcinoma with difficult diagnosis of the primary lesion.

A 57-year-old male patient presented with an immobile ellipsoid mass of 6-cm diameter in the right occipitoparietal region. Cranial computed tomography showed the mass with dense contrast enhancement causing bone destruction. After embolization of the mass, total resection was performed. Histological examination showed the mass had a capsule, with no invasion of the dura mater or dermis, and the follicles of various sizes covered with mono-lined thyrocytes were full of colloid. Immunohistochemical examination showed positive staining for thyroglobulin. Postoperatively, levels of thyroid hormones were normal, and thyroid ultrasonography and technetium-99m scintigraphy showed no abnormalities. Fine needle aspiration biopsy performed at various locations of the thyroid gland revealed no atypical thyroid cells. Whole body technetium-99m scintigraphy found no abnormal bone involvement. The histological evidence was suggestive of follicular carcinoma metastasis. Surgical treatment was planned for the thyroid gland, but the patient did not consent. Two years later, the patient presented with the pain and sensitivity in the sacrum, the right iliac wing, and the right caput femoris. Computed tomography revealed lytic lesions in these areas. Bone metastases were identified. Whole body scintigraphy showed increased activity in these regions, but the cranium and all other tissues were normal. The patient underwent total thyroidectomy under a diagnosis of follicular carcinoma. The present case of a lytic skull lesion associated with normal thyroid tissue on admission but finally treated as follicular thyroid cancer emphasizes the difficulty in histological discrimination of follicular carcinoma from normal thyroid tissue.

Seprafilm superior to Gore-Tex in the prevention of peridural fibrosis.

OBJECT: This is an investigation into the effects of two barrier membranes in the prevention of peridural fibrosis in an animal model. METHODS: Seprafilm or Gore-Tex was applied to a laminectomy defect overlying the dura mater in rats separated into treatment groups. A third group of rats underwent laminectomy only and served as controls. Two months postoperatively a histological study was performed to compare the amount of scar tissue in each group. The gross dissection demonstrated that both membranes created a controlled dissection plane, facilitated access to the epidural space, and provided a reduction in the amount of tissue adhering to the dura mater. Statistically, Seprafilm was superior to Gore-Tex in preventing peridural fibrosis (p < 0.05). CONCLUSIONS: Seprafilm can prevent peridural fibrosis better than Gore-Tex and can be used in humans in spinal surgery.

Meningocele with cervical dermoid sinus tract presenting with congenital mirror movement and recurrent meningitis.

Dermoid sinuses and meningoceles are seldom encountered in the cervical region. Besides, to the best of our knowledge, the coexistence of these types of congenital abnormalities with recurrent meningitis, as well as with mirror movement, has never been reported before. A 14-year-old female with the diagnosis of recurrent meningitis was referred to our clinic from the Department of Infectious Diseases. She had a cervical meningocele mass that was leaking cerebro-spinal fluid (CSF) and an associated mirror movement symptom. Spina bifida, dermoid sinus and meningocele lesions were demonstrated at the C2 level on computed tomography (CT) and magnetic resonance imaging (MRI). She underwent an operation to remove the sinus tract together with the sac, and at the same time the tethered cord between the sac base and the distal end of the spinal cord was detached. The diagnosis of dermoid sinus and meningocele was confirmed histopathologically. These kinds of congenital pathologies in the cervical region may also predispose the patient to other diseases or symptoms. Herein, a case of meningocele associated with cervical dermoid sinus tract which presented with recurrent meningitis and a rare manifestation of mirror movement is discussed. Neurosurgeons should consider the possible coexistence of mirror movement and recurrent meningitis in the treatment of these types of congenital abnormalities.

The mechanism of injury of the abducens nerve in severe head trauma: a postmortem study.

The aim of this study is to investigate the mechanism of injury of abducens nerve at petroclival region in severe head trauma. Twenty specimens provided from 10 autopsied cases due to severe head trauma were investigated macroscopically and histopathogically. The slices of the abducens nerve taken consecutively along its course at petroclival region were stained with Hematoxylline-Eosin and evaluated under light microscope. In addition, coexisting cervical injuries in these cases were assessed macroscopically. Edema and perineural hemorrhagia of abducens nerve were identified in all cases. Nerve injury was found more exaggerated at the sites of dural entry point and petrous apex than any other parts of the abducens nerve. Furthermore, microscopically, also remarkable perineural hemorrhage of the abducens nerve was observed at the site of its anastomoses with the sympathetic plexus on the lateral wall of the internal carotid artery (ICA). Abducens nerve is injured at the sites of dural entry point, petrous apex and lateral wall of the ICA, directly proportional with the severity of the trauma. This finding is also significant in verification of the severe head trauma.

Melatonin reduces glial reactivity in the hippocampus, cortex, and cerebellum of streptozotocin-induced diabetic rats.

Hyperglycemia plays a critical role in the development and progression of diabetic neuropathy. One of the mechanisms by which hyperglycemia causes neural degeneration is via the increased oxidative stress that accompanies diabetes. Metabolic and oxidative insults often cause rapid changes in glial cells. Key indicators of this response are increased synthesis of glial fibrillary acidic protein (GFAP) and S100B, both astrocytic markers. In the present study, we examined glial reactivity in hippocampus, cortex, and cerebellum of streptozotocin (STZ)-induced diabetic rats by determining the expression of GFAP and S-100B and we evaluated the effect of melatonin on the glial response. Western blot measurement of contents in brain regions after 6 weeks of STZ-induced diabetes indicated significant increases in these constituents compared with those in nondiabetic controls. Administration of melatonin prevented the upregulation of GFAP in all brain regions of diabetic rats. Using GFAP immunohistochemistry, we observed an increase in GFAP immunostaining in the hippocampus of STZ-diabetic rats relative to levels in the control brains. Treatment with melatonin resulted in an obvious reduction of GFAP-immunoreactive astrocytes in hippocampus. Like GFAP, S100B levels also were increased in all three brain areas of diabetic rats, an effect also reduced by melatonin treatment. Finally, the levels of lipid peroxidation products were elevated as a consequence of diabetes, with this change also being prevented by melatonin. These results suggest that diabetes causes increased glial reactivity possibly due to elevated oxidative stress, and administration of melatonin represents an achievable adjunct therapy for preventing gliosis.

Effects of prostaglandin E1, melatonin, and oxytetracycline on lipid peroxidation, antioxidant defense system, paraoxonase (PON1) activities, and homocysteine levels in an animal model of spinal cord injury.

STUDY DESIGN: Investigation of the effects of prostaglandin E1, melatonin, and oxytetracycline on lipid peroxidation, antioxidant and paraoxonase activities, and homocysteine levels in an experimental model of spinal cord injury. OBJECTIVES: To determine the antioxidant efficacy of prostaglandin E1, melatonin, and oxytetracycline and whether paraoxonase and homocysteine can be used as monitoring parameters in the acute oxidative stress of spinal cord injury. SUMMARY OF BACKGROUND DATA: Melatonin has been found useful in spinal cord injury in previous studies. No study exists investigating the effects of melatonin, prostaglandin E1, and oxytetracycline as well as the response type of paraoxonase enzyme and homocysteine levels in the acute oxidative stress of spinal cord injury. METHODS: Sixty-three male albino Wistar rats were anesthetized with 400 mg/kg chloral hydrate and divided into 5 groups. The G1 (n = 7) control group provided the baseline levels. G2-G5 underwent T3-T6 total laminectomies and spinal cord injuries by clip compression at the T4-T5 levels. Medications were applied to G3-G5 right after clip compression. Hence, G2 constituted laminectomy + injury, G3 laminectomy + injury + prostaglandin E1; G4 laminectomy + injury + melatonin, and G5 laminectomy + injury + oxytetracycline groups. Animals were decapitated either the first or fourth hour after injury. Spinal cord tissue and blood malonyldialdehyde and plasma homocysteine levels, plasma glutathione peroxidase, superoxide dismutase, paraoxonase activities were assayed. The SPSS 9.0 program was used for statistical analysis and graphics. Intergroup comparisons were made by Bonferroni corrected Mann Whitney U test (P < 0.025) and intragroups comparisons by Wilcoxon Rank test (P < 0.03). RESULTS: In injury groups, plasma homocysteine levels decreased and paraoxonase activities increased as erythrocyte superoxide dismutase levels and plasma glutathione peroxidase activities decreased in parallel to increases of tissue and blood malonyldialdehyde levels. These alterations were relatively suppressed by prostaglandin E1, melatonin, and oxytetracycline administrations in varying degrees. Melatonin was the most powerful agent, particularly at the fourth hour. Oxytetracycline was also effective, both at the first and fourth hour. Prostaglandin E1 was effective in comparison to injury group, but not as much as melatonin and oxytetracycline. CONCLUSIONS: Melatonin and oxytetracycline are effective in preventing lipid peroxidation in spinal cord injury. Paraoxonase and homocysteine can be used in monitoring the antioxidant defense system as well as superoxide dismutase and plasma glutathione peroxidase, both in injury and medicated groups.

Asymptomatic interval in delayed traumatic intracerebral hemorrhage: report of two cases.

Delayed traumatic intracranial hemorrhage (DTICH) is seen mostly in trauma to the occipitoparietal region by countercoup mechanism. It is most encountered within the first posttraumatic 10 days, particularly in the first 3. Herein, two cases of delayed traumatic intracerebral hemorrhage were discussed, first one presented with headache and vomiting who had been asymptomatic for 168 days after head trauma and the other presented with dysarthria and hyperkynesias after 92 days of asymptomatic interval, either being longer than that of the previous cases reported in the literature. Despite a long time elapse, DTICH should be considered in the differential diagnosis in the patients with history of head trauma that manifests at later stages with intracranial pressure elevation symptoms such as headache, vomiting.

Duplication of the abducens nerve at the petroclival region: an anatomic study.

OBJECTIVE: During its course between the brainstem and the lateral rectus muscle, the abducens nerve usually travels forward as a single trunk, but it is not uncommon for the nerve to split into two branches. The objective of this study was to establish the incidence and the clinical importance of the duplication of the nerve. METHODS: The study was performed on 100 sides of 50 autopsy materials. In 10 of 11 cases of duplicated abducens nerve, colored latex was injected into the common carotid arteries and the internal jugular veins. The remaining case was used for histological examination. RESULTS: Four of 50 cases had duplicated abducens nerve bilaterally. In seven cases, the duplicated abducens nerve was unilateral. In 9 of these 15 specimens, the abducens nerve emerged from the brainstem as a single trunk, entered the subarachnoid space, split into two branches, merged again in the cavernous sinus, and innervated the lateral rectus muscle as a single trunk. In six specimens, conversely, the abducens nerve exited the pontomedullary sulcus as two separate radices but joined in the cavernous sinus to innervate the lateral rectus muscle. In 13 specimens, both branches of the nerve passed beneath the petrosphenoidal ligament. In two specimens, one of the branches passed under the ligament and the other passed over it. In one of these last two specimens, one branch passed over the petrosphenoidal ligament and the other through a bony canal formed by the petrous apex and the superolateral border of the clivus. In all of the specimens, both branches were wrapped by two layers: an inner layer made up of the arachnoid membrane and an outer layer composed of the dura during its course between their dural openings and the lateral wall of the cavernous segment of the internal carotid artery. This finding was also confirmed by histological examination in one specimen. CONCLUSION: Double abducens nerve is not a rare variation. Keeping such variations in mind could spare us from injuring the VIth cranial nerve during cranial base operations and transvenous endovascular interventions.

Complete superior and inferior sagittal sinus thromboses with multiple cranial nerve pareses and transient ischemic attack--case report.

A 27-year-old woman with headache and right peripheral facial nerve paresis persisting for over 25 days, and left hemiparesis for 2 days, which had all been gradually improving, was admitted to our hospital as she suddenly developed horizontal and vertical diplopia. She had right fourth and sixth cranial nerve pareses, papilledema, and right orbital venous congestion, and also experienced a seizure on the day of admission. Magnetic resonance (MR) imaging and MR venography revealed complete superior and inferior sagittal sinus thromboses and significant collateral venous channels, but no parenchymal lesion. Fourth and seventh cranial nerve pareses and the left hemiparesis resolved completely within 2 days, but she concurrently developed an episode of right hemiparesis, which lasted for 30 minutes. The patient recovered with medical therapy. MR venography showed recanalization of both sinuses. She was neurologically intact except for minimal right abducens nerve paresis at discharge, 40 days after admission. Multiple cranial nerve pareses with transient ischemic attack is an extremely rare manifestation of superior sagittal sinus thrombosis. Transient functional disturbance due to temporary reduction of tissue perfusion caused by overload of the collateral channels is more likely to be responsible for the transient ischemic attack and reversible ischemic neurological deficit.

Dural and arachnoid membraneous protection of the abducens nerve at the petroclival region.

The goal of this study was to determine the membranous protection of the abducens nerve in the petroclival region. The petroclival portion of the abducens nerve was studied in ten dissections from five cadaveric head specimens. One of the heads was used for histological sections. Four heads were injected with colored latex for microsurgical dissections. The histological sections were prepared from petroclival dura mater, embedded in paraffin blocks, stained, sectioned in the axial, coronal, and sagittal planes, and evaluated by light microscopy. The abducens nerve was covered by a dural sleeve and arachnoidal membrane during its course within the petroclival area. Following the petrous apex, the abducens nerve was fixed by a sympathetic plexus and connective tissue extensions to the lateral wall of the cavernous segment of the internal carotid artery and to the medial wall of Meckel's cave. Fibrous trabeculations inside the venous space were attached to the dural sleeve. The lateral clival artery accompanied the dural sleeve of the abducens nerve and supplied the petroclival dura mater. The arterioles accompanying the abducens nerve through the subarachnoid space supplied the nerve within the dural sleeve. The arachnoid membrane covered the abducens nerve within the dural sleeve to the petrous apex, and arachnoid granulations found on the dural sleeve protruded into the venous space. The extension of the arachnoid membrane to the petrous apex and the presence of arachnoid granulations on the dural sleeve suggest that the subarachnoid space continues in the dural sleeve.