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Multipl skleroz geniþ bir klinik bulgu spektrumu olan, inflamatuvar demiyelinizan santral sinir sistemi hastalýðýdýr. Multipl skleroz lezyonlarý sýklýkla optik sinirleri, periventriküler ak maddeyi, beyin sapý, spinal kord ve serebellumu etkiler. Multipl skleroz geliþim mekanizmasý, hastalar arasýnda ve hastalýk dönemlerine göre kompleks ve heterojen özellik göstermektedir. Günümüze kadar, multipl skleroz kesin taný ve prognozuna yönelik spesifik yöntemler bulunmamaktadir. Aferent görsel yol, retinadan primer görsel kortekse uzanýr ve multipl sklerozda en sýk etkilenen alanlardan biridir (%94-99). Etkilenen optik sinirlerde gözlenen patolojik bulgular arasýnda inflamasyon, demiyelinizasyon, akson ve retinal sinir liflerinin (RNFL) hasarlanmasý ve RNFL incelmesi bulunmaktadýr. RNFL miyelinsiz aksonlardan oluþur, RNFL kalýnlýðýnýn deðerlendirilmesi akson hasarýný yansýtarak hastalýk progresyonunun deðerlendirilmesinde yardýmcý olur. Aferent görsel yolun klinik, görüntüleme ve elektrofizyolojik metodlarla deðerlendirilmesi multipl skleroz patofizyolojisinin anlaþýlmasý ve hastalýk prognozunun deðerlendirilmesinde önem taþýmaktadýr. Optik koherans tomografi RNFL kalýnlýðýný ölçerek multipl sklerozun santral sinir sistemi üzerine etkilerini deðerlendiren, pratik uygulanýmý olan, tekrarlanabilir bir metottur. Bu derleme ile optik koherans tomografinin multipl skleroz taný, hastalýk prognozu ve tedavi yaklaþýmlarýnýn etkilerinin deðerlendirilmesindeki yeri tartýþýlacaktýr.

Multiple sclerosis is an inflammatory demyelinating disorder of the central nervous system with a wide spectrum of clinical signs and symptoms. Multiple sclerosis lesions have a predilection for the optic nerves, periventricular white matter, brainstem, spinal cord, and cerebellum. The mechanisms responsible for multiple sclerosis are complex and heterogeneous across patients and disease stages. No specific markers exist for the definite diagnosis and prognosis of multiple sclerosis. The afferent visual pathway, which extends from the retina to the primary visual cortex including the optic nerve, is one of the most commonly affected sites in multiple sclerosis (94-99%). Pathology of affected optic nerves exhibits inflammation, demyelination, gliosis, axonal injury, and thinning of the retinal nerve fiber layer (RNFL). The RNFL is composed of unmyelinated axons, and measuring RNFL thickness is a viable method to monitor axonal loss reflecting disease progression. Optical coherence tomography is a noninvasive and reproducible tool in assessing the impact of multiple sclerosis on the thickness of the RNFL. Assessment of the afferent visual pathway using clinical, imaging and electrophysiological methods provides insights into the pathophysiology of multiple sclerosis and may also serve a prognostic role in multiple sclerosis.

AMAÇ: Bu çalýþmada ana karotid arter (AKA) intima-media kalýnlýðý (ÝMK) ve internal karotid arter (ÝKA) intima-media kalýnlýðý ile serebral infarkt hacmi arasýndaki iliþkinin araþtýrýlmasý planlandý.
YÖNTEMLER: Çalýþmaya, kliniðimize akut iskemik inme tanýsýyla ilk 24 saatte baþvurarak yatýrýlmýþ olan 40 hasta alýndý. Hastalarýn ilk baþvuru anýnda ve 72 saat sonra bilgisayarlý beyin tomografileri çekilerek infarkt hacimleri hesaplandý. Ýki yanlý Doppler ultrasonografi ile AKA ve ÝKA ÝMK’larý ölçüldü.
BULGULAR: Hastalarýmýzýn %77.5’inde karotis intima-media kalýnlýðý artýþý bulundu. Tek aterom plaðý olan grupta AKA ÝMK, plak olmayan gruba göre istatistiksel olarak anlamlý ölçüde daha fazla bulundu.
SONUÇ: Hem AKA hem de ÝKA ÝMK ile infarkt hacmi arasýnda istatistiksel anlamlýlýða ulaþan bir iliþki saptanmadý.

OBJECTIVE: In this study, it was aimed to determine the relation between the cerebral infarction volume and common carotid artery (CCA) intima-media thickness (IMT) and internal carotid artery (ICA) intima-media thickness.
METHODS: Forty patients diagnosed with acute ischemic stroke and admitted to our clinic within the first 24 hours were accepted into this study. The brain computed tomographies taken at admission and 72 hours after the onset of the first symptoms were analyzed. The volume of the infarct areas was measured. The bilateral carotis (C) IMT was measured by Doppler ultrasonography.
RESULTS: CCA IMT was significantly thicker in the group with single plaque compared to the group without plaque.
CONCLUSION: No statistically significant relation between the infarct volume and ICA IMT or CCA IMT was observed.

AMAÇ: Spastisite, inmeli hastalarda sýk karþýlaþýlan bir komplikasyondur. Spastisite günlük aktiviteleri gerçekleþtirmeyi önemli derecede engeller ve yaþam kalitesini düþürür. Bu çalýþmada inme sonrasý geliþen fokal spastisiteli olgularda, botulinum toksin A tedavisinin özürlülük, kas tonusu, aðrý ve günlük yaþam aktiviteleri üzerindeki etkilerinin araþtýrýlmasý amaçlanmýþtýr.
YÖNTEMLER: Botulinum toksin uygulama polikliniðinde takip edilen, inme nedeniyle botulinum toksin A uygulanan fokal spastisiteli 15 hasta deðerlendirilmiþtir. Hastalarýn tedavi öncesi ile tedavi sonrasý birinci ve üçüncü ay kontrolde spastisitenin þiddeti (Modifiye Ashworth Skalasý-MAS), kas gücü skoru (Medical Research Council Scale-MRC), özürlülük ölçeði, görsel aðrý derecelendirilme ölçeði (Visual Analogue Pain Scale), Barthel indeksi karþýlaþtýrýlmýþtýr.
BULGULAR: Biz çalýþmamýzda; tüm olgularda, klinik durumu yansýtan ölçekler kullanarak, botulinum toksin A tedavisinin etkili olduðunu saptadýk. Kas tonusu ve özürlülükte belirgin azalma elde ettik (p< 0.05). Bu sonuçla birlikte aðrýdaki anlamlý azalmanýn (p< 0.05) da fonksiyonel düzelmeye ciddi katkýsý olduðunu gözlemledik (p< 0.01). Skorlardaki düzelmenin yaný sýra, yaþam kalitesinin artmasý, kiþinin kendini iyi hissetmesi, fizyoterapiye yardýmcý olmasý, diðer sistemik ilaçlara gereksinimi azaltmasý açýsýndan da spastisite tedavisinde botulinum toksin A’nýn önemli bir yeri olduðunu düþünmekteyiz.
SONUÇ: Spastisite, etkilenen olgularda önemli özürlülüðe neden olan karmaþýk bir hastalýktýr. Botulinum toksini, spastisite gibi aþýrý motor aktivite içeren birçok hastalýðýn tedavisinde tercih edilmektedir. Uzun süreli ancak geri dönüþümlü etkisi, uygulama kolaylýðý, uygun güvenilirlik ve yan etki profili botulinum toksin A’yý fokal spastisitenin farmakolojik tedavisinde ilk seçenek haline getirmiþtir.

OBJECTIVE: Spasticity is a common dysfunction in stroke patients. It hinders the performance of everyday living activities and lowers the quality of life. In this study, it was aimed to investigate the effects of botulinum toxin A therapy on various aspects, such as muscle tone, pain, daily living activities and disability.
METHODS: Fifteen patients with stroke presenting with focal spasticity in the botulinum toxin outpatient unit were evaluated. Results before and after treatment were evaluated by applying different scales. Modified Ashworth Scale was applied for the severity of spasticity. The Medical Council Research Scale was used to test muscle power, and the disability scoring scale, Visual Analogue Pain Scale and Barthel index were the other measures tested.
RESULTS: It was found that therapy with botulinum toxin A was effective in spasticity. The increased muscle tone and the disability scores decreased prominently after the treatment (p< 0.05). Lower values in pain scores (p< 0.05) also contributed to better functional outcome (p< 0.01). Along with the significantly good outcome according to the scales, the higher scores in quality of life, feeling of well-being, good performance during the physiotherapy sessions, and less medications needed for spasticity were also indications in commencing the therapy of botulinum toxin A in spasticity.
CONCLUSION: Spasticity is a complicated condition causing serious disability. Botulinum toxin A is a preferred therapy when there is an increased motor activity. The effects of the agent are reversible and reliable. The duration of the treatment is long-lasting. Since botulinum toxin A is easily applied and the outcome in focal spasticity is favorable, it is recommended as the first-line choice in the treatment of focal spasticity.

Bu olgu sunumunda, multipl miyeloma baðlý kronik böbrek yetmezliði zemininde kemoterapötik ajanýn (zoledronik asit) derinleþtirdi¬ði hipokalsemi ve bu metabolik bozukluða baðlý olarak parkinsonizm epizotlarý geliþmiþ olan özgün bir olgu sunulmaktadýr. Multipl miyelom tanýsý almýþ ve altý aydýr aylýk bifosfonat tedavisi almakta olan 80 yaþýnda kadýn hasta, acil servisimize iki defa parkinsonizm epizodlarý ile baþvurdu. Replasman tedavisiyle düzelen parkinsonizm semptomlarýna, her iki epizotta da düþük kalsiyum düzeyleri eþ¬lik etmekteydi. Görüntülemelerde bazal gangliyonlarda herhangi bir patoloji izlenmedi. Her iki seferde de hastanýn kliniðinin kalsiyum replasmaný ile düzeltilmiþ olmasý, epizodlarýn asýl nedeninin hipokalsemi olduðunu düþündürmektedir. Bu, bazal gangliyonlarda olu¬þan yýkým sürecine baðlý bir hasardan ziyade, kemoterapötik ajanýn metabolik yan etkilerine baðlý geri dönüþlü fonksiyonel bir bozuk¬luðu yansýtan özgün bir olgu olarak yorumlanmaktadýr.

In this report, we present a unique case in which the chemotherapeutic agent, i.e., zoledronic acid, deepened the hypocalcemia on the basis of chronic renal failure secondary to multiple myeloma and caused parkinsonism episodes. An 80-year-old female patient, who had been diagnosed as multiple myeloma and had been administered bisphosphonate therapy monthly for six months, was ad¬mitted to our emergency room with two parkinsonism episodes. Low serum calcium levels accompanied parkinsonism symptoms, which subsided with calcium replacement therapy in both episodes. Imaging did not reveal any pathology in the basal ganglia. The fact that the patient was cured both times with calcium replacement suggests that hypocalcemia was the actual cause. This can be interpreted as a unique case, reflecting the reversible functional impairment due to metabolic side effects of a chemotherapeutic agent rather than destructive changes in the basal ganglia.

Heerfordt sendromu; ateþ, parotis bezinde büyüme, anterior üveit ve fasiyal sinir felcinin kombinasyonundan oluþan bir nörosarkoidoz formudur. Sunduðumuz 38 yaþýndaki kadýn hastanýn her iki gözde kýzarýklýk ve yanma, halsizlik, gece terlemeleri ve kilo kaybý þikayetleri baþladýktan 20 gün sonra her iki kulak arkasýnda sert aðrýlý þiþlikler ortaya çýktýðý öðrenildi. Üç hafta sonra sað periferik fasiyal paralizi geliþen hasta polikliniðimize baþvurmuþtu. Fizik muayenede her iki parotis bezinde solid ve aðrýlý kitleler palpe edildi. Nörolojik muayenesi sað periferik fasiyal parezi dýþýnda normaldi. Oftalmolojik muayenede bilateral anterior üveit saptandý. Kraniyal manyetik rezonans görüntüleme normaldi. Parotis manyetik rezonans görüntüleme tetkikinde her iki parotis bezinin boyutlarýnda artýþ, lobülasyon ve kistik lezyonlar ile heterojen kontrast tutulumu izlendi. Parotis biyopsisinde nonnekrotizan granülomatöz siyaladenit saptandý. Mediasten bilgisayarlý tomografi tetkikinde her iki akciðerde multipl nodüller mevcuttu. Laboratuvar tetkiklerinde C-reaktif protein 0.75, sedimentasyon 26 mm/saat ve anjiyotensin dönüþtürücü enzim 83 U/L (N: 8-52 U/L) idi. Heerfordt sendromu tanýsý konulan hastaya evre I sarkoidoz tanýsýna raðmen çoklu organ tutulumu nedeniyle 45 mg/gün steroid tedavisi baþlandý. Sonuç olarak, Heerfordt sendromu nörosarkoidozun nadir bir formu olmakla birlikte fasiyal sinir paralizisi ayýrýcý tanýsýnda akla gelmelidir.

Heerfordt syndrome is a form of neurosarcoidosis with the combination of fever, enlargement of the parotid gland, anterior uveitis, and facial nerve paralysis. We present a 38-year-old female patient who had a solid and painful swelling behind each ear 20 days after the complaints of redness of both eyes, fatigue, night sweat, and weight loss. Three weeks later, right facial paralysis developed, and the patient was seen in our outpatient clinic. On physical examination, bilateral solid and painful masses were observed on the parotid glands. Neurological examination was normal except for the right facial nerve paralysis. Ophthalmologic examination revealed bilateral anterior uveitis. Cranial magnetic resonance imaging was normal. On parotid gland magnetic resonance imaging, enlargement, lobulation and cystic lesions on both parotid glands with heterogeneous contrast involvement were observed. Parotid biopsy showed non-necrotizing granulomatous sialadenitis. There were multiple nodules on both lungs on mediastinum computerized tomography. Laboratory tests revealed: C-reactive protein 0.75 mg/dL, erythrocyte sedimentation rate 26 mm/hour and angiotensin-converting enzyme 83 U/L (N: 8-52 U/L) Though the patient, diagnosed as Heerfordt syndrome, had phase 1 sarcoidosis, she was treated with 45 mg/day steroid because of the multiple organ involvement. In conclusion, Heerfordt syndrome, a rare manifestation of neurosarcoidosis, must be kept in mind in the differential diagnosis of facial nerve paralysis.

Serebral malarya Plasmodium infeksiyonunun ender görülen bir komplikasyonudur. Ýnfekte eritrositlerin yaptýðý kapiller blokaj, sitokinlerin parankime sýzmasý sonucu oluþan mikroglial aktivasyon ve astrositlerin apopitozu etyopatogenezde suçlanan ana nedenlerdir. Son zamanlarda metabolik deðiþikliklerin de ensefalopati ve epilepsi patofizyolojisinden sorumlu olabileceði belirtilmektedir. Yirmi beþ yaþýnda erkek hasta epileptik nöbet ve ensefalopati kliniði ile baþvurdu. Serebral malarya tanýsý konan hastanýn kliniði antiödem, antiepileptik ve antimalaryal tedavi ile düzeldi. Literatür eþliðinde hastalýðýn patofizyolojisi, kliniði ve laboratuvar özellikleri tartýþýldý.

Cerebral malaria is a rare complication caused by Plasmodium infection. Capillary blockage caused by infected erythrocytes, microglia activation and apoptosis of astrocytes as a result of cytokine leakage to the parenchyma are cited in the pathogenesis. Recently, a concept has evolved that metabolic changes in the brain in malaria infection may also be responsible for the epilepsy and encephalopathy pathogenesis. A 25-year-old male was admitted to our clinic for seizures and encephalopathy. The patient, diagnosed with cerebral malaria, recovered with antiedema, antiepileptic and antimalarial therapy. The pathophysiology and clinical and laboratory findings are discussed in light of the literature.

Santral pontin miyelinolizis pons ve beynin bazal gangliyon, lateral genikulat cisimler, eksternal ve internal kapsül ve serebellumda miyelin kaybý ile giden nörolojik bir bozukluktur. Biz santral pontin miyelinolizisi olan üç ve hem santral pontin hem de ekstrapontin miyelinolizisi olan bir hastanýn klinik ve radyolojik bulgularýný sunduk.

Central pontine myelinolysis is a neurological disorder characterized by loss of myelin in the central pons as well as in the other parts of the brain like basal ganglia, lateral geniculate bodies, external and internal capsules, and cerebellum. We report the clinical and radiological findings of three patients with central pontine myelinolysis and one patient with both pontine and extrapontine myelinolysis.

POEMS sendromu, polinöropati ve multisistemik tutulum ile seyreden oldukça ender görülen bir plazma hücre diskrazisidir. Semptomlardan plazmasitom tarafýndan salgýlanan vasküler endotelyal büyüme faktörü sorumlu tutulmaktadýr. Distal simetrik sensörimotor polinöropati kliniði ile baþvuran, yaný sýra organomegali, endokrin bozukluk ve deri deðiþiklikleri de olan olgunun immünelektroforezinde serum ve idrarda M proteini saptanmasý nedeniyle POEMS sendromu düþünülmüþtür. Edinsel nöropatilerin ayýrýcý tanýsýnda akla gelmesi gereken bu sendrom ender görülmesi nedeniyle sunulmuþtur.

Presented with characteristic polyneuropathy and multisystemic manifestations, POEMS syndrome is a rare plasma cell disorder. Vascular endothelial growth factor, secreted by plasmacytoma, is considered responsible for these symptoms. The first symptoms in this patient were arthralgia, distal sensory impairment ascending proximally and motor impairment of distal lower extremities. By immunoelectrophoresis, M protein in serum and urine was detected. In addition to polyneuropathy and monoclonal gammopathy, the patient presented with organomegaly, endocrine dysfunction and skin changes, and was diagnosed as POEMS syndrome. This rare syndrome should be included in the differential diagnosis of acquired neuropathies associated with multisystemic manifestations.

Kýrk dört yaþýnda Miller Fisher sendromu tanýsý alan, Graves hastalýðý bulunan ve santral sinir sistemi demiyelinizasyonu saptanan bir erkek hasta sunuldu. Klinik ve laboratuvar bulgularý Miller Fisher sendromu tanýsýný destekliyordu. Olgunun kraniyal manyetik rezonans görüntülemesinde bilateral derin beyaz cevherde çok sayýda ovoid, T2 aðýrlýklý kesitlerde hiperintens gözlenen lezyonlar saptandý. Lezyonlar manyetik rezonans görüntüleme spektroskopi ile incelendiðinde demiyelinizasyon ile uyumlu olarak NAA/Cr oraný düþük olarak elde edildi. Periferik sinir sistemi ve santral sinir sisteminin kombine demiyelinizan süreçleri son derece nadir olarak ortaya çýkmaktadýr. Miller Fisher sendromu tanýlý bu olguda periferik sinir sistemi ve santral sinir sisteminin immünolojik etkilenimi ve Graves hastalýðý birlikteliði literatür eþliðinde tartýþýldý. Ýntravenöz immünglobulin G tedavisinden olumlu yanýt alýndý.

A 44-year-old male patient with a diagnosis of Miller Fisher syndrome, Graves disease and central nervous system demyelination is presented. Clinical and laboratory findings supported the diagnosis of Miller Fisher syndrome. On T2-weighted sections of cranial magnetic resonance imaging, many ovoid-shaped, hyperintense lesions in bilateral deep white matter were detected. Magnetic resonance imaging spectroscopy demonstrated low N-acetylaspartate to creatine (NAA/Cr) ratio consistent with demyelination. Combined peripheral nervous system and central nervous system demyelinating processes are rare. In this Miller Fisher syndrome case, an immunological mechanism affecting both the peripheral nervous system and central nervous system with association of Graves disease is discussed in light of the relevant literature. A positive response to intravenous immunoglobulin G treatment was obtained.