Belgin Koçer

Vitiligo and multiple sclerosis in a patient treated with interferon beta-1a: a case report.

Dear Sir, Interferon (IFN) beta-1a is an approved immunomodulating treatment for relapsing-remitting multiple sclerosis. Subcutaneous injections were given three times weekly. The most frequent side effects of IFN beta-1a are inflammatory reactions at the injections sites (72%) and flu-like symptoms (69%) [1]. It has been reported that IFN-alfa therapy induce vitiligo or make it worse [2,3]. However, the development of vitiligo in response to IFN-beta treatment has not been reported. Although the mechanism for interferoninduced vitiligo is not known, it is believed that IFN-alfa causes vitiligo via induction of antimelanocyte autoantibodies or activation of cytotoxic T cells [2]. It has been stated that vitiligo lesions completely resolved after discontinuation of IFN-alfa treatment [4]; however, Seckin et al. stated that the lesions did not resolve after the cessation of treatment and new lesions continued to evolve despite of withdrawal of treatment [2]. We present the case of a 33-year-old female patient who developed vitiligo lesions after receiving 22 mcg of subcutaneous recombinant IFN beta-1a therapy three times weekly for relapsing-remitting multiple sclerosis. Her baseline value of the complete blood count, biochemical test, ferritin, vitamin B12, folate, homocysteine levels and thyroid function tests were with in normal limits. Her blood vasculitis marker, brucella agglutination, VDRL, angiotensin converting enzyme and Borrelia Burgdorferi, hepatitis markers, anti-human immunodeficiency virus antibody were negative. She tolerated the therapy well, and no concurrent steroid treatment was given. After 2 years of therapy, she developed depigmented patches on the dorsal aspects of her hands (Fig. 1). The patient gave permission for the publication of the photographs. The therapy was continued despite these skin lesions. Twenty-two months after the appearance of first skin lesions, new depigmented patches occurred on periorificial areas and on chin (Fig. 2). After the appearance of vitiligo lesions on the perioral region and the chin, the laboratory evaluation of the patient was repeated. The free T3 and free T4 levels were normal, whereas the TSH values were above the normal limits (12.97 IU/ml; normal range, 0.35–4.94 IU/ml). She was treated with 0.05% Clobetasone butyrate for the lesions on the periorofacial and chin region, and with 0.05% Clobetasol 17-propionate for the lesions on the both dorsum of the hands. No improvement was observed after the treatment of topical corticosteroid for 1.5 months; there was no any progression in that period also. She was planning to become pregnant; so her IFN beta-1a treatment was terminated and there was a mild decrease in the dimensions of the lesions at the 45th day follow-up. She was treated with levothyroxine 50 mcg/day for hypothyroidism. The free T3 and free T4 levels were normal, while the TSH level was still high (8.27 IU/ml) at 3rd month. The TSH level became in normal limit at the fourth months. The vitiligo lesions significantly improved 3 months post-cessation of IFN beta-1a and were stable in follow-up 6 months. Figure 1 Depigmented patches on the dorsal aspects of both hands.

Blink reflex abnormalities in diabetes mellitus.

Damage of the peripheral nervous system is particularly frequent in diabetes mellitus (DM), but somatic cranial neuropathies usually presenting as mononeuropathies are rare. Oculomotor and facial nerves are among the most commonly affected, whereas the Vth, IXth and Xth cranial nerves are less often affected. While existing neurophysiological tests in the subclinical diagnosis of damage to the peripheral nerve in diabetic patients have advanced, the same does not hold true for the subclinical diagnosis of the central nervous system (CNS). Electrophysiological studies such as the blink reflex was shown to be an effective method for revealing subclinical involvement of cranial nerves in generalised neuropathies.

Evaluating sub-clinical cognitive dysfunction and event-related potentials (P300) in clinically isolated syndrome

ObjectiveThis study investigated the presence of sub-clinical cognitive dysfunction in patients with clinically isolated syndrome (CIS) and the abnormalities of cognitive event-related potentials (ERPs).MethodsSubclinical cognitive dysfunction was assessed in 20 patients with CIS and in 20 healthy controls.ResultsPatients had impairments in verbal learning and long-term memory, evaluating attention, executive function and visuospatial skills, in decreasing order of frequency. SDLT and SIT were the most, and COWAT and BNT were the least affected tests. The N200 and P200 latencies were prolonged, and N100, N200 and P200 amplitudes were reduced in the patients relative to the controls, from the Fz, Cz and Pz electrode positions (p<0.05).ConclusionDetailed cognitive testing is valuable in determining subclinical cognitive dysfunction in CIS patients. ERP abnormalities as well as abnormalities in detailed cognitivetesting in patients with CIS are helpful in the diagnosis of sub-clinical cognitive dysfunction.

The value of diffusion-weighted imaging in the diagnosis of Marchiafava-Bignami disease: apropos of a case.

Marchiafava‐Bignami disease (MBD) is characterized by demyelination and necrosis of corpus callosum encountered in chronic alcoholic patients. Etiology is the deficiency of vitamin B complex. Magnetic resonance imaging (MRI) in MBD typically reveals focal lesions of high T2 and FLAIR signal intensity in the corpus callosum. We here present a 42‐year‐old male alcoholic diagnosed as MBD on the basis of MRI and diffusion‐weighted imaging (DWI) features. The patient totally recovered following appropriate vitamin B complex replacement therapy, despite reduced diffusion in the initial setting. This case report emphasizes on the important role played by MRI and DWI in the early diagnosis and follow‐up of this potentially fatal disease.

Pathological Laughing As a Manifestation in a Clinically Isolated Brainstem Syndrome: A Case Report

The prevalence of pathological laughing and crying in multiple sclerosis (MS) is 10%. It has been speculated that the anatomical lesion responsible for the pathological laughing is located in the pontine base, prefrontal cortex, and cerebellum. We report an 18‐year‐old male patient presenting with pathological laughing and hypomania. In his neurological examination, he had a euphoric effect with ataxic walking and dysarthria speech. He had a bilateral conjugated gaze limitation, with a prominent bilateral horizontal nystagmus on left gaze, dysmetria, dysdiadokokinesia, and remarkable dysfunction in a heel‐to‐shin test on the left. The IgG index in cerebrospinal fluid was normal with an oligoclonal band was present. In cranial MRI, there was a lesion on central pons which was hypointense in T1 images with contrast enhancement and hyperintense in T2 and flair images. Also another lesion in right brachium pontis which did not contrast enhancement but was hyperintense on T2 and flair images was present. There was an elevation of myoinositol/creatine ratio and choline and a reduction of NAA in proton MR spectroscopy. MR spectroscopic evaluation of the patient demonstrated the demyelination process. There has been no report of patients in whom pathological laughter was the presenting symptom of clinically isolated brainstem syndrome.

Cognition, depression, fatigue, and quality of life in primary Sjögren's syndrome: correlations.

The aim of the present study was to investigate the prevalence and pattern of cognitive dysfunction observed in primary Sjögrens syndrome (PSS) and to examine the relationships between cognitive abilities, depression, fatigue, and quality of life.

Overactive bladder symptoms in patients with multiple sclerosis: Frequency, severity, diagnosis and treatment

Objective: To determine the frequency and severity as well as the diagnosis and treatment of overactive bladder problems in patients with multiple sclerosis (MS) followed up at five centers in Turkey. Design: Survey study. Setting: Outpatient tertiary clinics of physical medicine and rehabilitation and neurology. Participants: Consecutive MS patients scheduled for outpatient follow-up (n = 309). Intervention: MS patients were asked to complete a questionnaire regarding the frequency and severity, as well as the diagnosis and treatment of their overactive bladder problems. Results: The mean age ± SD was 39.3 ± 10.6 years. Urinary urgency was the most common urinary symptom (62%), followed by frequency (50.4%), urge incontinence (44.7%) and nocturia (33%). Residual urine volume was measured using a portable ultrasound instrument in 13.3% of the patients and by catheterization in 16.2% of them. Urodynamic investigations and urinary tract ultrasound were performed on 26.5% and 35.3% of the patients, respectively. Anticholinergic medications were prescribed for 27.5% of the patients. Intermittent catheterization and indwelling catheterization were used on 8.1% and 1.9% of the patients, respectively. The overactive bladder symptom score (OABSS) was significantly higher in patients who had had residual urine measurement (P < 0.001), upper urinary tract assessment by ultrasound (P < 0.001), urodynamic assessment (P < 0.001), admitted to a doctor for urinary symptoms (P < 0.001), and current or past catheter use (P = 0.002). Conclusion: Urgency was the most common urinary symptom followed by frequency, urge incontinence and nocturia in MS patients. The patients with lower OABSS had detailed urological assessments less frequently than the patients with higher OABSS.