Mehmet Guney Senol

The effects of gabapentin on acute and chronic pain after inguinal herniorrhaphy.

Background and objective To find out whether preoperative gabapentin use had a favourable effect on long-term postoperative pain in patients undergoing inguinal herniorrhaphy. Methods Sixty male patients – aged 20–40 years – who were scheduled for unilateral inguinal herniorrhaphy under spinal anaesthesia were included in this prospective, randomized, double-blind study. The patients were randomly allocated to two groups: the gabapentin group (n = 30) received single-dose 1.2 g oral gabapentin 1 h before surgery, and the placebo group received a placebo capsule instead. Spinal anaesthesia was performed with heavy bupivacaine, and all operations were performed by the same surgeon with the same technique. Postoperative analgesia was evaluated during sitting and lying with a visual analogue scale. Assessment of postoperative pain at 1, 3 and 6 months was carried out with an 11-point numerical rating scale; 0 indicating ‘no pain’ and 10 indicating ‘worst pain imaginable’. Patients who had numerical rating scale scores of more than 0 were further evaluated with regard to the impact of pain on their daily activities. Results When compared with the placebo group, the gabapentin group displayed significantly lower visual analogue scale scores (lying and sitting) and total tramadol consumption at 8, 12, 16, 20 and 24 h after surgery (P < 0.05) and higher postoperative patient satisfaction scores (P < 0.05). Numerical rating scale scores at 1, 3 and 6 months after surgery were lower in the gabapentin group than in the placebo group (P < 0.05). The number of patients whose daily activities were adversely affected by pain was smaller in the gabapentin group at the first month; however, the two groups were found to be similar at 3 and 6 months. Conclusion We conclude that preoperative single-dose gabapentin decreases the intensity of acute postoperative pain, tramadol consumption and the incidence and intensity of pain in the first 6 months after inguinal herniorrhaphy.

Sonographic appearances of the normal ulnar nerve in the cubital tunnel

To investigate the sonographic characteristics of the normal ulnar nerve in the cubital tunnel, as well as any differences related to age, sex, and dominant arm.

Cerebral white-matter lesions in asymptomatic military divers.

INTRODUCTION There is some concern that over a period of years, diving may produce cumulative neurological injury even in divers who have no history of decompression sickness. We evaluated asymptomatic divers and controls for cerebral white-matter lesions using magnetic resonance imaging (MRI). METHODS The study enrolled 113 male military divers (34.4 +/- 5.6 yr) and 65 non-diving men (33.1 +/- 9.0 yr) in good health. Exclusion criteria included any condition that might be expected to produce neurological effects. Patent foramen ovale was not assessed. A questionnaire was used to elicit diving history. A 1.5-T MRI device was used to acquire T1, T2-weighted, and fluid attenuated inversion recovery (FLAIR) images of the brain. A lesion was counted if it appeared hyperintense on both T2-weighted and FLAIR images. RESULTS MRI revealed brain lesions in 26 of 113 divers (23%) and in 7 of 65 (11%) controls, a difference that was statistically significant. There was no significant difference between the groups with respect to blood pressure, smoking history, or alcohol consumption, and no subject reported a history of head trauma or migraine. There was no relationship between MRI findings and age, diving history, or lipid profile in divers. DISCUSSION The higher incidence of lesions in the cerebral white matter of divers confirms the possibility that cumulative, subclinical injury to the neurological system may affect the long-term health of military and recreational divers.

Carbon Monoxide-Induced Cortical Visual Loss: Treatment with Hyperbaric Oxygen Four Years Later

Objective: We present a patient who developed visual loss after carbon monoxide (CO) poisoning and was treated with hyperbaric oxygen. Clinical Presentation and Intervention: A 21-year-old woman poisoned with CO (with coma lasting 4 h and carboxyhemoglobin level 46%) developed seizures and cortical blindness 3 days after poisoning. Four years later, her visual acuity was 0.2 in both eyes. An 18F-fluorodeoxyglucose positron emission tomography (PET) scan showed reduced metabolism in the bilateral posterior temporal and occipital lobes. The patient received a total of 50 hyperbaric oxygen sessions over 3 months for visual loss and the visual acuity improved to 0.5 in both eyes. In addition, increased metabolism was detected in the brain in post-treatment PET scans. Conclusion: PET documented brain hypoperfusion 4 years after CO poisoning and hyperbaric oxygen therapy improved visual acuity. However, we cannot endorse routine use of hyperbaric oxygen for such patients, until results of further clinical trials demonstrate efficacy of hyperbaric oxygen in CO-induced chronic brain injury.

Comparison of regeneration results of prefabricated nerve graft, autogenous nerve graft, and vein graft in repair of nerve defects

The purpose of this study was to evaluate the effectivity of prefabricated nerve grafts in the repairing nerve defect and to compare them with the autogenous nerve graft and vein graft. Four groups were created, each containing 10 rats. First, nerve prefabrication was carried out in groups I and II during 8 weeks. For this purpose, jugular vein graft was sutured to the epineural windows on the peroneal and tibial nerve at the right side in an end‐to‐side fashion. To create neurotrophic stimulus, partial incision was performed on the nerves in group I, and gene therapy was performed by plasmid injecting to the adjacent muscles in group II. At the end of the eighth week, prefabricated nerve grafts, jugular vein, and the axons passing through it were taken. Then, gap was created on the left peroneal nerve in all groups. Defect on the peroneal nerve was repaired by using the prefabricated nerve grafts in groups I and II, the autogenous nerve graft in group III, and the vein in group IV. Assessment of nerve regeneration was performed by using electromyography. Morphological assessment was performed after follow‐up period. According to electrophysiological and morphological results, the results of first three groups were similar. There was no statistically significant difference between three groups. Prefabricated nerve graft is as effective as autogenous nerve graft, and it can be used in the repair of nerve defects as autogenous nerve graft as an alternative.

Incidence of ischemic brain lesions in hyperbaric chamber inside attendants

Concern is growing about the negative long-term effects of hyperbaric exposure on the central nervous system of divers. This study was conducted with magnetic resonance imaging (MRI) to evaluate attendants that work inside hyperbaric chambers (known as inside attendants) for hyperintense brain lesions. Ten inside attendants and 10 healthy nondiving subjects were included in the study. A questionnaire was used to obtain information about subjects’ medical history, hyperbaric exposure history, alcohol intake, and smoking habits. T1-weighted, T2-weighted, and fluid-attenuated inversion recovery images were acquired with a 1.5-T MRI device. A lesion was included in the count if it was hyperintense on both T2-weighted and fluid-attenuated inversion recovery images. Although MRI revealed 3 hyperintense brain lesions in 2 of 10 inside attendants and in none of the controls, the differences between groups were not statistically significant (P=.147). The number of brain lesions counted did not correlate with the age of the inside attendants (r=0.007;P=.978), the number of hyperbaric exposures (r=-0.203;P=.574), or the duration of work as an inside attendant (r=0.051; P=.890). Investigators found a correlation, however, between the number of cigarettes smoked in a day and the number of brain lesions identified (r=0.779;P < .01). An increased incidence of hyperintense brain lesions was not observed in inside attendants who had never experienced decompression sickness compared with nondiving controls. Additional multicenter epidemiologic studies are needed if the occupational safety of inside attendants is to be enhanced.

Diagnostic Role of ECG Recording Simultaneously With EEG Testing

Arrhythmia is not uncommon in the etiology of syncope which mimics epilepsy. Data about the epilepsy induced vagal tonus abnormalities have being increasingly reported. So we aimed to evaluate what a neurologist may gain by a simultaneous electrocardiogram (ECG) and electroencephalogram (EEG) recording in the patients who underwent EEG testing due to prediagnosis of epilepsy. We retrospectively evaluated and detected ECG abnormalities in 68 (18%) of 376 patients who underwent EEG testing. A minimum of 20 of minutes artifact-free recording were required for each patient. Standard 1-channel ECG was simultaneously recorded in conjunction with the EEG. In all, 28% of females and 14% of males had ECG abnormalities. Females (mean age 49 years, range 18-88 years) were older compared with the male group (mean age 28 years, range 16-83 years). Atrial fibrillation was more frequent in female group whereas bradycardia and respiratory sinus arrhythmia was higher in male group. One case had been detected a critical asystole indicating sick sinus syndrome in the female group and treated with a pacemaker implantation in the following period. Simultaneous ECG recording in conjunction with EEG testing is a clinical prerequisite to detect and to clarify the coexisting ECG and EEG abnormalities and their clinical relevance. Potentially rare lethal causes of syncope that mimic seizure or those that could cause resistance to antiepileptic therapy could effectively be distinguished by detecting ECG abnormalities coinciding with the signs and abnormalities during EEG recording.

Comments on 'oxidative stress increases in carbon monoxide poisoning'

We read with great interest the article by Kavakli et al. in which the total oxidant and the antioxidant status were investigated in patients with carbon monoxide (CO) poisoning. Although lipid peroxidation has been linked to CO-induced neuropathology for more than two decades, serum levels of oxidative stress markers have not been investigated before. In this study, they measured, in patients with CO poisoning (n 1⁄4 88) and control subjects (n 1⁄4 37), serum levels of total oxidant and antioxidant status and calculated oxidative stress index (1⁄4 total oxidant status/total antioxidant status). They found that total oxidant status and oxidative stress index, but not total antioxidant status significantly increased in patients with CO poisoning when compared with controls. Additionally, they found that carboxyhemoglobin (COHb), total oxidant status and oxidative stress index were significantly reduced after 6 h of treatment. We applaud their efforts to gain insight into the pathophysiology of CO poisoning, which is a frequent cause of morbidity and mortality in Turkey. In the discussion, they conclude that ‘ . . . oxidative stress index may be a useful guide in planning treatment of CO poisoned patients’ and ‘ . . . in decision of hyperbaric oxygen therapy application, oxidative stress index levels should be taken into consideration’. We think that the data presented in this article is not sufficient to support their conclusion that oxidative stress index is a marker of severity and can be used in the selection of patients for hyperbaric oxygen therapy. Oxygen is first-line therapy in CO poisoning. Severely poisoned patients are referred to hyperbaric oxygen therapy. In order to argue that oxidative stress index can discriminate severely poisoned patients, they should have compared oxidative stress index levels in mild, moderate and severely poisoned patients. They could also analyze whether there is a correlation between COHb and oxidative stress markers. If the data is available, the authors could also analyze the correlation between oxidative stress markers and the number of clinical manifestations. Interestingly, in a recent study Garrabou et al. measured serum levels of lipid peroxidation (oxidative stress) in patients with CO poisoning and analyzed its correlation with clinical findings. Although, serum levels of lipid peroxidation were similar in patients with moderate and severe CO poisoning, pretreatment lipid peroxidation level was strongly correlated with the total number of symptoms along the 3 months follow-up. In addition, pretreatment lipid peroxidation was significantly higher in patients who developed late neurological sequel (LNS) compared with those without LNS. Since COHb poorly correlates with severity of CO poisoning, new serum markers are needed to evaluate severity and outcome of patients with CO poisoning. Further studies are needed to elucidate the value of oxidative stress markers in the management of CO poisoning.

Simultaneous posterior and middle cerebral artery infarct

On the follow-up, the patient developed painful, erythematous skin lesion of 15 cm in diameter, located on the lateral malleolus and dorsum of the foot [Figure 2]. MEFV gene investigation revealed homozygote mutation for M694V gene. Five pyrin gene mutations (E148Q, M680I, M694V, M694I and V726A) were detected by using the PRONTOTM FMF Basic Kit according to the manufacturer’s instructions. Biopsy specimens from the duedonum and rectum were negative for amyloidosis. A diagnosis of FMF with CNS demyelination was considered and colchicine therapy was started. With colchicine therapy, her symptoms regressed and no further progression of the disease was observed during two years follow-up.

Relationship between tuberculous otomastoiditis and tuberculous meningitis

OBJECTIVE The aim of this study was to determine the correlation between tuberculous meningitis and tuberculous otomastoiditis. MATERIALS AND METHODS Meningeal involvement sites were investigated by magnetic resonance imaging in 32 patients (21 males, 11 females) who had previously been diagnosed with tuberculous meningitis. Clinical and laboratory findings and responses to anti-tuberculous treatment were evaluated, and the presence of concomitant tuberculous otomastoiditis was also investigated. RESULTS The meningeal involvement site was unilateral (in the sylvian fissure and the perimesencephalic cistern) in 28 patients (87.5 per cent), and bilateral and widespread in four patients (12.5 per cent). Tuberculous otomastoiditis was found in 11 of the patients with tuberculous meningitis (34.3 per cent). Otomastoiditis was on the same side as the meningeal involvement in nine of these 11 patients. Bilateral otomastoiditis with meningeal involvement was observed in two patients. CONCLUSIONS Tuberculous meningitis is frequently accompanied by otomastoiditis, although the exact causal relationship between the two conditions is unclear. Since meningitis is a serious clinical condition, concomitant otomastoiditis generally remains unrecognised. Tuberculosis should be considered in the differential diagnosis of patients with otitis or otomastoiditis who do not respond to antibiotic therapy.