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Chemotherapy induced peripheral neuropathy is a syndrome with distal symmetrical sensorial-dominant pain, tingling and numbness caused by neurotoxic chemotherapeutic agents. The severity increases with cumulative doses of chemotherapy, besides decrease in quality of life, may lead to cessation of treatment which may effect survival. Neurotoxicity causes large fiber and small fiber neuropathy through many pathologic mechanisms including mitochondrial dysfunction and oxidative stress. Dose related neuropathic pain is most commonly seen with taxanes, platins, vinca alkaloids, bortezomib and brentuximab. There is a limited effect of anticonvulsant and antidepressant medication for treatment. In this review awareness about chemotherapy induced peripheral neuropathy, prevention and treatment are discussed. [ABSTRACT FROM AUTHOR]

Copyright of MN Opthalmology / MN Oftalmoloji is the property of Medical Network and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Tepecik Education & Research Hospital / İzmir Tepecik Eğitim ve Araştırma Hastanesi Dergisi is the property of Logos Medical Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Diabetic neuropathy (DN) is the most common complication of diabetes mellitus. It causes microvascular and macrovascular damages and diagnosis can easily be overlooked by most physicians. Generally; the diagnosis of DN can be omitted by physicians dealing with diabetes treatment since it starts with non-specific findings, shows slow progression and can be confused with complaints in many diseases. It is estimated that there will be 578 million people diagnosed with DN in the world in 2030. Chronic hyperglycemia, microvascular insufficiency, oxidative and nitrosative stress, impaired neurotropism and autoimmunity are some of the factors that cause nerve destruction. Paresthesias such as tingling, burning, electrical shock-like sensations, numbness, throbbing, compression, pinpricks to the skin, complaints are the most common symptoms. There is no treatment for pathogenetic mechanisms in diabetic neuropathy that completely eliminates neuronal damage. The purposes of treatment is slowing down the progression of the disease, controlling the pain, preventing complications, quick and adequate treatment of occurred complications, maintaining the functional capacity of the patient. In this review, we aimed to comprehensively address the general approach to diabetic neuropathy, diagnosis and treatment.

Copyright of Journal of Physical Medicine & Rehabilitation Sciences is the property of Turkiye Klinikleri and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Traditional Medical Complementary Therapies is the property of Turkiye Klinikleri and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction:Chronic hypoxia is known to be one of the risk factors for peripheral neuropathy. However, the effect of intermittent hypoxia on peripheral nerves is not fully understood. This study evaluated the relation between intermittent hypoxia and peripheral nerve function in Obstructive Sleep Apnea (OSA) patients.Materials and Methods:In this retrospective study, 86 patients who underwent polysomnography (PSG) and electroneuromyography were enrolled. Participants with diseases affecting peripheral nerves and lung function were excluded from the study. Hypoxia parameters were obtained from the PSG study. Lower extremity motor and sensory nerve conduction studies of all patients were evaluated.Results:In patients with OSA, peroneal nerve distal motor latency and sural sensory nerve action potential amplitude was low and velocity was significantly slower than controls (p

Copyright of Journal of Health Sciences of Kocaeli University / Kocaeli Üniversitesi Sağlık Bilimleri Dergisi is the property of Institute of Health Sciences of Kocaeli University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Agri: Journal of the Turkish Society of Algology / Türk Algoloji (Ağrı) Derneği'nin Yayın Organıdır is the property of KARE Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

With the rising prevalence of morbid obesity, the numbers of bariatric surgical procedures are also increasing, thus resulting in more neurological complications to be recognized. Among these complications, the most well-defined are Wernicke's encephalopathy and peripheral neuropathies. Guillain Barre Syndrome (GBS) has been reported as a very rare complication of bariatric surgery and reported cases are mostly axonal types. An 18-year-old female patient applied to our outpatient clinic with complaints of pain and weakness in her arms and legs. She had bariatric surgery 3 months ago. The electrophysiological findings of the patient who had proximal muscle strength loss in the lower extremities were consistent with subacute anterior root anterior horn involvement in the L3-S1 innervated muscles. After the intravenous immunoglobulin therapy, the patient improved almost completely. We think that in neurological complications after bariatric surgery, nutritional deficiencies should be taken into consideration as well as inflammatory damage and these cases should be followed up and treated in a multidisciplinary manner in order to prevent permanent neurological damage. [ABSTRACT FROM AUTHOR]

Purpose: The blink reflex (BR) is a useful electrodiagnostic method for evaluating neuropathies. The aim of our study was to investigate the role of the BR in the early diagnosis of neuropathy in simple steatosis. Material and Methods: A total of 86 subjects were enrolled in this study: 56 patients (29 female, 27 male) with simple steatosis and 30 healthy controls (17 female, 13 male). After the electrical stimulation of the supraorbital nerve, two responses in the orbicularis oculi muscle occur, the early ipsilateral response and the late bilateral response latencies, which were recorded. Results: The triglyceride levels and lipid accumulation products were higher in the patients with steatosis than in the controls. When compared to the control group, the patient group had early right ipsilateral latency, late right ipsilateral latency, late right contralateral latency, early left ipsilateral latency, late left ipsilateral latency, and late left contralateral latency. Conclusion: There is a slowdown of the BR in the steatosis stage; therefore, by performing the BR, neuropathy can be detected at an early stage in patients with steatosis. [Cukurova Med J 2015; 40(4.000): 714-722]

Amaç: Blink refleks (BR) nöropatileri değerlendirmek için kullanılan yararlı bir elektrodiagnostik yöntemdir. Biz bu çalışmada basit steatozda nöropatinin erken tanısında BR’in rolünü incelemeyi amaçladık. Materyal ve Metod: Çalışmaya basit steatozlu 56 hasta (29 kadın, 27 erkek) ve 30 sağlıklı kontrol (17 kadın, 13 erkek) olmak üzere toplam 86 kişi dahil edildi. Supraorbital sinirin elektriksel uyarımından sonra orbikularis okuli kasında ortaya çıkan iki cevap, erken ipsilateral cevap ve geç bilateral cevap gecikme zamanları kaydedildi. Bulgular: Trigliserid düzeyi ve lipid akümülasyon skoru steatozlu hastalarda kontrol grubundan daha yüksekti. Kontrol grubuyla karşılaştırıldığında hasta grubunda erken sağ ipsilateral gecikme, geç sağ ipsilateral gecikme, geç sağ kontralateral gecikme, erken sol ipsilateral gecikme, geç sol ipsilateral gecikme ve geç sol kontralateral gecikme zamanı uzundu. Sonuç: Steatoz aşamasında BR’de yavaşlama vardır. Steatozlu hastalarda BR ölçülerek nöropati gelişimi erken aşamada tespit edilebilir

Objective: We have evaluated the functional scores of in situ ulnar nerve decompressed cubital tunnel sendrome patients. Materials and Methods: Between january 2006 and december 2010, 32 cubital tunnel syndrome patients operated in our clinic with ulnar neuropathy were evaluated retrospectively from 43 patients. All patients were diagnosed with clinically and electromyography, follow up period was at least 3 years. And also any patient have surgical history about cubital tunnnel syndrome before. McGowan's classification was used for preoperative scoring and the Wilson Krout classification for postoperative clinical evaluation. Results: Preoperatively 24 patient were degree 2, 8 patients were degree 3. There were excellent results in 22 patients (%), good in 7 (%), fair in 2 (%), and poor in one (%). Any of patients re-opereted cause of complaints. Conclusion: In situ decompression is an effective, simple and safe methode for cubital tunnel syndrome without ulnar nerve subluxation and with nöral continuity is intact. [ABSTRACT FROM AUTHOR]

Transthyretin-related familial amyloid polyneuropathy (TTR-FAP) is caused by gain-of-toxic-function of TTR, which dissociates from its native tetramer form to a monomer form and aggregates in several tissues and organs. Mutations in the TTR gene lead to this amyloidogenic transformation and cause autosomal dominant disease. TTR-FAP typically causes sensorimotor FAP accompanied by autonomic involvement, but considerable phenotypic diversity is noted between different mutation types. In the event of clinical suspicion, TTR gene sequencing and pathologic confirmation are the recommended paths to follow. Significant improvement has been achieved in treating the disease over the past 20 years, starting with liver transplantation, followed by tetramer stabilizers and TTR-lowering therapies. Although there are still some uncertainties in diagnosing and treating TTR-FAP, recent advances are promising, especially in the field of treatment. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Physical Medicine & Rehabilitation Sciences is the property of Turkiye Klinikleri and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: In terms of prevention and therapy, in patients with diabetes mellitus it is important to foresee chronic complications as neuropathy. In this study we aimed to evaluate the contribution of uric acid to development of neuropathy and uric acid of the patients with type 2 diabetic with and without neuropathy. Material and methods: 90 patients with diabetic peripheral neuropathy, 92 patients with diabetes mellitus but without chronic complications and 90 healthy volunteers were included in the study. Serum HbA1c, C-reactive protein, uric acid, total cholesterol, LDL, HDL cholesterol, creatinin and fasting blood glucose levels were analyzed. Result: The mean age and gender of groups of patient and control were similar. Besides, in the patient groups, therapy options, duration of the illness, fasting blood glucose, and HbA1c were statistically similar, too. Fasting blood glucose, HbA1c, uric acid and trigliceride levels of the patient groups were significantly higher, whereas HDL levels were significantly lower than control group. When the patient groups were compared with each other, although it was not statistically significant, C-reactive protein, creatinin and uric acid levels were higher in the patients with neuropathy in comparison with the diabetic group. Discussion: Our results were partly similar with the other studies. This may be due to the diversity of the regional nourishment and genetically different serum levels of the uric acid. We believe that further studies are needed to exhibit the role of uric acid levels in the development of neuropathy [ABSTRACT FROM AUTHOR]

Guillain-Barre syndrome (GBS) is an acute inflammatory demyelinating polyradiculoneuropathy characterized by bilateral progressive symmetrical paralysis. GBS is rarely seen neuropathy in cancer patients. In the literature some cases of GBS associated with anticancer chemotherapy. In this case; the guillain-barre syndrome developed after the treatment of a 59-year-old male patient with metastatic small cell lung carcinoma who admitted to hospital with neutropenic fever after cisplatin/etoposide chemoteraphy regime is presented. The patients complained of bilteral progressive symmetrical paralysis in upper and lower limbs with depressed deep tendon reflexes and hypoesthesia. There was no pathological findings on electromyography. There was no a sign at radiological imaging that explained cranial and spinal mestastasis. The cerebrospinal fluid had albuminocytologic dissociation. Decline in tumoral lesions were detected on chest radiography. Accompanied by clinical and laboratory findings, a diagnosis of Guillain-Barre syndrome was considered. Semptoms completely disapperared after intravenous immunoglobulin for five days. Recurrence did not during follow-up. The patients was administered a total of 4 cycles of cisplatin / etoposide chemotherapy. The patient died due to disease progression six months later. We think that, in this case GBS was not a paraneoplatic syndrome because there was more than 50% tumor shrinkage. We propose GBS was induced by infection and chemotherapy rather than malignancy. [ABSTRACT FROM AUTHOR]

Thoracic outlet syndrome (TOS) is a heterogeneous group of disorders which occures with the compression of one or more neurovascular elements at the cervicobrachial region. It is also a cause of neck and shoulder pain due to complex mechanisms. Diagnosing TOS can be difficult due to a great variety of symptoms may be seen in this disorder. These symptoms can simulate different diseases such as neck, shoulder and elbow pathologies and peripheric neuropathies or TOS may associate with other peripheric neurpathies. Thus once a peripheric neuropathy diagnosed, the possibility of an additional TOS should be investigated. Despite all these challenges, a clinical practice guideline for differential diagnosis of TOS is not determined yet. A careful history and thorough clinical examination are the most important components of the diagnosis. This article aims to discuss the clinical features and physical examination methods of the other related upper extremity and cervical pathologies in order to make an accurate differential diagnosis for TOS. [ABSTRACT FROM AUTHOR]

Thoracic outlet syndrome (TOS) is a complex of symptoms that occur when subclavian artery, vein and brachial plexus become subject to pressure at the superior thorax outlet. In this paper principally, attempt was made to scrutinize the physiopathology of the peripheral nerve lesion and analysis methods. Lowest level of a nerve injury is an injury where there is no damage in the nerves but it causes interruption in the signal conduction, and it is referred to as neurapraxia. Second level is the injury where the connective tissue is sound but it causes interruption in the axons within the nerve cell and it is referred to as axonotmesis. The third level of the injury is the injury that inflicts damage on both the axons and the connective tissue whereby obliterating the nerve integrity completely and it is referred to as neurotmesis. The degeneration observed through the disruption of the peripheral nerve is called Waller degeneration. They are the findings observed more frequently in neurapraxia and less frequently in axonotmesis, and neurotmesis TOS as a result of nerve pressures and compactions. In TOS, in order to evaluate the nerve pressure, electroneu-romyography (ENMG) findings are important. Motor neuron disease, radiculopathy, plexopathy, peripheral nerve lesion, peripheral neuropathy, entrapment neuropathy, neuromuscu-lar junction disease and myopathies are present among the diseases that can be evaluated through electroneuromyog-raphy ENMG. In EMG, the examinations that are interference patern, analysis during rest, motor unit potentials (MUP) examination and motor unit participation (recruitment) analysis distinguish myopathy and denervation from each other. In the TOS diagnosis, tests like nerve conduction velocity works (NCV), F response, and Hoffman (H) reflex are used. Ulnar nerve's normal conduction rate is 72 m/sec and more at the thoracic outlet. Values under 70 m/sec show the nerve pressure on TOS. When the ulnar nerve conduction rate is below 55-60 m/sec, surgical treatment can be considered. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Physical Medicine & Rehabilitation Sciences is the property of Turkiye Klinikleri and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Varicella zoster infection is an important cause of cranial neuropathy. Ramsay Hunt Syndrome occurs as a result of the reactivation of the latent varicella zoster virus infection in geniculate ganglion through the facial nerve. Paresis or paralysis of the 7th cranial nerve, vesicles along the course of the nerve and otalgia are the major clinical manifestations of the syndrome. Here we present a 75 year old female patient with hypertension, diagnosed with Ramsey Hunt syndrome who had 7th, 10th cranial nerve involvement and ipsilateral vocal cord paralysis. Etiologies other than herpes zoster infection were excluded by extensive laboratory and imaging studies. This case was one of very rare occasions, with herpes zoster oticus presenting with ipsilateral right periferal facial nerve paralysis and ipsilateral vocal cord paralysis. [ABSTRACT FROM AUTHOR]

A sixty one years old patient who sufferred from visual loss in the left eye upon awakening, presented with optic atrophy in the right eye and hyperemic optic disc edema combined with flame shaped hemorrhages in the left eye. He was diagnosed as Non-Arteritic Anterior Ischemic Optic Neuropathy (NA-AION) after ophthalmological examination. Optical Coherence Tomography (OCT) revealed cystoid macular edema (CME) in the left eye. NA-AION is a common disease which is associated with optic disc edema and painless visual loss. In this case report, a patient who probably experienced NA-AION in the right eye and sufferred from NA-AION and CME in the left eye is reported, and the combination and pathogenesis of NA-AION and CME have been discussed. [ABSTRACT FROM AUTHOR]

The purpose of this paper is to report a patient who diagnosed with acute zonal occult outer retinopathy (AZOOR). A 31-year-old female referred with a chief complaint of headache and photopsia of her right eye for 2 years. At her detailed ophthalmologic examination, her best-corrected visual acuities were 20/20 and intraocular pressures were 16 mm-Hg bilaterally. Biomicroscobic examination showed no pathological view in anterior segment, ocular media and retina. Bilateral optical coherence tomography (OCT) showed no abnormalities. Humphrey visual field examination (full threshold 30-2) revealed periferic arcuat visual field defect at inferior temporal quadrant of the right eye. No visual field defect was seen in her left eye. ERG and multifocal ERG were abnormal. [ABSTRACT FROM AUTHOR]

During the course of human immunodeficiency virus (HIV) infection, which leads to a chronic infectious disease that suppresses the cellular immune system, various types of peripheral neuropathies can be seen in different stages from seroconversion to the advanced stage. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) usually occurs in early or mid-stage of the disease. In this study, we are presenting a 66 year-old man who was admitted to our clinic due to progressive and predominantly sensorial symptoms and signs of CIDP, who had recently been operated for carpal tunnel syndrome which was suggested by electromyography even though he had complains of diffuse polyneuropathy symptoms from the beginning. During his diagnostic work-up cerebrospinal fluid (CSF) analysis had revealed elevated protein and pleocytosis, and further investigation revealed HIV-1 infection. Areas of demyelination are very common in usual entrapment zones in the course of CIDP, which is a neuropathy with multi-segment demyelination in peripheral nerves and/ nerve roots. Without a detailed patient history and examination, and a detailed EMG evaluation, a diffuse neuropathy can be misdiagnosed as an entrapment neuropathy. As it is in our case, this can lead to an unnecessary surgery and a delay in the actual diagnosis. CSF examination is very valuable for the investigation of the etiology of chronic demyelinating polyneuropaties. In CIDP patients, only protein elevation can be seen in CSF analysis; however, in the presence of pleocytosis, other diseases such as chronic infections, particularly HIV infection, other chronic inflammatory diseases, and malignant infiltration of nerve roots should be investigated. [ABSTRACT FROM AUTHOR]

Objective: We retrospectively investigated the epidemiological, clinical, laboratory and electrophysiological features of patients with Guillain Barre Syndrome (GBS) and their relationship with prognosis. Methods: We reviewed the medical records of patients hospitalized with the diagnosis of GBS at our neurology clinic from January 2001 through January 2012. Results: Sixty-four patients with the diagnosis of GBS included 40 males (mean age 50; range 17-79) and 24 (mean age 45; range 20-76) females. Based on clinical and electrophysiological features, 70.3% of the patients had acute inflammatory demyelinating polyneuropathy (AIDP), 15.6% had acute motor axonal neuropathy, 9.4% had acute motor and sensory axonal neuropathy and 4.7% had Miller Fisher Syndrome. GBS scores and muscle forces of the patients with axonal forms were worse than those of the patients with AIDP (p<0.05). Thirty patients had medical records of control examinations after discharge. Eighty percent (24/30) of these patients were able to walk without aid, and 20 patients (66.6%) had minimal or no symptoms after approximately 12 months (range 8-34 months). Patients' Medical Research Council (MRC) sum-scores exhibited a significant correlation with prognosis (p<0.001, r>0.75). Findings of autonomic involvement, respiratory distress requiring mechanical ventilation, axonal findings on electromyography and axonal forms were associated with poor prognosis (p<0.05). Conclusions: The demographic, clinical and electrophysiological features of GBS in our study were consistent with the literature. A clinical approach based on awareness that axonal involvement, autonomic dysfunction, respiratory distress requiring mechanical ventilation and severe muscle weakness are poor prognostic factors will contribute to patient care and planning of treatment. [ABSTRACT FROM AUTHOR]

Background: The aim of our study is to investigate the prevalence and association of diabetic rethinopathy and diabetic neuropathy in patients with foot ulceration. Methods: Diabetic patients with foot ulcers who admitted to our diabetic council and surgical debridement was recommended were included in the study. Only 43 patients (10 female, 33 male) who were followed up regularly during the wound healing period were included in the study. Diabetic retinopathy, independent co-morbidites (hypertension, hyper-lipidemia), tobacco use, and history of diabetes mellitus was recorded. Diabetic foot ulcers were classified according to the Wagner-Meggit classification. Results: The average follow up period for diabetes mellitus was 11.46 (range, 2-30) years. The average follow up period was 135.3 (33-285) days. Particularly the prevalence of diabetic neuropathy in patients with diabetic rethinopathy (66.7%) and in patients with diabetic neuropathy (64.3%) were very close. This result reveals a strong relationship between diabetic retinopathy and neuropathy in patients with neuropathic foot ulceration. Conclusion: Diabetic foot ulcers are the most common indication for amputation and they have strong contribution with high morbidity rate. For this reason we think that diabetic retinopathy and diabetic foot research is very important for early diagnosis and proper treatment. [ABSTRACT FROM AUTHOR]

Transient acute elevations of intraocular pressure occur following many ocular surgical and laser procedures. These intraocular pressure spikes, although well-tolerated in healthy eyes, may cause progression of nerve fiber damage and visual field defects in eyes with glaucoma and may lead to serious complications such as anterior ischemic optic neuropathy, and retinal artery occlusion may occur in eyes with sclerotic vessels. In this review, transient acute intraocular pressure elevations seen early after ocular surgeries, except for glaucoma surgery and laser procedures, are being evaluated. [ABSTRACT FROM AUTHOR]

Background: Sensorimotor polyneuropathy or mononeuropathy caused by damage of axon or myelin have been reported in patients with clinical hypothyroidism; however, there are conflicting results concerning peripheral neuropathy involvement due to subclinical hypothyroidism. Our aim in this study was to investigate the electrophysiological changes in median and ulnar nerves in patients with clinical hypothyroidism or subclinical hypothyroidism that is asymptomatic from the neurological point of view. Method: 15 patients (30 hands) with clinical hypothyroidism (group 1) and 18 patients (36 hands) with subclinical hypothyroidism (group 2), who were asymptomatic from the neurological point of view, were included in the study. 27 age- and gender-matched healthy individuals (54 hands) were taken as a control group. The median and ulnar nerves were assessed electrophysiologically in the groups. Results: Slowing of ulnar motor nerve conduction velocity (uMNCV) and ulnar nerve sensory latency (uSDL) elongation values in group 2 were found to be significant compared to the control group. When group 1 was compared with the control group, elongation in the median motor distal latency (mMDL), slowing in median motor conduction velocity (mMNCV), reduction in median nerve compound muscle action potential (mCMAP), and a significant decrease in ulnar motor conduction velocity (uMNCV) were found in group 1. When group 1 was compared with group 2, in patients with clinical hypothyroidism, elongation in mMDL and amplitude reduction in mCMAP were found, no statistically significant differences were found between the groups in terms of median sensory nerve conduction velocity (mSNCV), mMNCV, median distal sensory latency (mSDL), uMNCV, ulnar sensory nerve conduction velocity (uSNCV), ulnar compound muscle action potential (uCMAP), and uMDL values. Conclusion: Even before the emergence of neurological symptoms in patients with clinical and subclinical hypothyroidism, abnormalities can be detected in nerve conduction studies. We believe that, assessment of these patients for peripheral neuropathy by conducting routine nerve conduction studies will contribute to early diagnosis and treatment. [ABSTRACT FROM AUTHOR]

A 47-year-old female patient was admitted to our clinic with the chief complaint of sudden onset visual loss in the right eye that had occurred 25 years ago. Her visual acuity was count fingers OD and was 1.0 OS with the Snellen chart. The anterior segment evaluation showed normal OU. There was optic atrophy in the OD and the fundus examination showed a normal OS. There was a relative afferent pupillary defect (RAPD) in the OD. The patient had had two still-births and two normal deliveries in her past medical history. A laboratory work-up was performed with a preliminary diagnosis of nonarteritic ischemic optic neuropathy and mutations were found in the methylene tetrahydrofolate reductase (MTHFR) C677T and p-fibrinogen genes. Younger patients with NAION should be examined for thromboembolic diseases and preventive measures should be taken if any diseases are found. [ABSTRACT FROM AUTHOR]

Glaucoma is an optic neuropathy that progresses with loss of ganglion cells. Retinal nerve fiber layer (RNFL) are composed of ganglion cell axons and extend in 4-5 layers in the macula, comprising 35% of the retinal thickness. It has been reported that macular thickness can be used in evaluating glaucoma. In advanced glaucoma, reduced macular volume has been shown on optical coherence tomography (OCT). Peripapillary RNFL and macular thickness on OCT have been reported to be correlated in glaucoma cases. In monitoring macula functions, visual acuity, 10-2 standard perimetry (SAP), and newly introduced fundus microperimetry (MP) are used. However, visual acuity does not reflect macula functions to the fullest extent, and SAP is known to have some drawbacks. MP-1 can evaluate macula and fixation stability and combine the macula morphology and functional parameters in real and simultaneous timing in glaucoma evaluations. In this review, the use of microperimetry in glaucoma has been evaluated based on relevant literature. [ABSTRACT FROM AUTHOR]

Ramsay Hunt Syndrome (RHS) (Herpes zoster oticus) is a cranial polyneuropathy which is caused by the reactivation of varisella zoster virus. Respectively 7, 8, 9, 5, 10, and 6 cranial nerves and the servical nerves are involved. In this syndrome, 7 cranial nerve involvement constitutes 3-12% of all facial paralysis patients. Diagnosis depends on determining the ear pain, vesiculer rush around the earlap, and facial paralysis caused sequelae. Due to skin lesions on the head and neck region and neurological symptoms, RHS was suspected. Early treatment may effect prognosis. A 65-year-old individual, with right facial paralysis andpainfull ipsilateral herpetic vesicules on one side of the head and neck has been diagnosed RHS. The case has been discussed for the purpose of determining prognosis because servical dermatome involvement is rare in RHS. [ABSTRACT FROM AUTHOR]

The aim of this review is to provide a commentary on recent studies with the new IOP-lowering fixed-combination product brinzolamide 1%/timolol 0.5%. Glaucoma is a progressive optic neuropathy leading to visual field loss and a major leading cause of blindness in the world. It is estimated that approximately 60.5 million suffer from glaucom. Elevated intraocular pressure (IOP) is a key risk factor in disease progression. Treatment is aimed at reduction of IOP to minimize continued optic nerve head damage. The uses of fixed combinations reduce the number of daily instillations and washout effect, which promotes adherence to the prescribed medication and diminishes the exposition of the ocular surface to preservatives. One option is the fixed combination of brinzolamide 1% and timolol maleate 0.5%, which is commercially available in some countries as Azarga. It is more potent than either of its ingredients alone. Compared with another carbonic anhydrase inhibitor-containing product- dorzolamide 2%/timolol 0.5%- brinzolamide/timolol has similar IOP-lowering efficacy but better tolerated than the dorzolamide/timolol fixed combination. This is explained by the more physiologic pH of brinzolamide/timolol. In conclusion, brinzolamide/timolol fixed-combination is equally effective and more comfortable than dorzolamide/timolol fixed-combination, a fact that may positively impact adherence, leading to an increased likelihood of reaching target IOP goal. [ABSTRACT FROM AUTHOR]

Mercury (Hg) is a well-known environmental toxicant and Hg intoxication is a rare but life threate-ning condition and may cause serious complications (e.g., impairment of the developing central nervous system). In 19th Century, particularly hatters suffered Hg intoxication. They presented ne-uropsychiatry symptoms including shaking, aggressiveness, irritability, mood lability, excessive ti-midity, loss of self-confidence and anxiety. These psychological symptoms have inspired the na-ming "mad as a hatter" disease. In this case report we present a 4-year-old girl with history of Hg exposure. She was presented with the signs and symptoms suggestive of mercury intoxication such as prominent irritability and mood swings. We aimed to discuss the "mad as hatter" disease in children who have overblown psychiatric symptoms beside the symptoms of Hg intoxication like hypertension, skin rash, peripheral neuropathy and behavioral changes. [ABSTRACT FROM AUTHOR]

Introduction: Most recently, it was accepted that diabetes mellitus (DM) is the most important disease from the point of view mortality and morbidity. It is possible to determine subclinic neuropathy recording Auditory Brainstem Response (ABR) to avoid complication of DM. If it is determined pahtological condition on the ABR recording, it must be followed more tightly serum glucose levels of patients and it must be avoided especially hipoglisemia and ketoasidosis. It can be obtained information about last three monthly blood glucose controlling HbA1c levels of patients together with fasting blood glucose following in the outpatient controls. It should not give permission excessive undolation of blood glucose patients must be recorded assaying several times their blood glucose. It is important that ABR records of patients must be compared according to ages repeating with spesific intervals. Materials and Methods: In our study, it was compared evoked brainstem responces with serum HbA1c levels of 30 patients with Diabetes Mellitus and 30 control group patients when working groups compared with respect whether I, III and V wave latences. Results: No statistical difference was found between groups that examined. It was observed smilar results to our study, it was determined clear axtend on the patients with neuropathy. Statistically significance was found between diabetes period and serum HbA1c levels with wave latences (p<0.05) but no difference was found in diabetes period when compare to the serum HbA1c levels in the literature. Conclusion: Diabetes Mellitus is the disease showing a latent period before complications of DM and it is possible to determine complications of DM using electrophysiological tests in this period and to take measures. For this reason, ABR can provide a good monitorisation. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is a metabolic disease, which results in microvascular and macrovascular complications in later stages. It has been known that with elevated glucose concentrations, proteins in both the circulation and the tissues are non-enzymatically glycated and this results in the production of advanced glycation end-products. Advanced glycation end-products alter cell structure and function which lead to the synthesis and release of cytokines and growth factors. Therefore, advanced glycation end-products contribute to the microvascular and macrovascular complications of diabetes mellitus. Inhibition of advanced glycation was found to reduce diabetic complications such as nephropathy, retinopathy and neuropathy. Some of the agents that are used for the treatment of advanced glycation end-products formation and accumulation are summarized in this review [ABSTRACT FROM AUTHOR]

Guillain Barre Syndrome is an acute inflammatory demyelinating polyneuropathy and it is a rare event in pregnancy. Active treatment such as plasmapheresis and intravenous immunoglobulin together with vigilant follow up in intensive care has improved maternal and fetal outcome. In this case report, we discussed the diagnosis and treatment modalities and intensive care approaches in a 26 year old pregnant patient with Guillain Barre Syndrome. [ABSTRACT FROM AUTHOR]

Normal tension glaucoma is a progressive optic neuropathy characterized by glaucomatous optic nerve cupping and visual field effects yet with measured Intraocular pressure (IOP) levels within the normal range. The purpose of these two case reports is to emphasize the clinical characteristics and differential diagnostic considerations. The first case discusses the clinical features of a normal tension glaucoma case with normal cranial imaging findings. The second case highlights the association of a compressive intracranial mass causing asymmetric disc cupping and normal IOP readings. The differential diagnosis of this case is discussed. [ABSTRACT FROM AUTHOR]

Inhalant substance dependence is generally seen at 14-15 years of age and its prevalence decreases in adulthood. Inhalant use is common among disadvantaged groups, street children, people with history of crime, depression, suicide, antisocial attitudes, history of abuse, violence and any other drug dependence. Psychosocial factors are important in the beginning of inhalant dependence. Medical and neurological problems are frequently seen in chronic inhalant users. The duration of inhalant use is positively correlated with morbidity and mortality. In this report, medical and neuropsychiatric results of chronic inhalant dependence will be discussed. In our patient, chronic inhalant use caused central and peripheral neuropathy, cognitive impairment, depression, psychotic disorder, upper motor neuron type destruction in muscles and mild anemia. Neuropsychiatric destructive effects are prominent in chronic abuse. Mirtazapine and olanzapine treatment decreased depressive and psychotic symptoms, but cognitive impairment, neuropathy, upper motor neuron type destruction didn't recover completely. Given serious and sometimes irreversible consequences of chronic inhalant dependence, early medical and psychosocial interventions seem very important. [ABSTRACT FROM AUTHOR]

Chronic inflammatory demyelinating polyneuropathy (CIDP), which is characterized by a progressive or recurrent loss of motor and sensory peripheral nerves, could be due to many reasons such as diabetes mellitus, cancer, sarcoidosis. Although, CIDP could develop in patients with Hepatitis B virus infection (HBVi), HBVi wasnot found to present itself as CIDP. Our case is a 60 years old-man whom suddenly developed numbness and weakness in hands and feet. He was tetraparetic with hypoactive deep tendon reflexes, hypoesthesia and parestesia. Electroneuromyography (ENMG) revealed mixed type demyelinating and sensorial sensorimotor polyneuropathy. At the time of the diagnosis, high values of AST and ALT; later on, positivity of HBsAg and HBV-DNA were detected. Although liver biopsy showed chronic hepatitis and liver fibrosis, he didnot have any history of hepatitis. In conclusion, while investigating the etiology of CIDP, HBVi should be considered even if patients didnot mention or know any history of hepatitis. [ABSTRACT FROM AUTHOR]

Cauda equina syndrome is a neurological state with bilateral ischiatic pain, lower extremity weakness, and bladder and bowel dysfunction due to multiple compressive neuropathies of the lumbar and sacral nerves. Even though the relationship between cauda equina syndrome and voiding dysfunctions is a well known fact, data on the clinical management of the condition is limited. The aim of this paper is to review the pathophysiological relationship between voiding dysfunctions and cauda equina syndrome and to refresh our knowledge about the clinical approach to this group of patients. [ABSTRACT FROM AUTHOR]

Osteoporosis and rheumatismal diseases have some findings that affecting all layers of the eye. Adult and Juvenile rheumatoid arthritis, Sjögren's syndrome and ancylosing spondylitis are frequently together with eye symptoms and signs. Eye findings frequently precede the symptoms of systemic disease. Uveitis, iridocyclitis, vitritis, keratitis, scleritis, anterior ischemic optic neuropathy and retinal vasculitis are the most frequent ocular inflammatory findings. Ocular inflammation may be either related to disease process itself, or secondary to anti-inflammatory agents. In present study, in the light of literature review, ocular findings of osteoporosis and rheumatismal diseases that most frequently accompanied by ocular signs were reviewed. [ABSTRACT FROM AUTHOR]

Arthrogryposis multiplex congenita is a syndrome characterized by non-progressive multiple congenital joint contractures. The exact etiology of arthrogryposis is unknown. It may be due to neuropathic or muscular pathologies, connective tissue disorders, conditions limiting the uterine space, intrauterine vascular abnormalities, or maternal diseases. In the early period of the disease, establishment of the correct diagnosis is crucial for determining the prognosis and initiation of the appropriate therapy. Herein, a 69-year-old female patient initially admitted with shoulder pain and later diagnosed to have both shoulder lesion and multiple joint contractures is presented. [ABSTRACT FROM AUTHOR]

Objective: In this study, we aimed to investigate the change in dorsal sural nerve (DSN) conduction studies in early diabetic neuropathic patients and to evaluate whether high sensitive C-reactive protein (hs-CRP), inflammatory marker, and adiponektin, important role in insulin resistance and diabetes, have any effect on DSN studies or not. Material and Method: Forty-six patients with early stages (Dyck classification N1) diabetic neuropathy and age-sex matched forty-four control subject were included in the study. Informed consent was obtained after approval of ethical committee. In all subject DSN conduction studies were performed with conventional electrophysiological studies. DSN electrophysiological parameters of diabetics were compared with controls. The relationship between plasma adiponectin and hs-CRP levels and DSN conduction study parameters were analyzed. Results: In diabetic patients, DSN parameters were significantly different than controls. The level of adiponectin was found to be lower in diabetic (p:0.01) but not statistically significant for hs-CRP levels (p:0.40). There was not any relationship between DSN parameters and the level of adiponectin or hs-CRP (p>0.05). Sixty-three % of diabetics, whom routine electrophysiological studies were in normal limits, had abnormal DSN parameters. Fifty% of diabetics had bilateral abnormalities. However, there was no difference in hs-CRP and adiponectin levels between patients with abnormal and normal DSN studies (p>0.05). Conclusion: DSN studies are useful methods to detect subclinical early diabetic polyneuropathy according to the results of our study. Although adiponectin level was found lower in early diabetic neuropathic patients, both adiponectin and hs-CRP do not have any relationship with DSN studies. [ABSTRACT FROM AUTHOR]

Background and Design: Central nervous system involvement is well known in patients with Behcet's disease but studies evaluating peripheral nervous system is not usual. The aim of this study is to evaluate the frequency and characteristics of subclinical neuropathy in patients with Behcet's disease. Material and Method: Thirty three Behcet's disease patients (23 male, 10 women) with no evident neurological sign and symptom and 33 healthy volunteers were enrolled to the study. To exclude the other causes of peripheral neuropathy, some laboratory investigations were made. Electrophysiological studies of peripheral nerves were performed to all patients and healthy volunteers. The results were assessed according to the American Diabetes Association Diabetic Neuropathy Protocol. Results: Nerve conduction studies were abnormal in 11 of 33 patients (7 men, 4 women; 33.3%). Five patients (15%) had sensorymotor polyneuropathy, 4 (12%) has sural sensory polyneuropathy, 1 (3%) had median and tibial motor neuropathy. Sural nerve were unobtainable in 7 (21%) patients. 2 patients (6%) had prolonged F latency. Control group were normal electrophysiologically and the difference was statistically important (p<0.0001). There was no correlation between peripheral neuropathy and gender (p=0.696). Conclusion: Despite the detailed neurological examination, subclinical peripheral neuropathy can be seen in patients with Behçet's disease. Electrophysiological studies are useful for the early detection of peripheral neuropathy in these patients. [ABSTRACT FROM AUTHOR]

Purpose: Gabapentin is an antiepileptic agent used for the treatment of neuropathic pain. This study was aimed to evaluate the usage and efficacy of gabapentin in neuropathic pain. Material and Methods: A hundred and six patients who prescribed gabapentin for neuropathic pain were assessed. Demographic data, initial diagnosis, symptom duration, previous medications, medications used with gabapentin, duration and dosage of gabapentin were recorded retrospectively. Patients were asked to evaluate efficacy of treatment by Likert scale (0-4) via phone visits. Results: Mean age of patients was 56.8±12.6 and 57.5% of them were female. Mean duration of symptoms and duration of gabapentin usage were 5.35±5.0 years and 11.13±9.9 months respectively. Mean gabapentin dosage was 1606.6±505.3 mg. Global assessment of treatment efficacy was 1.9±1.3. 51% of our patients rated the efficacy of treatment as mild or moderate, whereas 32% of them rated as good or very good. No statistically significant difference was detected between patients with central and peripheral neuropathic pain based on global assessment of treatment efficacy. Conclusion: Gabapentin was evaluated as moderately effective for the treatment of neuropathic pain. Majority of patients had radiculopathy and spinal cord compression due to spinal stenosis. Prospective, randomized controlled trials are needed to investigate efficacy of gabapentin in these particular neuropathic pain conditions. [ABSTRACT FROM AUTHOR]

Objective: Polyneuropathy is the most frequent complication of diabetes mellitus (DM), which is a common disorder worldwide. Early diagnosis of this complication is critical for treatment planning. Recently, intra-epidermal nerve fiber (IENF) analysis has been used for the early diagnosis of diabetic neuropathy and was reported to be superior to both conventional fascicular nerve biopsy and other diagnostic tests. The present study aimed to determine the effect of early glucose metabolism disorders on the peripheral nerves using IENF analysis. Patients and Method: This prospective study compared IENF nerve fiber density in 10 patients with early-stage DM and 12 patients with impaired glucose tolerance (IGT) to that of healthy controls in order to investigate fiber loss in the asymptomatic stage. Results: Mean age of the DM and IGT groups was 53.4 ± 10.9 years and 50.8 ± 10.6 years, respectively. Neither the IGT nor DM patients had paresthesia. Neurological examination results of the patients were all in the normal range. Mean fiber density was 6.4 ± 2.7 mm-1 in the DM group, 7.5 ± 3.2 mm-1 in the IGT group, and 13.7 ± 2.7 mm-1 in the control group (p< 0.0001). Paired analysis of the groups showed a significant difference between the 2 patient groups and the control group. There was a statistically significant difference in mean nerve fiber density between the DM and control groups (p< 0.0001, Mann-Whitney U test), and between the IGT and control groups (p< 0.0001, Mann-Whitney U test); however, there wasn't a significant difference between the DM and IGT groups (p= 0.5, Mann-Whitney U test). Conclusion: The results show that IENF density in the IGT and DM groups decreased in the asymptomatic stage of DM. This means that polyneuropathy can begin in the prediabetic period in patients with glucose metabolism disorders. This critical information highlighs the importance of the early diagnosis and treatment of glucose metabolism disorders in preventing neurological complications. [ABSTRACT FROM AUTHOR]

Neuropathic pain is brieşy defined as pain caused by a lesion in the nervous system and is common in clinical practice. Pharmacotherapy and neurostimulation therapy are the two most recommended therapies for the treatment of this condition. It is generally accepted that pharmacotherapy remains the mainstay of neuropathic pain management. First-line treatments include gabapentin, 5% lidocaine patch, opioid analgesics, tramadol hydrochloride, and tricyclic antidepressants. Neurostimulation techniques recommended in the treatment of neuropathic pain are transcutaneous electrical nevre stimulation (TENS), peripheral nerve stimulation (PNS), nerve root stimulation (NRS), spinal cord stimulation (SCS), deep brain stimulation (DBS), epidural motor cortex stimulation (MCS) and repetitive transcranial magnetic stimulation (rTMS). Treatment decisions for patients with neuropathic pain can often be difficult. Recently, growing interest in the mechanisms of chronic neuropathic pain has resulted in significant advances in treatment. In this review, recent knowledge on therapeutic management of chronic neuropathic pain is reviewed. [ABSTRACT FROM AUTHOR]