Background: Multiple sclerosis (MS) is a chronic autoimmune, inflammatory demyelinating disease of the central nervous system. Commonly, MS patients present with accompanying degenerative vertebral disc diseases. Simultaneous disc herniations situated in the cervical or lumbosacral spine can mimic the clinical symptoms of MS and worsen patients’ quality of life.Objective: to investigate the incidence rate and clinical impact of accompanying disc herniations in patients with MS.Material and methods: Our study covered 330 patients (220 females and 110 males, mean age 40.5±12.4 years) with clinically definite MS, according to McDonald’s criteria. Comprehensive neurological examinations, EDSS (Expanded Disability Status Scale) assessments, and MRI neuroimaging were carried out. Statistical data processing was performed by using the method of variation analysis.Results: Relapsing-remitting MS (RRMS) was diagnosed in 280 patients while 50 patients presented with secondary progressive MS (SPMS). Disc herniation was found in 64 (19.4%) of our patients. Cervical disc pathology was detected in 38 patients (11.5% of the cases) and lumbosacral - in 26 (7.9% of the cases). EDSS scores ranged from 2.5 to 5.5. EDSS evaluation showed statistically significantly worse scores in MS patients with disc herniation comorbidity (p<0, 05).Conclusion: Our own data confirm the assumption that MS patients often present with accompanying degenerative disc pathology. We suggest that comorbidity of disc herniation and MS exert an additional unfavorable effect on patient’s disability and individual quality of life

ABSTRACT:Idiopathic intracranial hypertension (IIH) or benign intracranial hypertension is a neurological syndrome characterized by elevated intracranial pressure. This uncommon disorder occurs primarily in obese women aged 10 to 50 years, sometimes in association with endocrine and metabolic dysfunction, with systemic diseases or when treated with multiple medications.We describe a case of IIH in a 43-year-old woman with schizophrenia treated with risperidone, demonstrating a typical clinical picture of benign intracranial hypertension. For the 5 years of treatment with risperidone she put on 35 kg in total (BMI> 35); for the last 2-3 months she began to complain of visual obscurations, nausea with vomiting. Ophthalmoscopy revealed bilateral asymmetric papilledema (OD>OS). Magnetic resonance imaging was normal, intracranial pressure was elevated IIH was diagnosed. Risperidone was discontinued and replaced with Seroquel 200 mg daily. Treatment with furosemide and mannitol 10% was initiated. Papilledema resolved completely over the next 2 months. The patient was followed-up for four years after risperidone withdrawal. Weight loss of 28 kg was noted for four years. There were no relapses of headache, nausea, visual obscuration. Ophthalmologic examination revealed no papilledema.We suggest that prolonged use of antipsychotics, such as risperidone, should require proper surveillance for possible development of IIH and routine ophthalmologic examinations should be performed.

Lyme disease is a multi-system disorder caused by the spirochete Borrelia burgdoferi. Eye manifestations are a rare involvement. We report two cases of patients who developed a retrobulbar optic neuritis and a cystoid macular edema as a sole clinical presenting in Lyme disease. A 42-year-old female presented with left eye decreased visual acuity and painful ocular movement. Dilated funduscopy and neurological examination were normal. A diagnosis of left eye retrobulbar optic neuritis was made. The brain and spinal cord MRI showed typical lesions characteristic of MS. Serological tests for Lyme disease revealed positive results for IgM ELISA and Western blot. The possible serologically proven Lyme disease was diagnosed. Visual acuity returned to normal following a course of high-dose steroids and intravenous antibiotic, after by oral antibiotic. A 28-year-old male presented with left eye blurred vision and intermittent blurring vision in his right eye. Dilated funduscopy revealed bilateral cystoid macular edema (left more than right). He was positive for Lyme serology, IgM ELISA and Western blot, and intravenous antibiotic therapy was commenced, followed by oral antibiotic. Visual acuity was restored and fuduscopy was normal. In summary, although Lyme disease is an uncommon cause of these neuro-ophthalmic complications, our two patients highlight the importance of considering this disorder as a differential diagnosis and to initiate an early adequate therapy.

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