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The aim of this study was to perform a genome-wide expression analysis of whole-blood samples from people with optic neuritis (ON) and to determine differentially expressed mRNAs compared to healthy control subjects. The study included eight people with acute ON and six healthy control subjects. Gene expression was analyzed using DNA microarrays for whole-human-genome analysis, which contain 54,675 25-base pairs. The additional biostatistical analysis included gene ontology analysis and gene set enrichment analysis (GSEA). Quantitative RT-PCR (qPCR) was used to confirm selected differentially expressed genes. In total, 722 differently expressed genes were identified, with 377 exhibiting increased, and 345 decreased, expression. Gene ontology analysis and GSEA revealed that protein phosphorylation and intracellular compartment, apoptosis inhibition, pathways involved in cell cycles, T and B cell functions, and anti-inflammatory central nervous system (CNS) pathways are implicated in ON pathology. qPCR confirmed the differential expression of eight selected genes, with SLPI , CR3 , and ITGA4 exhibiting statistically significant results. In conclusion, whole-blood gene expression analysis showed significant differences in the expression profiles of people with ON compared to healthy control subjects. Additionally, pathways involved in T cell regulation and anti-inflammatory pathways within CNS were identified as important in the early phases of MS.

Objective: To investigate the correlation of the vestibular evoked myogenic potential (VEMP) score with Timed 25-Foot Walk (T25FW), 9-Hole Peg Test (9HPT), Paced Auditory Serial Addition Test (PASAT) and EDSS in patients with multiple sclerosis (MS)., Methods: This prospective, cross sectional study included 52 patients with clinically isolated syndrome (CIS). Cervical VEMP (cVEMP) and ocular VEMP (oVEMP), analyzed in the form of the cVEMP, oVEMP and VEMP scores, T25FW, 9HPT, PASAT and Expanded Disability Status Scale (EDSS) were performed., Results: The only predictor of walking impairment in this study was general disability as measured by the EDSS, after controlling for age, gender, PASAT and EDSS the effect of VEMP score was non-significant (p=0.419). 9HPT of the dominant hand did not correlate with the oVEMP score (rs=0.258, p=0.065), however after controlling for age, gender, PASAT and EDSS, the effect of the oVEMP score on 9HPT of the dominant hand was statistically significant (p=0.017). After controlling for age, gender and oVEMP score, the effect of the PASAT on 9HPT variable for the non-dominant hand was statistically significant (p=0.001)., Conclusion: We found possible effects of brainstem dysfunction on walking impairment, however they were not seen after correction for EDSS and cognitive dysfunction. On the other hand, dominant hand function seems to be influenced by upper brainstem dysfunction measured with oVEMP, while cognitive dysfunction is related to non-dominant hand function., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Context: Alemtuzumab, an anti-CD52 monoclonal antibody, increased the risk of thyroid dysfunction in CAMMS223, a phase 2 trial in relapsing-remitting multiple sclerosis., Objective: The objective of the study was a detailed description of thyroid dysfunction in CAMMS223., Design: Relapsing-remitting multiple sclerosis patients (n=334) were randomized 1:1:1 to 44 μg sc interferon-β-1a (SC IFNB-1a, Rebif) or annual courses of 12 or 24 mg iv alemtuzumab. Thyroid function tests (TSH, free T3, free T4) and thyrotropin-binding inhibitory immunoglobulin (TBII) were assessed at screening, month 1, and quarterly thereafter; antithyroid peroxidase antibodies were assessed at screening and every 6 months. Thyroid dysfunction episodes were categorized post hoc by an endocrinologist., Results: During a median follow-up of 57.3 months, 34% of alemtuzumab and 6.5% of SC IFNB-1a patients had thyroid dysfunction (P<.0001). Ten percent of alemtuzumab and 3% of SC IFNB-1a patients had more than one episode of thyroid dysfunction. With alemtuzumab, Graves' hyperthyroidism occurred in 22%, hypothyroidism in 7%, and subacute thyroiditis in 4%. Of patients with overt Graves' hyperthyroidism, 23% spontaneously became euthyroid and an additional 15% spontaneously developed hypothyroidism. Of patients with overt hypothyroidism, 74% were TBII positive. The annual incidence of a first episode of thyroid dysfunction increased each year through year 3 and then decreased each subsequent study year., Conclusions: Thyroid dysfunction was more common with alemtuzumab than with SC IFNB-1a. There were few serious episodes. Regular monitoring facilitated early detection. Unique features of this population included high prevalence of Graves' hyperthyroidism, multiple episodes of thyroid dysfunction in individual patients, spontaneous hypothyroidism after overt Graves' hyperthyroidism, and a high prevalence of TBII-positive overt hypothyroidism.

Acute disseminated encephalomyelitis (ADEM) is an idiopathic inflammatory demyelinating disease of the CNS that is particularly difficult to differentiate from the first episode of multiple sclerosis. ADEM typically occurs as a post-infectious phenomenon, and usually presents a monophasic episode, but also includes recurrent and multiphasic forms. We report a case of ADEM associated with hepatitis B virus (HBV) reinfection. After steroid and IV immunoglobulin treatment, neurologic symptoms were improved. We suppose that the HBV reinfection was the cause of ADEM, but possible pathogenetic mechanism is still obscure., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Objectives: To compare retinal nerve fiber (RNFL) thickness and conventional and non-conventional MRI characteristics of healthy controls (HCs) from the general population (non-fHC) to healthy relatives of multiple sclerosis (MS) patients (fHC)., Methods: Sixty-eight (68) HCs underwent optical coherence tomography (OCT) and 3T MRI examination. Subjects were classified based on whether or not there was a family history of MS. The study enrolled 40 non-fHC who had no relatives with MS and 28 fHC with at least one relative affected with MS. The associations between OCT parameters and conventional and non-conventional MRI measures were investigated., Results: There were no significant OCT or conventional and non-conventional MRI measureable differences between the non-fHC and fHC groups. Periventricular localization and total volume of white matter (WM) signal abnormalities (SA) were more common in the fHC group but the differences did not reach a level of significance. A significant association between decreased RNFL thickness with increased volume (p=0.001), number (p=0.003) and frequency of ≥ 9 T2 (p=0.003) WM SAs on MRI was found in the fHC group. No association between OCT and MRI parameters was detected in the non-fHC group., Conclusion: There is an association between decreased RNFL thickness on OCT and increased WM injury in healthy relatives of MS patients. Further studies should explore the pathophysiology of these findings., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Background: Alemtuzumab is a humanised monoclonal antibody that depletes lymphocytes, causing long-term immunomodulation. In a 3-year, rater-blinded phase 2 study (the CAMMS223 study) in patients with relapsing-remitting multiple sclerosis (RRMS), alemtuzumab reduced relapse rate and the risk of sustained accumulation of disability compared with subcutaneous interferon beta-1a, and the mean expanded disability status scale (EDSS) score of the alemtuzumab cohort improved compared with baseline. Adverse events included infusion-associated reactions, predominantly mild to moderate infections, thyroid disorders, and immune thrombocytopenia. In this study, we further analysed the CAMMS223 data with the aim of determining whether demographic and baseline disease-related characteristics affect the beneficial effects of alemtuzumab. Additionally, we aimed to describe a new outcome measure in multiple sclerosis research: sustained reduction in disability., Methods: 334 treatment-naive patients with active, early RRMS were randomly assigned in a 1:1:1 ratio to receive interferon beta-1a (44 μg subcutaneously three times per week), or 24 mg per day or 12 mg per day alemtuzumab intravenously for 2 or 3 annual cycles. We analysed freedom from clinical disease activity (CDA; defined as no relapses and no sustained accumulation of disability) and occurrence of sustained reduction in disability (SRD; a ≥1 point decrease on the EDSS sustained for 6 consecutive months for patients with a baseline EDSS ≥2), and analysed efficacy outcomes for subgroups based on age, sex, geographic region, MRI-T1 brain volume, MRI-T2 lesion volume, disease duration, number of previous relapses within 2 years, and EDSS., Findings: 322 patients were analysed. 161 of 215 patients treated with alemtuzumab were free of CDA at 36 months (Kaplan-Meier estimate 71·8%, 95% CI 63·1-78·8%) compared with 52 of 107 patients treated with interferon beta-1a (42·6%, 32·4-52·4%; hazard ratio [HR]=0·31, 0·20-0·46; p<0·0001). For the 199 patients with a baseline EDSS score greater than or equal to 2, SRD was more likely (HR=2·61, 1·54-4·43; p=0·0004) among patients treated with alemtuzumab (66 of 133 patients, Kaplan-Meier estimate 51·6%, 95% CI 43·2-60·7%) than patients treated with interferon beta-1a (15 of 66 patients, 27·2%, 17·2-41·4%). All disability and relapse outcomes showed evidence of beneficial effects of alemtuzumab compared with interferon beta-1a across all analysed patient subsets, and no subgroup of patients consistently responded better than others to alemtuzumab., Interpretation: Alemtuzumab reduced disease activity compared with interferon beta-1a in most of the analysed subgroups. Significantly greater numbers of patients experienced sustained improvement in disability after treatment with alemtuzumab than interferon beta-1a. The efficacy offered by alemtuzumab is a substantial advance in the treatment of multiple sclerosis., Funding: Genzyme and Bayer Schering Pharma., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Multiple sclerosis and lichen ruber planus are clinically and histologically distinct complex disorders of putative autoimmune aetiology that are fairly commonly observed in isolation but rarely found in combination. Only two previous reports have described lichen skin disorders in association with multiple sclerosis. The present report describes the case of a 51-year-old Caucasian woman exhibiting both familial multiple sclerosis and lichen ruber planus. This combination may have occurred by chance or it might imply that these disorders share common mechanisms in their pathogenesis.

Immunopathogenesis of multiple sclerosis is a complex process involving T cell mediated autoimmunity at initial stage of disease. A long standing view that Th1 cells are critical for early inflammatory development of lesions is challenging by recent findings that Th1 helper cells with Th17 phenotype are even more important. A complex autoimmunity of MS is further complicated with evidence that CD8 cells, regulatory T cells, clonal expansion of B cells, cells of myelin lineage, antibodies and complement, as well as process intrinsic to central nervous system contribute to the tissue destruction. Although there are a lot of evidences about inflammatory phase of MS, far less is known about mechanisms involved in degenerative phase of disease. It is not known weather quantitative, or qualitative differences in inflammatory response contributes to destruction of the tissue, or as it was shown experimentally demyelination may sometimes occur independent of T cells. Understanding of immunopathogenesis of MS especially regarding various stages of disease is necessary for clinicians in choosing optimal therapy of MS in individual patients. Influences of immunomodulatory treatment on various stages of MS immuno-pathogenesis are presented.

Objective: Myelin oligodendrocyte glycoprotein (MOG) is a highly immunogenic minor component on the outside surface of CNS myelin which is believed to be one of the autoantigens in multiple sclerosis. The aim of this study was to evaluate the diagnostic potential of anti-MOG IgG antibody levels in cerebrospinal fluid (CSF) and serum of patients with relapsing-remitting multiple sclerosis (RRMS), primary progressive multiple sclerosis (PPMS) and non-inflammatory neurological diseases (NIND) as markers for the different clinical types of multiple sclerosis., Patients and Methods: Consecutive serum and cerebrospinal fluid samples were taken from 21 patients with RRMS, 7 patients with PPMS and 19 patients with NIND. The antibody responses to MOG were determined in paired samples of these different clinical groups by enzyme-linked immunoassay using a recombinant human MOG protein., Results: The performed analysis indicated that the differences in levels of anti-MOG IgG antibody in serum and cerebrospinal fluid from the patients with RRMS, PPMS or NIND were not statistically significant., Conclusion: The assay is not sensitive or specific enough to be used as a differential diagnostic tool for the clinical types of MS, nor for MS itself.

The spectrum of optic neuromyelitis (ONM) ranges from monophasic or recurrent idiopathic forms of the disease, to ONM associated with autoimmune disorders. A distinct form of the disease, called recurrent ONM with endocrinopathies, characterized by spinal cord involvement (cavitations with syringomyeloid sensory disturbance), rapid evolution to blindness and paraplegia, characteristic cerebrospinal fluid (CSF) findings, and association with hypothalamus-pituitary dysfunction, has recently been described. The first case of ONM with endocrinopathies in a female Caucasian from Europe is presented, supporting the existence of this syndrome as a separate entity.

Multiple sclerosis (MS) has several clinically different forms. Whereas the illness progresses slowly in most of the patients, 10% have an aggressively progressive course with fatal outcome without signs of remyelination capability. The process of remyelination depends on numerous interactive factors, including the presence of various growth factors, the most important of which in the adult is insulin growth factor-I (IGF-I). On the other hand, the most powerful postnatal regulator of IGF-I is growth hormone (GH), which also acts as a neuroprotective and an antiapoptotic agent, and has direct influence on myelination. Levels of these growth factors have never been examined in the cerebrospinal fluid (CSF) of patients with MS. The levels of IGF-I and GH were measured in serum and CSF of 46 MS patients and compared with those of 49 patients with no evidence of demyelinating disease. The only positive finding was a deficiency of GH in the CSF of MS patients. The possible implications of those findings in the etiopathogenesis of MS will be discussed.

Recent data indicate that the apoptotic process, mediated by the CD95/Fas cell surface receptor, is impaired in activated lymphocytes of patients with relapsing-remitting multiple sclerosis. Using flow cytometric-immunophenotyping, we analyzed the expression of CD95/Fas on peripheral blood CD4+ and CD8+ T lymphocytes (PBL) in 10 MS patients in relapse, and the effect of pulse corticosteroid therapy on the apoptosis of autoreactive lymphocytes. The proportions of CD8+ and CD8+CD95+ T lymphocytes were significantly higher in MS patients in relapse before than after pulse corticosteroid therapy. Conversely, the proportions of CD4+ and CD4+CD95+ T cells were significantly lower before than after therapy, but not significantly different from healthy persons. The different expression of CD95/Fas on peripheral blood CD8+ T lymphocytes in relapsing RRMS and in healthy controls suggests a possible involvement of apoptosis in the pathogenesis of MS. Our results also show that pulse corticosteroid therapy influences the CD95/Fas expression on CD8+ and CD4+ T lymphocytes in patients with RRMS.

Leigh's disease is a mitochondrial disease of infancy and early childhood, and is rare in adults. Following a febrile illness, a 21-year-old woman developed ataxic paraparesis and was originally diagnosed as multiple sclerosis. Her illness progressed to somnolence and quadriparesis. The unusual MR images, the discovery of elevated blood lactate and pyruvate levels, the results of muscle biopsy and the lack of response to corticosteroid treatment, led to the correct diagnosis of Leigh disease. Initiation of a ketogenic diet resulted in a rapid partial response. She recovered sufficiently to be able to walk after 6 months.

The aim of the study was to determine diagnostic value of magnetic resonance angiography (MRA) of the carotid artery, performed with less expensive machine of 0.5 T, and value of duplex ultrasonography (DU) in the same patients. Diagnostic values of MRA and DU were examined by comparison with the results of digital subtraction angiography (DSA) or with the operative finding. All MRA examinations were performed in the same diagnostic center, but DU diagnostic procedures were performed in five different centres. In total, we examined 70 arteries in 37 patients. Among them, 66 arteries in 33 patients were compared with DSA and four arteries in four patients with operative findings. All patients were referred to DSA after MRA and DU. In four patients four carotid arteries were operated without DSA due to previous allergic reaction to iodinated contrast agent. The positive result in present examination was stenosis of the carotid artery more than 70% of the arterial lumen. Such stenosis is considered as an indication for active therapeutic approach using vascular surgery or transluminal angioplasty. Results indicate more true positive results for MRA (21 patients) than for DU (20 patients). Also, we found more true negative results for MRA (45 patients) than for DU (44 patients). MRA had one false positive and three false negative results, and DU two false positive and 4 false negative results. Sensitivity of MRA in our group of patients was 88% and specificity 98%. In the same group DU had sensitivity 83% and specificity 96%. Our results showed that neither MRA nor DU separately could replace DSA in diagnosis of high grade carotid stenosis. Because of high specificity, negative MRA or DU can exclude significant stenosis and avoid DSA. In the case of similar positive results of MRA and DU, the number of DSA can be reduced.

The importance of laboratory methods for multiple sclerosis (MS) diagnosis and differential diagnosis is often overestimated now. The role of several methods including MRI, evoked potentials, examination of the cerebrospinal fluid and some others methods are discussed in this review. Several conditions may in some patients mimick the appearance of MS and it is easy to understand why there is a tendency among many clinicians to embark on extensive- and expensive-laboratory investigations to establish the correct diagnosis at early stages of the disease. Disorders like cerebrovascular diseases, vasculitis, Lyme disease, neurosarcoidosis, acute disseminated encephalomyelitis, progressive multifocal leukoencephalopathy, HIV-associated encephalitis may cause very close changes of the results of these examinations. A detailed, exhaustive history and the neurological examination, along with a careful scrutiny of the actual MRI films by the neurologist experienced in the diagnosis of MS, will obviate the need for additional tests in the overwhelming majority of cases. So, the MS diagnosis and differential diagnosis is still based mainly of the data of clinical observation.

In this study we compared the performance of 39 multiple sclerosis (MS) patients with 28 age-, sex- and education-matched controls on both the Mini-Mental State Examination, a global cognitive assessment tool, and the Sternberg Short-Term memory scanning task, a standardized test of short-term memory (STM) processes. While the STM span of our MS patients did not differ from that of our controls, STM scanning time of the MS group was reliably slower than that of the controls and a significant correlation was observed between STM scanning time and duration but not severity of illness. Our results suggest that processing stages other than the manipulation of data within the STM buffer are also affected by MS., (Copyright 1999 Lippincott Williams & Wilkins)

A 37-year-old patient with Creutzfeldt-Jakob disease (CJD) is presented, who had received a cadaveric dura matter graft 12 year before the onset of neurologic symptoms. Initial clinical presentation included cerebellar symptoms, with dementia and myoclonus developing in later stages of the disease. EEG showed diffuse slowing with sporadic triphasic periodic activity. CT was normal in the early stage but pronounced cerebral and cerebellar atrophy with widened sulci were seen on MRI in the late stage of the disease. The prion protein (PrP) gene was homozygous for valin at the polymorphic codon 129. Cerebrospinal fluid analysis for 14-3-3 protein was positive. We believe that this patient is the first Croatian to acquire CJD by dural implant. Based on this case and a review of 66 cases from the literature, it is manifest that the awareness of iatrogenic transmission of CJD and adoption of preventive measures are the only effective way to stop the spread of CJD among surgically treated patients.

We observed seven patients who developed their first signs and symptoms of motor neuron disease together with signs of protrusion/prolapse of intervertebral disc. The age of the patients was between 55 and 67, of which one female and six male patients. All of them suffered from cervical spine pain or low back pain. The female patient and one male patient developed weakness in the small feet muscles as initial symptom and they complained of paresthesia along dermatomes L5S1 and of severe pain. The other five patients developed wasting of the hands muscles. They had a rather mild pain in the cervical spine and early morning paresthesia as well as severe causalgia along dermatomes C5C6 or C6C7. After the diagnosis of compressive radiculopathy in all patients, they underwent surgical treatment and very soon developed very severe progression of muscle wasting which included muscles of limbs, trunk and bulbar innervated muscles with signs and symptoms of lower and upper motor neuron lesion. Five patients died from 12 to 15 months after surgical treatment and two patients are still living.

The disturbances of autonomic cardiovascular reflexes have already been described in patients with multiple sclerosis (MS). It seems that this disturbances are the result of reflex pathways impairment in the central nervous system. We have tested 28 patients with MS and control group of 21 healthy volunteers using a set of autonomic cardiovascular reflexes tests. In all of patients zones of demyelinization have been discovered with magnetic resonance imaging (MRI). The biggest number of abnormal results was found in respiratory sinus arrhythmia (RSA) test (60.7%) and cortical activation test (35.7%). In 11 patients we found abnormal results in 2 or more tests. Patients with abnormal results in 4 or more tests had clinical impairment of other autonomic functions (urinary bladder regulation). The results of autonomic dysfunction tests show positive correlation to the MRI findings.

Seventy-nine patients admitted in the neurological Intensive care unit because of severe disturbances of consciousness has been evaluated. Protocol based on previous experiences in evaluation of unconsciousness patients was used. Forty-four patients died and thirty-five survived. In 46 patients cause of illness was intracerebral hemorrhage. In 44 of them the cause of hemorrhage was arterial hypertension and in two of them rupture of a-v malformation. The majority of patients actually 41 of them showed hemispheral localization of intracerebral hematoma and five subtentorial. Pontien hemorrhages was found in three and cerebellar in two patients. In majority of 24 patients with hemispheral localization of intracerebral hematoma who showed progressive deterioration of consciousness the signs of descendent transtentorial herniation were found. The symptoms of uncal herniation were rare. In three patients with subtentorial localization of intracerebral hematoma who died signs of upward transtentorial herniation were observed. In 16 patients with ischemic cerebrovascular accident who showed disturbances of the consciousness at the admittance or soon after, nine patients died and seven survived. The cause of their condition were great hemispheral, smaller brain stem ischemic lesion, or deterioration of consciousness was related to the somatic illness. Patients with great ischemic lesions showed similar course of consciousness deterioration as it was observed in patients with hemispherical intracerebral hematomas with difference that biphasic course of illness characterized with temporary stagnation or even slight improvement of patients condition and than secondary progression of deterioration was seen only in patients with intracerebral hematoma, probably because of secondary ischemic complications. Ten patients were admitted because of subarachnoidal and two of them because of intraventricular hemorrhage. Six of them died and four survived. These patients has rupture of great sacular aneurysm with fast development of high intracranial pressure. In two of them the cause of death was rerupture of aneurysm. Stuporous patient with hemispheral neoplasm showed development of descendent transtentorial herniation which was stopped by anti oedematous and corticosteroid therapy. Comatose patient with brisk response on oculocephalic stimulation and normal papillary light reflexes was suspected on intoxication rather than structural brain lesion. He recovered by diuretics and forced rehydratation. After becoming conscious barbiturate intoxication was confirmed. Three patients were admitted in coma because of poisoning with CO, two patients died. Two patients admitted in epileptic status showed late diencephalic state of coma and they survived after anti epileptics and antioedematous treatment.

The authors evaluate the most frequent causes of seizures in 562 patients admitted at the emergency out-patient ward because of fits. 194 patients were admitted because of the first occurrence of seizures, in 12 of them the first manifestation was status epilepticus of the generalized (8), or focal type (4). The commonest causes of seizures were alcoholism (82), disturbances of the brain blood flow (74), posttraumatic states (20), brain tumor (4), or encephalopathies. In 11 patients the cause of seizures was not found. Besides the causes, the authors stressed the most frequent type of seizures, as well as therapeutic measures. They pointed out that in alcoholism generalized seizures, and grand mal status were the commonest expression of seizures. The same was found in patients with posttraumatic seizures, but they mostly suffered single attacks, and the same in encephalopathies. In patients with vascular lesions focal seizures were not rare. The antiepileptic therapy is not applied in the first occurrence of convulsions, therapy is causal, linked primarily to basic etiopathogenic mechanism responsible for triggering seizures.

In order to determine genetic differences between 50 examinees with ischemic cerebrovascular accident (iCVA) and those of comparative group, we have chosen 1883 persons from phenotypic healthy population divided into 5 different subgroups. The purpose of our investigation was exploring hereditary characteristics of antigenes linked to erythrocyte membrane. The highest discriminating value in genetic distance had MN and ABO genetic loci. The frequency of M antigen in stroke patients was 70% (in the comparative group 55%), N antigen had frequency 30% in patients with iCVA and 45% in the comparative group. The frequency of the blood group A in the patients with iCV was 32.68% and 27.16% in the comparative group. Blood group B had frequency in the patients 10.69% and in the comparative group 6.72%. O blood group had frequency in the patients 56.73% and in the comparative group 66.12%. Genetic distance between patients with iCVA and the comparative group were determined with gene frequencies, that was shown on the dendrogram. The dendrogram clearly shows that patients with iCVA are separated from all other comparative subgroups. The results of our investigation presented the highest discriminating value of MN and ABO genetic loci. The possibility of linkage between genetic loci for these erithrocyte antigenes (on the 4th and 9th chromosome) and genetic loci which determine iCVA cannot be excluded. Finally we consider that this method can support earlier identification of persons who belong to "high risk group for cerebrovascular disease".

Stress response measured as the cortisol secretion rate as well as urinary 17 oxogenic steroid (17 OGS) and 17 oxosteroid (17 OS) excretion was investigated in a group of 28 patients with stroke (11 with hypertensive intracerebral hemorrhage and 17 with ischemic cerebrovascular insult). Significantly higher cortisol secretion values were found in the group of patients who died (p less than 0.01). Similarly, the first day urinary 17 OGS excretion pointed to the greater adrenocortical response in patients who died (p less than 0.05). Urinary 17 OS excretion was normal or below normal in the majority of patients and no difference was found between either male or female patients who survived or died. Our findings indicate that adrenocortical changes which maximize the production of cortisol are operative soon after the onset of stroke. The cortisol secretion rate appeared to be a good indicator of the severity of the stress caused by stroke and may be useful in predicting the prognosis of the illness.

Brainstem auditory evoked responses (BAERs) were recorded in 30 patients with brainstem lesions. The aim of the study was to find the correlation between an abnormal BAER and the adequate level of a brainstem lesion. The correlation noted between an abnormal BAER and level of a brainstem lesion (medulla, pons, midbrain) was not statistically significant (p = 0.073 Kruskal-Wallis H-test). This could be explained partly by the fact that a brainstem generators for the BAERs are complex and the various components of the BAERs may actually depend on multiple generators. In patients with unilateral lesions the most prominent abnormality was noted in BAERs generated by stimulating the ear ipsilateral to the lesion, except for wave V. The present study supports the concept that ipsilateral pathway (uncrossed fibres) and crossing fibres contribute to its generation.