Objectives: Emergent computed tomography angiography with contrast is commonly performed for acute ischaemic stroke, but potentially delayed pending admission renal function assessment due to purported risk of contrast-induced acute kidney injury. Such clinical dilemma warrants further evaluation. Methods: We retrospectively examined the incidence of contrastinduced acute kidney injury in acute ischaemic stroke patients who underwent a single initial contrasted computed tomography angiography or two serial contrasted computed tomography angiographies, versus acute kidney injury in patients with no contrast exposure. Acute kidney injury and extended renal dysfunction were defined as increase by >50% in serum creatinine from admission, within 5 days and after 30 days respectively. Results: Of 465 patients with acute ischaemic stroke, 372 underwent computed tomography angiography (203 with single initial contrasted computed tomography angiography, 169 with two serial contrasted computed tomography angiographies), and 93 patients had no contrast exposure. 33% of entire cohort had diabetes mellitus and 9.4% had chronic kidney disease, both comparable between subgroups. Acute kidney injury occurred in 2.5%, 2.4%, and 9.7% with single initial contrasted computed tomography angiography, two serial contrasted computed tomography angiographies, and no contrast exposure, respectively (p = 0.004). Corresponding rates of extended renal dysfunction were 1.5%, 0.6%, and 6.5% (p = 0.185). On multivariate analysis, diabetes mellitus and lower baseline estimated glomerular filtration rate were independently associated with acute kidney injury, while lower estimated glomerular filtration rate was associated with extended renal dysfunction (p < 0.05). Contrast-exposed patients did not have higher risk for acute kidney injury (odds ratio, OR = 0.25, 95% CI 0.096–0.647, p = 0.004) or extended renal dysfunction (OR = 0.083, 95% CI 0.008–0.810, p = 0.032) versus non-contrasted patients. Receiving two computed tomography angiographies within 24 hours did not confer added risk for contrast-induced acute kidney injury. Conclusions: Emergent or serial computed tomography angiographies in acute ischaemic stroke were associated with very low risk of acute kidney injury and extended renal dysfunction, and these risks were not significantly higher than in acute ischaemic stroke patients with no early contrast exposure.
Aim of the study: On financial or facility constraints of brain imaging, score model is used to predict the occurrence of acute haemorrhagic stroke. Accordingly, this study attempts to develop a new score model, called Soetomo score. Material and methods: The researchers performed a cross-sectional study of 176 acute stroke patients with onset of ≤24 hours who visited emergency unit of Dr. Soetomo Hospital from July 14th to December 14th, 2014. The diagnosis of haemorrhagic stroke was confirmed by head computed tomography scan. There were seven predictors of haemorrhagic stroke which were analysed by using bivariate and multivariate analyses. Furthermore, a multiple discriminant analysis resulted in an equation of Soetomo score model. The receiver operating characteristic procedure resulted in the values of area under curve and intersection point identifying haemorrhagic stroke. Afterward, the diagnostic test value was determined. Results: The equation of Soetomo score model was (3 × loss of consciousness) + (3.5 × headache) + (4 × vomiting) − 4.5. Area under curve value of this score was 88.5% (95% confidence interval = 83.3–93.7%). In the Soetomo score model value of ≥−0.75, the score reached the sensitivity of 82.9%, specificity of 83%, positive predictive value of 78.8%, negative predictive value of 86.5%, positive likelihood ratio of 4.88, negative likelihood ratio of 0.21, false negative of 17.1%, false positive of 17%, and accuracy of 83%. Conclusions: The Soetomo score model value of ≥−0.75 can identify acute haemorrhagic stroke properly on the financial or facility constrains of brain imaging.
Aim of the study: The prevalence of cognitive impairment increases with age and features lesions observed in Alzheimer’s disease, vascular dementia, Parkinson’s disease and dementia with Lewy bodies. The aim of the study was to determine whether individuals without diagnosed dementia are affected by any reduction of cognitive functioning and to what extent such reduction occurs. Material and methods: The study enrolled 156 individuals, including 110 aged <75 years and 46 aged ≥75 years. Cambridge Neuropsychological Test Automated Battery was used in assessment of Motor Screening Task (Mean Latency and Mean Errors), Paired Associated Learning (Total Errors and Errors Shapes), Stocking of Cambridge (Mean Initial Thinking Time, Mean Subsequent Thinking Time, Problems Solved in Minimum Moves) and Graded Naming Test. Individuals who aborted tests were categorized as below the reference threshold. Results: Prevalence of results below the reference threshold were as follows: 8.97% in Motor Screening Task – Mean Latency, 57% in Paired Associated Learning – Total Errors, 57% in Paired Associated Learning – Errors Shapes, 30% in Stocking of Cambridge – Mean Initial Thinking Time, 28% in Stocking of Cambridge – Mean Subsequent Thinking Time, 57% in Stocking of Cambridge – Problems Solved in Minimum Moves and 32% in Graded Naming Test. The results of Motor Screening Task were above the threshold. Motor Screening Task – Mean Error was higher in the +75 group (p < 0.001), whereas the Motor Screening Task – Mean Latency did not differ between the groups. Also Paired Associated Learning outcomes were higher in the +75 group (p = 0.01). Graded Naming Test and Stocking of Cambridge – Mean Subsequent Thinking Time were lowered in the +75 group (p = 0.01), whereas other Stocking of Cambridge tests did not differ. The age ≥75 years was associated with 2.3 times higher risk of decreased Stocking of Cambridge – Mean Initial Thinking Time, 2.7 times higher risk of decreased Stocking of Cambridge – Mean Subsequent Thinking Time and 3.3 times higher risk of decreased Graded Naming Test. Conclusions: The link between cognitive functions and the age, despite the lack of diagnosis of dementia, confirms the need of neuropsychological assessment in patients without dementia.
Trigeminal neuralgia is one of the most severe facial pains. Although it has been broadly described by many researchers, it is referred to as Fothergill’s disease to commemorate the researcher who gave the first full and accurate description of trigeminal neuralgia in 1773. Trigeminal neuralgia incidence ranges from 2 to 5 cases per 100,000 people, with women being affected more often than men. The trigeminal nerve has a sensory and motor function, and along with the glossopharyngeal nerve, the vagus nerve, the suboccipital nerve, the greater and lesser occipital nerves and the great auricular nerve innervate the skin of the head. Fibres that convey pain stimuli through the trigeminal ganglion terminate in the spinal nucleus, from where, passing through the nuclei of the thalamus, they reach the sensory cortex, the limbic system and the insular cortex. The reasons behind painful sensation in neuralgia may be the damage of the thick Aβ nerve fibres and the appearance of focuses of ectopic excitation which is then transferred to the damaged structural thin Aδ and C nerve fibres in neural connections referred to as ephapses. There are two types of trigeminal neuralgia: classic and symptomatic. Both types are characterised by a sudden, electric shock-like pain that lasts from a couple of seconds to two minutes. More often than not, the pain affects the area innervated by the second and the third branch of the trigeminal nerve, namely the maxillary and the mandibular nerve. Trigger zones are characteristic for this condition, and – when irritated by non-pain stimuli – they cause an attack of neuralgia. The management of trigeminal neuralgia involves surgical and conservative treatment. The golden standard for the conservative treatment is to use carbamazepine or oxcarbazepine. Should the aforementioned treatment fail, baclofen, lamotrigine or other anticonvulsant drug used in the treatment of epilepsy may be introduced. The following are the most frequently used surgical methods of treatment: decompression of the neurovascular conflict, the use of trigeminal ganglion balloon compression, the use of percutaneous glycerol block of the Gasserian ganglion, cutting postganglionic nerve fibres with radiofrequency and stereotactic radiosurgery (gamma knife).
Treatment of multiple sclerosis with interferon-beta involves the risk of the development of immunological response to this protein. The response consists in the production of antibodies that bind or neutralise interferon-beta. The binding antibodies are detectable in the majority of the treated patients and do not influence the efficacy of treatment. Simultaneously, large clinical studies provide evidence that the neutralising antibodies reduce and in high titres suppress the effect of interferon, which causes the frequency of exacerbations and the number of new and intensified outbreaks in magnetic resonance imaging to increase. What is more, it may even result in the accelerated progression of disability. The incidence of the neutralising antibodies depends on the preparation as well as the route of administration and concerns from 2 to 42% of the treated patients; it reaches its maximum between the 6th and the 24th month of treatment. The neutralising antibodies may be present temporarily (once they disappear, the efficacy of interferon returns to its initial level), yet a high titre predicts their long-term persistence, even after the drug has been discontinued. Various ways of detecting the neutralising antibodies have been devised – from methods that take advantage of a cytopathic effect to those based on the induction of a luciferase reporter gene. Reliable markers of the in vivo activity of interferon-beta that may complement marking of the antibodies are being sought. For many years, the issue of anti-interferon antibodies was accompanied by controversy that resulted from methodological difficulties in studying their clinical utility. At present, in view of the gathered data, European experts unanimously recommend a repeated screening examination of the neutralising antibody titre for patients treated with interferon and considering the results when making therapeutic decisions.
Changes in human behaviour resulting from the brain injury are of great interest to neurology and neuropsychology. The frontal area of the brain is interesting in terms of neuropsychological assessment, as it is responsible for a proper function of multiple cognitive processes. The analysis of the frontal lobe dysfunction expands to other areas: emotional and behavioural. Oftentimes, it is important to take into account remarks made by the patient’s family as they immediately notice dramatic changes in his or her personality and behaviour. The diagnostic process is complex and includes all areas of o the patient’s activities. In the course of analysis of disorders resulting from an injury of the brain’s frontal region stages can be distinguished – these stages relate to the assessment of: the level of psychomotor activity and motivational sphere, cognitive functioning, changes in personality and emotional area. In addition, knowing the exact location of damage in the frontal lobe provides the basis for the diagnosis of specific frontal lobe syndrome. Data on the lateralization of damage facilitate the identification cognitive deficits. Prefrontal area – the youngest, in terms of phylogenetics, area of the frontal part of cerebral cortex – is particularly associated with emotional disorders. It is responsible for the control of the most complex acts of human behaviour. This paper discusses cognitive and emotional deficits as well as personality changes of the reported patient. Authors focus on the role of the frontal lobe in the control of executive functions. Moreover, they highlighted the role of the frontal region in the development of many mental disorders. Structural neuroimaging studies provide a number of data that show the relationship between changes in the activation of the frontal area and the development of emotional disorders.
Acute transverse myelitis is a pathological condition leading to the damage of the spinal cord’s structures. It is also a rare manifestation of systemic lupus erythematosus affecting 1 to 2% of patients. It usually occurs shortly after the diagnosis is established, most often within the first five years of the disease. This article reports a 35-year-old man, with no history of any diseases, who suddenly had the following signs and symptoms: deterioration of mood, hyperhidrosis, headaches, thoracic-lumbar spine pain, sensory disorders around the torso, difficulties urinating and defecating. Magnetic resonance imaging of the spine revealed long-segment myelitis. In order to establish the aetiology of the disease, a number of laboratory and imaging examinations were performed. Based on the Systemic Lupus International Collaborating Clinics/American College of Rheumatology criteria – SLICC–ACR 2012, systemic lupus erythematosus was diagnosed. The patient was subjected to glucocorticosteroid pulse therapy without delay, and eventually improved satisfactorily. The reported case shows that transverse myelitis may be the first clinical manifestation of systemic lupus erythematosus. The authors have highlighted the necessity of an early diagnosis as well as establishing the disease’s aetiology and determining the risk of relapse, as all three affect prognosis.