Multiple sclerosis is an insidious, intermittent or chronic progressive inflammatory, autoimmune disease of the central nervous system; it is a major cause of disability, especially in young adults. It affects women twice as often as men. The prevalence varies from 50 to 100 per 100,000 in moderate climate zones. Interferon beta-1b reduces frequency and severity of clinical attacks of relapsing-remitting multiple sclerosis and prolonged time until the progression of disability and time patients suffering from secondary progressive multiple sclerosis become wheelchair-bound.

The aim of the study was to analyze the 5-year survival after first-ever ischemic stroke and intracerebral hemorrhage. In this study 836 patients were analyzed with a first-ever stroke admitted at the Department of Neurology Tuzla, Bosnia and Herzegovina, from January 1(st) 1997 to December 31(st) 1998. Of these 613 (73,3%) were ischemic strokes and 223 intracerebral hemorrhages (26,7%) Subarachnoid hemorrhages were excluded. After hospitalization surviving patients examined periodically, and a final examination was performed 5 years after the stroke. Overall, case-fatility at the first month was 36% (301/836) and the mortality rate was significantly higher in the patients with intracerebral hemorrhage (58,3% vs. 27,9%, p<0,0001). The first year survived 60% patients with ischemic stroke, and 38% with intracerebral hemorrhage. After 5 years, 188 (31%) patients with ischemic stroke and 53 (24%) with intracerebral hemorrhage were alive (p=0,5), and the cumulative survival rate for the entire study was 29%. Among 30-day survivors (n=535) surviving rate after 5 years was significantly higher in patients with intracerebral hemorrhage (57% vs. 42,5%, p=0,01). The survival rate was the highest for those 50 years and younger (57%), and the lowest for those aged over 70 years (9%). Predictors of 5-year mortality were older age and hypertension for both types of stroke, heart diseases for ischemic stroke and diabetes for intracerebral hemorrhage. Long-term survival after first-ever ischemic stroke and intracerebral hemorrhage is similar. However, among 30-day survivors the 5-year survival is better in patients with intracerebral hemorrhage.

It was performed electroneurographic (ENG) studies with surface electrodes and examined nervus medianus (NM) in 60 patients (38 females), average age of 50,28 years (X+/-SD=50,28+/-11), with clinical diagnosis of carpal tunnel syndrome (CTS) and at least one border or discrete abnormal value of conventional electrophysiological tests. It was also examined 57 healthy individuals (33 females) as control group, average age of 45,65 years (X+/-SD=45,65+/-9,68). The sensitivity and specificity of sensory-motor index (SMI), terminal latency index (TLI) and residual latency (RL) were calculated and compared. SMI is determinate by using following formula: distal distance (DD) (in cm)/distal motor latency (DML) (in ms) + sensory conduction velocity (SCV) (in m/s)/motor conduction velocity (MCV) (in m/s) of NM. SCV of NM was measured by antidromic technique in segment wrist-index finger and MCV of NM in forearm segment above wrist. SMI mean value of control group was 3,45 (X+/-SD=3,45+/-0,45) with lower limit of normal value 2,82 and in patients with CTS 2,13 (X+/-SD=2,13 +/-0,37). The sensitivity of SMI in patients with CTS was 98,51%. SMI is useful parameter in electroneurographical diagnosis of CTS and it's determination is easy and fast and specially important in cases with border or discrete abnormal values of other NM electrophysiological parameters, when SMI values can indicate incipient phase of CTS evolution. In rare cases (about 1%) of CTS with selective NM motor axons affection, SMI may have normal value (false negative result), but DML is always prolonged in this cases. SMI is not dependent on age and DD values in patients with CTS and control subjects.

Acute disseminated encephalomyelitis (ADEM) is a monophasic, immuno-mediated disease with multifocal demyelinated lesions in the central nervous system (CNS). However, the course of disease could be with multiple sclerosis (MS)-like relapses. ADEM is a childhood disease (children 10 years of age and younger) and could be the first phase of MS in 25% or more children. Onset of the disease is acute. The clinical picture depends on the intensity of the process itself, and the parts of the CNS affected. It correlates with an infectious syndrome affecting the menings and different parts of the brain and spinal cord. Prognosis is very uncertain, and the disease is lethal in 1/3 of cases. MS is a chronic inflammatory, non-contagious, progressive multifocal demyelinated, autoimmune disease of the CNS (white matter of the brain and spinal cord) with many and various neurological symptoms. In 85-90% of cases the symptoms come and go in “attacks” (exacerbations and remissions), or slowly progress over time. The cause and pathogenesis of MS still is not well known. Inheritance could have an important possible precipitating role. The pathogenesis of MS includes inflammation, demyelinisation and axonloss. Although demyelinisation could generate relapse, long-term disability is primarily due to irreversible loss of axons and cell death. MS is most frequent in patients 30 to 40 years of age, although it can be seen prior and after this age range. Childhood onset is reported in 3-5% of cases. It is estimated that 2.5% to 5% of all MS patients experience the first MS “attack” before 16 years of age. Onset before the age of 10 occurs in only 0.2% cases. Diagnosis of ADEM and/or MS is based on cerebrospinal liquor analysis, brain evoked potentials (EP’s), and magnetic resonance imaging (MRI) of the brain and spinal cord. Computed tomography (CT) of the brain could be useful, not to diagnose MS but to exclude some other brain disorders (tumors, stroke etc.). Recently, for secure diagnose of MS revised McDonald’s criteria for MS are used. Patients with ADEM are treated with anti-inflammatory medications (corticosteroids) and immunosuppressive therapy administered in the same manner as in MS. Interferon I² (1a, 1b), as well as glatiramer acetate are used to slow the progress of MS.