BENİN ÇOCUKLUK ÇAĞI MYOZİTİ: AKUT OLARAK YÜRÜMEYİ REDDEDEN BİR ÇOCUKTA AYIRICI TANIDA DÜŞÜNÜLMESİ GEREKEN BİR HASTALIK

Benign childhood myositis is a disease of childhood which is characterised with calf pain and sudden onset of refusal to walk. The disease must be differentiated from more serious causes of refusal to walk or limb pain. Elevated creatin kinase, muscle tenderness, normal muscle power and deep tendon reflexes are the most important clues to reach the diagnosis. We report an eight year old boy who presented with acute onset of inability to walk. Based on history, clinical and laboratory findings, the diagnosis of benign childhood myositis is established. All pediatricians should be aware of this condition in order to prevent unnecessary investigations. Benign çocukluk çağı myositi, baldır ağrısı ve ani olarak yürümeyi reddetme ile karakterize bir çocukluk çağı hastalığıdır. Bacak ağrısı ve yürümeyi reddetmeye yol açacak çok daha ciddi hastalıklardan ayrımı yapılmalıdır. Artmış kreatin kinaz, kaslarda hassasiyet, normal kas gücü ve derin tendon refleksleri tanıya ulaşmada en önemli ipuçlarıdır. Bu yazıda ani olarak yürüme yetisini kaybeden sekiz yaşında bir erkek hasta sunulmaktadır. Vakaya öykü, klinik ve laboratuar bulguları ile benign çocukluk çağı myositi tanısı konulmuştur. Gereksiz incelemeleri önlemek için tüm pediatristler bu hastalık hakkında bilgi sahibi olmalıdır

PARTIAL CYTOCROM C OXIDASE DEFICIENCY RELATED LEIGH SYNDROME: A CASE REPORT

Leigh sendromu en çok ‘'sitokrom c oksidaz'' eksikliği sonucu ortaya çıkan ve erken süt çocukluğu döneminde nöbet, gelişme geriliği, hipotoni, solunum bozuklukları ve laktik asit yüksekliği ile karakterize bir mitokondrial ensefalomyopatidir. Enzim eksikliği parsiyel olan vakalarda klinik seyir ve laboratuvar bulguları daha farklı olabilmektedir. Bu yazıda altı aylıkken dirençli nöbetler ve psikomotor gerilik ile getirilen, yenidoğan döneminde laktik asit ve kraniyal MRG tetkiki normal olmasına rağmen izlemde laktik asiti yükselen ve kortikal atrofi gelişen parsiyel "sitokrom c oksidaz'' eksikliği ile ilişkili Leigh sendromlu bir vaka sunulmaktadır. SUMMARY Leigh disease is a mitochondrial encephalomyopathy that is frequently caused by "cytocrom c oxidase'' deficiency and is characterised with seizures, psychomotor deficiency, hypotonia, respiratory arrest and lactic acidosis in the early infancy period. Patients who have partial deficiency of the enzyme have different laboratory and clinical findings. We report a case with partial ‘'cytocrom c oxidase'' deficiency associated Leigh Syndrome who was admitted with refractory seizures and psychomotor retardation when she was 6-months-old with a raised lactic acid and cortical atrophy although the lactic acid level and cranial MRI were in normal ranges in her newborn period

Olanzapine attenuates brain damage after focal cerebral ischemia in vivo

Atypical antipsychotic drugs are widely used in the treatment of schizophrenia. These agents are discovered to have some additional beneficial effects beyond their effectiveness as antipsychotic drugs. Among these initially unexpected effects are their potential effects as mood stabilizers in bipolar disorder and their efficacy in improving long-term outcome in schizophrenia. These effects recently raised the question whether these drugs may also have some neuroprotective effect in the brain. To examine this matter, in this study we evaluated the neuroprotective effect of olanzapine after permanent focal cerebral ischemia. Anaesthetized male C57BL/6j mice were submitted to permanent thread occlusion of the middle cerebral artery (MCA). Olanzapine (0.1 and 1 mg/kg) or vehicle was applied intraperitoneally just after permanent ischemia. Twenty-four hours after permanent ischemia, brain injury was evaluated by triphenyltetrazolium chloride staining (TTC). Olanzapine (0.1 and 1 mg/kg) showed significant neuroprotection after permanent focal cerebral ischemia