Remote Cerebellar Hemorrhage Presenting with Cerebellar Mutism after Spinal Surgery: An Unusual Case Report.

Dural injury during spinal surgery can subsequently give rise to a remote cerebellar hemorrhage (RCH). Although the incidence of such injury is low, the resulting hemorrhage can be life threatening. The mechanism underlying the formation of the hemorrhage is not known, but it is mostly thought to develop after venous infarction. Cerebellar mutism (CM) is a frequent complication of posterior fossa operations in children, but it is rarely seen in adults. The development of CM after an RCH has not been described. We describe the case of a 65-year old female who lost cerebrospinal fluid after inadvertent opening of the dura during surgery. Computerized tomography performed when the patient became unable to speak revealed a bilateral cerebellar hemorrhage.

Affective Temperament Profiles in Patients with Multiple Sclerosis: Association with Mood Disorders.

INTRODUCTION: The aim of the present study was to screen for bipolarity and to investigate the affective temperaments of patients with multiple sclerosis (MS) and the possible association between the clinical and demographic characteristics of MS patients and temperament profiles. METHODS: A total of 65 patients with MS and 66 healthy volunteers completed the 32-item hypomania checklist (HCl-32), the Mood Disorder Questionnaire (MDQ), and the Temperament Evaluation of Memphis, Pisa, Paris, and San Diego-Autoquestionnaire (TEMPS-A) tests. The HCl-32, MDQ, and TEMPS-A scores were compared between the patients and healthy volunteers. RESULTS: MS patients had significantly higher scores for the depressive, cyclothymic, irritable, and anxious domains of the TEMPS-A scale than the control group, whereas relapsing remitting MS (RRMS) patients had higher MDQ and TEMPS-A hyperthymia scores than secondary progressive MS patients. MS patients who were being treated with interferon beta 1-b therapy had significantly higher MDQ scores than those being treated with interferon beta 1-a, glatiramer acetate, or who were without medication. Expanded Disability Status Scale (EDSS) scores were positively correlated with TEMPS-A depressive and hyperthymic temperaments. CONCLUSION: Our results suggest that higher scores for affective temperament in MS patients indicate subclinical manifestations of mood disorders. Higher hyperthymia scores and manic symptoms detected in the RRMS group could shed light on the relationship between bipolarity and MS. Thus, the screening of bipolarity and affective temperament profiles in MS patients could help clinicians predict future mood episodes and decrease their impact on disease severity.

Neuroprotective effect of p-coumaric acid in rat model of embolic cerebral ischemia.

OBJECTIVES: Stroke poses a crucial risk for mortality and morbidity. Our study aimed to investigate the effect of p-coumaric acid on focal cerebral ischemia in rats. MATERIAL AND METHODS: Rats were randomly divided into four groups, namely Group I (control rats), Group II (ischemia rats), Group III (6 hr ischemia + p-coumaric acid rats) and Group IV (24 hr ischemia + p-coumaric acid rats). Cerebral ischemia was induced via intraluminal monofilament occlusion model. In all groups, the brain was removed after the procedure and rats were sacrificed. Malondialdehyde, superoxide dismutase and nuclear respiratory factor-1 were measured in the ischemic hemisphere. The histopathological changes were observed in the right hemisphere within the samples. Functional assessment was performed for neurological deficit scores. RESULTS: Following the treatment, biochemical factors changed significantly. Histopathologically, it was shown that p-coumaric acid decreased the oxidative damage. The neurological deficit scores of p-coumaric acid-treated rats were significantly improved after cerebral ischemia. CONCLUSION: Our results showed that p-coumaric acid is a neuroprotective agent on account of its strong anti-oxidant and anti-apoptotic features. Moreover, p-coumaric acid decreased the focal ischemia. Extra effort should be made to introduce p-coumaric acid as a promising therapeutic agent to be utilized for treatment of human cerebral ischemia in the future.

Neuroprotective effects of daidzein on focal cerebral ischemia injury in rats.

Daidzein, a plant extract, has antioxidant activity. It is hypothesized, in this study, that daidzein exhibits neuroprotective effects on cerebral ischemia. Rat models of middle cerebral artery occlusion were intraperitoneally administered daidzein. Biochemical and immunohistochemical tests showed that superoxide dismutase and nuclear respiratory factor 1 expression levels in the brain tissue decreased after ischemia and they increased obviously after daidzein administration; malondialdehyde level and apoptosis-related cysteine peptidase caspase-3 and caspase-9 immunoreactivity in the brain tissue increased after ischemia and they decreased obviously after daidzein administration. Hematoxylin-eosin staining and luxol fast blue staining results showed that intraperitoneal administration of daidzein markedly alleviated neuronal damage in the ischemic brain tissue. These findings suggest that daidzein exhibits neuroprotective effects on ischemic brain tissue by decreasing oxygen free radical production, which validates the aforementioned hypothesis.

The protective effect of syringic acid on ischemia injury in rat brain.

BACKGROUND/AIM: Brain ischemia and treatment are important topics in neurological science. Free oxygen radicals and inflammation formed after ischemia are accepted as the most significant causes of damage. Currently there are studies on many chemopreventive agents to prevent cerebral ischemia damage. Our aim is to research the preventive effect of the active ingredient in syringic acid, previously unstudied, on oxidative damage in cerebral ischemia. MATERIALS AND METHODS: The rats were randomly divided into 4 groups: control group (no medication or surgical procedure), sham group (artery occlusion), artery occlusion + syringic acid group sacrificed at 6 h, and artery occlusion + syringic acid group sacrificed at 24 h. Obtained brain tissue from the right hemisphere was investigated histopathologically and for tissue biochemistry. RESULTS: Superoxide dismutase and nuclear respiratory factor 1 values decreased after ischemia and they increased after syringic acid treatment, while increased malondialdehyde levels after ischemia were reduced after treatment. Caspase-3 and caspase-9 values increased after ischemia and decreased after treatment; this reduction was more pronounced at 24 h. CONCLUSION: Our study revealed that syringic acid treatment in cerebral ischemia reduced oxidative stress and neuronal degeneration. In the light of the biochemical and histopathologic results of the present study, we think that syringic acid treatment may be an alternative treatment method.

The Neuroprotective Effect of Glycyrrhizic Acid on an Experimental Model of Focal Cerebral Ischemia in Rats.

Cerebral ischemia is still one of the most important topics in neurosciences. Our study aimed to investigate the neuroprotective and anti-oxidant effects of glycyrrhizic acid on focal cerebral ischemia in rats. Twenty-four rats were divided equally into three groups. A middle cerebral artery occlusion model was performed in this study where sham and glycyrrhizic acid were administered intraperitoneally following middle cerebral artery occlusion. Group I was evaluated as control. Malondialdehyde (MDA), superoxide dismutase (SOD), and nuclear respiratory factor-1 (NRF1) levels were analyzed biochemically on the right cerebral hemisphere, while ischemic histopathological studies were completed to investigate the anti-oxidant status. Biochemical results showed that SOD and NRF1 levels were significantly increased in the glycyrrhizic acid group compared with the sham group while MDA levels were significantly decreased. On histopathological examination, cerebral edema, vacuolization, degeneration, and destruction of neurons were decreased in the glycyrrhizic acid group compared with the sham group. Cerebral ischemia was attenuated by glycyrrhizic acid administration. These observations indicate that glycyrrhizic acid may have potential as a therapeutic agent in cerebral ischemia by preventing oxidative stress.

Effects of Tannic Acid on the Ischemic Brain Tissue of Rats.

Many studies of brain ischemia have shown the role played by massive ischemia-induced production of reactive oxygen species, the main mechanism of neuronal death. However, currently, there is no treatment choice to prevent cell death triggered by reactive oxygen species. In our study, we researched the effects of tannic acid, an antioxidant, on the ischemic tissue of rats with induced middle cerebral artery occlusion. The animals were divided into three groups of eight animals. The sham group were only administered 10 % ethanol intraperitoneally, the second group had middle cerebral artery occlusion induced and were given 10 % ethanol intraperitoneally, while the third group had middle cerebral artery occlusion with 10 mg/kg dose tannic acid dissolved in 10 % ethanol administered within half an hour intraperitoneally. The rats were sacrificed 24 h later, and brain tissue was examined biochemically and histopathologically. Biochemical evaluation of brain tissue found that comparing the ischemic group with no treatment with the tannic acid-treated ischemia group; the superoxide dismutase (SOD) levels were higher, malondialdehyde (MDA) levels were lower, and nuclear respiratory factor-1 (NRF-1) was higher in the tannic acid-treated group. Histopathological examination showed that the histopathological results of the tannic acid group were better than the group not given tannic acid. Biochemical and histopathological results showed that tannic acid administration had an antioxidant effect on the negative effects of ischemia in brain tissue.

Neuroprotective effect of humic Acid on focal cerebral ischemia injury: an experimental study in rats.

Stroke is still a major cause of death and permanent neurological disability. As humic acids are well-known antioxidant molecules, the purpose of this study was to investigate the potential neuroprotective effects of humic acid in a focal cerebral ischemia model. Twenty-four rats were divided equally into three groups. A middle cerebral artery occlusion model was performed in this study where control (group II) and humic acid (group III) were administered intraperitoneally following an ischemic experimental procedure. Group I was evaluated as sham. Malondialdehyde (MDA), superoxide dismutase (SOD), and nuclear respiratory factor-1 (NRF-1) levels were analyzed biochemically on the right side of the ischemic cerebral hemisphere, while ischemic histopathological studies were completed on the left side to investigate the antioxidant status. Biochemical results showed that SOD and NRF-1 levels were significantly increased in the humic acid group (III) compared with the control group (II) while MDA levels were significantly decreased. On histopathological examination, cerebral edema, vacuolization, degeneration, and destruction of neural elements were decreased in the humic acid group (III) compared with the control group (II). Cerebral ischemia was attenuated by humic acid administration. These observations indicate that humic acid may have potential as a therapeutic agent in cerebral ischemia by preventing oxidative stress.

Evaluation of platelet distribution width and mean platelet volume in patients with carotid artery stenosis.

Platelets contribute to the pathogenesis of atherosclerosis. Platelet activation has been linked with increased mean platelet volume (MPV) and platelet distribution width (PDW). We investigated the association between PDW, MPW, and the degree of carotid artery stenosis (CS). Patients (n = 229) were divided into 3 groups according to the North American Symptomatic Carotid Endarterectomy Trial criteria. Demographic and clinical features were collected retrospectively. Correlation analysis showed a positive association between PDW and the degree of CS. However, there was no significant correlation between CS and MPV. Moreover, we observed that PDW and low-density lipoprotein cholesterol were independent predictors of the degree of CS. This study showed that PDW, not MPV, is related to the degree of CS. Platelet distribution width could be a useful biomarker for CS. Whether targeting PDW will be of clinical benefit remains to be established.

Investigation of knee pain in osteoarthritic and neuropathic pain awareness.

The mechanism of neuropathic pain (NP) and osteoarthritic (OA) pain, although different, are both defined as chronic pain, and combinations are possible. In this study, the awareness of both types of chronic pain was investigated among patients and doctors. This prospective study was planned and coordinated by the orthopedic and internal medicine clinics and included 100 patients with a diagnosis of knee OA evaluated with the DN4 questionnaire. Patients with an OA diagnosis included those with NP linked to diabetes and those without NP, and these groups were compared using a visual analogue scale (VAS) and the Western Ontario and McMaster Universities Osteoarthritic Index (WOMAC). Data analysis of both groups focused on descriptive statistics of demographic and clinical characteristics. Twenty-four of the patients with type 2 diabetes mellitus (DM) were diagnosed with NP according to DN4 criteria, and began treatment. Of these patients, 21 (84%) had DM for 10 years or more, while 19 (86.4%) had HbA1c of 7 and above. The average WOMAC pain score for patients with NP was 4.33 ±â€ˆ1.2 while the score for VAS was 8.25 ±â€ˆ0.8. Patients without NP had a WOMAC pain score of 2.49 ±â€ˆ0.6 and a VAS of 6.28 ±â€ˆ1.8. It was observed that in these two knee OA patient groups, NP had a statistically significant enhancing effect on the WOMAC pain score and the VAS (p < 0.001). As underlying pathophysiological mechanism of pain caused by OA is complex, and OA is considered to have a component of NP, it has been proven to be useful to use drugs apart from conventional treatments for NP. We believe that, as a source of pain that is not relieved after arthroplasty, awareness level of NP among orthopedists should be increased and multidisciplinary studies are required on this topic.

Sleep disturbance among women with chronic pelvic pain.

OBJECTIVE: To investigate the effect of chronic pelvic pain (CPP), a debilitating condition, on sleep quality. METHODS: The present case-control study enrolled women older than 18 years attending the Gynecology Clinic of Çanakkale Onsekiz Mart University Hospital, Çanakkale, Turkey, with CPP between August 2011 and August 2012. The control group was selected from women attending the clinic for another complaint. Sleep quality was evaluated via the Pittsburgh Sleep Quality Index, and differences between the groups were compared by t and χ(2) tests. RESULTS: During the study period, 157 women were enrolled. Seventy-two had CPP symptoms, and 85 attended the clinic for other complaints. Poor sleep quality was found in 80% (n = 58) of the women with CPP, and 55% (n = 47) of the control group (P < 0.05). CONCLUSION: Women with CPP were found to have poor sleep quality. Sleep education should be recommended in psychiatry and neurology clinics to increase the awareness of sleeping problems among these women.

The neuroprotective effect of Sulindac after ischemia-reperfusion injury in rats.

PURPOSE: To investigate the neuroprotective effects of Sulindac on the hippocampal complex after global cerebral ischemia/reperfusion (I/R) injury in rats. METHODS: Thirty one Sprague-Dawley rats were used, distributed into group I (sham) n:7 were used as control. For group II (n:8), III (n:8) and IV (n:8) rats, cerebral ischemia was performed via the occlusion of bilateral internal carotid artery for 45 minutes and continued with reperfusion process. 0.3 mL/kg/h 0.9 % sodium chloride was infused intraperitoneally to the Group II rats before ischemia, 5µg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group III rats before ischemia and 5µg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group IV rats after ischemia and before reperfusion process. The levels of MDA, GSH and MPO activity were measured in the left hippocampus tissue. The hippocampal tissue of all group members were taken for histopathological study. RESULTS: The MDA and MPO levels increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). Beside these, the GSH levels decreased from group I (control) to group II (I/R) (P<0.05) and increased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05).The number of apoptotic neurons increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). CONCLUSION: The Sulindac may have neuroprotective effects on ischemic neural tissue to prevent the reperfusion injury after ischemia.

The neuroprotective effect of Sulindac after ischemia-reperfusion injury in rats

To investigate the neuroprotective effects of Sulindac on the hippocampal complex after global cerebral ischemia/reperfusion (I/R) injury in rats. Thirty one Sprague-Dawley rats were used, distributed into group I (sham) n:7 were used as control. For group II (n:8), III (n:8) and IV (n:8) rats, cerebral ischemia was performed via the occlusion of bilateral internal carotid artery for 45 minutes and continued with reperfusion process. 0.3 mL/kg/h 0.9 % sodium chloride was infused intraperitoneally to the Group II rats before ischemia, 5μg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group III rats before ischemia and 5μg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group IV rats after ischemia and before reperfusion process. The levels of MDA, GSH and MPO activity were measured in the left hippocampus tissue. The hippocampal tissue of all group members were taken for histopathological study. The MDA and MPO levels increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). Beside these, the GSH levels decreased from group I (control) to group II (I/R) (P<0.05) and increased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05).The number of apoptotic neurons increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). The Sulindac may have neuroprotective effects on ischemic neural tissue to prevent the reperfusion injury after ischemia.

Dural sinus filling defect: intrasigmoid encephalocele.

Filling defects of dural venous sinuses are considered to be a challenging problem especially in case of symptomatic patients. Many lesions have to be ruled out such as sinus thrombosis, arachnoid granulations and tumours. Encephalocele into dural sinus is also a rare cause of these filling defects of dural sinuses. Here, we report an extremely rare case with spontaneous occult invagination of temporal brain tissue into the left sigmoid sinus and accompanying cerebellar ectopia.