Aylin Bican

What Is the Efficacy of Nasal Surgery in Patients With Obstructive Sleep Apnea Syndrome

Purpose: Obstructive sleep apnea syndrome (OSAS) is characterized by repetitive episodes of partial or complete obstruction of the upper airway during sleep and is associated with increasing respiratory efforts, with a consequent oxyhemoglobin desaturation, sleep fragmentation, and daytime symptoms, most commonly excessive sleepiness. The effectiveness of continuous positive airway pressure (CPAP) is undoubtedly high in treating those patients who use it regularly, but for those who refuse it, the success rate is 0. It is for this subset of patients that surgical therapy can be useful. The purpose of this study was to evaluate the effects of nasal surgery on nasal resistance, sleep apnea, sleep quality, and nasal volumetric measurement in adult male patients with OSAS. Methods: Twenty male patients with complaints of hypersomnia and snoring were included in the study. Polysomnography of patients with the prediagnosis of OSAS was planned. All patients underwent CPAP treatment before and after surgery. Patients, who had anatomic structural defects causing nasal valve shrinkage, were operated on at the Plastic Reconstructive and Aesthetic Department. Volumetric measurements of the nose were obtained before and after the operation. Results: In our study, it was observed that respiratory tract space of patients increased subsequent to the surgery, and thereby OSAS level decreased, and tolerating CPAP device was easier. Measurements of internal nasal valve vertex and fields and external nasal valve fields before and after operation were significant. Conclusions: Surgical relief of this nasal obstruction may improve quality of life in patients with OSAS.

Hairy cell leukemia presenting with Guillain-Barre syndrome.

Hairy cell leukemia (HCL) is a chronic B-cell lymphoproliferative disorder, which mainly infiltrates the bone marrow and the spleen, resulting in peripheral cytopenias and splenomagaly [1]. Unusual complications including autoimmune phenomena have been described in HCL [2 – 4]. Of these, to the best of our knowledge, Guillain-Barre syndrome (GBS) was reported only in two cases so far [5,6]. Here, we describe a HCL patient who presented with GBS at the time of diagnosis. A 61-year-old previously healthy male was referred to our department complaining of weight loss, night sweats, and pain, weakness and parasthesia progressing from distal to proximal limb muscles for the last 3 weeks. There was no preceding history of viral illness or vaccination or any medication. His physical examination revealed pale appearance, hepatomegaly (3 cm) and splenomegaly (3 cm). Precise neurological examination demonstrated second motor neuron type tetraparesis prominent in the lower extremities (20% muscle strength in lower, 80% in the upper extremities) with hypoactive deep tendon reflexes and loss of vibration sense. Blood picture showed Hb 10.9 g/dl, MCV 96 fl, WBC 10.66 10 l with 44% lymphocytes, 37% hairy cells, 17% PNL, and 2% band leukocyte differentiation, and a platelet count of 2126 10 l. Erythrocyte sedimentation rate was elevated (130 mm/h). Biochemistry tests were normal except for alkaline phosphatase. Serum cobalamin level was found in normal limits. Cytomorphological examination of the bone marrow demonstrated a normocellular marrow with hairy cells infiltration. Flow cytometry of the bone marrow cells revealed positivity for CD19 (64%), CD20 (96.1%), CD11c (98.8%), CD25 (99.1%), CD22 (98.9%), and CD103 (29.3%) and negativity for CD23 (8.5%) and CD5 (3.4%). Histopathological examination of the bone marrow established the diagnosis of HCL (Figure 1). Then, the patient was referred to the Neurology department for consultation. Whole spine magnetic resonance imaging was normal. Lumbar puncture was performed. Protein content of cerebrospinal fluid (CSF) was 201 mg/dl and CSF was acellular. Electroneuromyography (ENMG) was consistent with sensorymotor demyelinating polyneuropathy. The patient was diagnosed as GBS with albuminocytologic dissociation of CSF and ENMG findings reflecting demyelination in both sensory and motor nerves. He was treated with

Effects of Propofol on Epileptiform Activity and Hippocampal Morphology inFebrile Convulsions and Pilocarpine Induced Seizures

Abstract Epidemiological and recent prospective analyses of long Febrile Seizures (FS) support the idea that such seizures can provoke Temporal Lobe Epilepsy (TLE) in some children. Because of the high prevalence of these seizures, if epilepsy was to arise as their direct consequence, this would constitute a significant clinical problem. Animal studies have revealed that exposure of hippocampal neurons to FS early in life, particularly prolonged or frequently repetitive FS, or together with brain malformation, may lead to sustained dysfunction of these cells including long-term memory impairment or epileptogenesis, in spite of the absence of neuronal damage. We established a hyperthermia model of febrile convulsions in young adult rats, and studied the effects of propofol treatment general anesthetic acting via GABA-A receptor on epileptiform activity and the morphological features of medial temporal lobe. We found statistically significant neuronal losses in the CA1, CA3 and dentate gyrus regions of hyperthermiaapplied rats as compared to the control rats. We also observed that propofol administration suppressed epileptic discharges in EEG and prevented clinical seizures behaviors. It took a median of 11 (range, 6-40) minutes for propofol to stop seizures. We conclude that prevention of epilepsy-related damage can be achieved via epileptogenesis-based clinical approaches, and that propofol is an effective agent in the hyperthermia-induced status epilepticus model.