Introduction: Neuroimaging is a standard examination implemented for diagnosis of various pathologies of the central nervous system. The fundamental diagnostic procedures in medical imaging of the central nervous system are computed tomography and magnetic resonance imaging. In case of a sudden focal or generalized onset of brain dysfunctions at first we should think about stroke. A very important test if stroke is suspected is computed tomography. In this paper we would like to check if it is possible to distinguish two pathologies of the cerebrum: ischaemic stroke and tumour, using quantitative analysis of selected abnormalities. Material and methods: Analysis is based on comparison of two pathologies (ischaemic stroke and tumour). Two sets of images were prepared. Analysis is performed to distinguish abnormalities observed on computed tomography brain images from healthy tissue. The image analysis includes data conversion, normalization of region of interest, estimation of the number of texture features, features selection based on four different methods of selection and finally classification based on artificial neural network classifier. Results: In the examination, different effectiveness of used methods was observed. Quantitative analysis of selected texture features allows to differentiate two classes of pathologies. Also an important observation is that the artificial neural network can be a useful tool in data classification and analysis. Conclusions: The performed analysis is effective but only for small number of data. That is why it still needs to be conducted on a larger set of data. It will be also necessary to repeat classification a number of times and to perform data validation in order to confirm effectiveness of the presented method. After that we can hope to get really satisfying results.
The advent of CT/MRI and modern antibiotics along with the progress in surgical techniques made both diagnosis and management of brain abscesses easier and safer. Nonetheless they remain one of the most challenging lesions, both for surgeons and internists. Atypical bacterial and fungal abscesses are frequently due to chemotherapy, immunosuppression, HIV infection, or prolonged antibiotic therapy. This paper gives an account of epidemiology, aetiology and pathogenesis of cerebral abscesses, discusses stages of the infection and stadia of the abscess formation as well as immune response, clinical presentation, diagnosis, management and prognosis. The specific clinical picture of mucormycotic abscesses and those caused by Aspergillus sp., Nocardia sp. and Scedosporium apiospermum were addressed, as were the contemporary MR techniques – diffusion weighted images (DWI) and proton spectroscopy (MRS). Up-to-date there has been no randomised controlled clinical trial comparing two methods of surgery: tap and aspiration versus excision. The review of the literature allowed a presentation of recommended management variants. Currently, mortality in brain abscesses decreased down to 17–32%. From 20% to 70% of patients have permanent neurological sequelae, often (30–50%) epilepsy. Immunosuppression and comorbidities, initial neurological status, and intraventricular rupture are significant factors influencing the outcomes of patients.
A spinal epidural empyema is a collection of pus between the bone and dura. It may be a sequela of discitis or vertebral body osteomyelitis but much more frequently it arises as a result of hematogenous spread, usually from urinary tract infection, endocarditis or pneumonia. Male to female ratio is two and patients are typically over 30 years old. Risk factors are as follows: the use of intravenous drugs, immunosuppression, diabetes mellitus, alcohol abuse, foci of infection, open spinal trauma, spinal surgery. The source of infection remains unidentified in <40% of patients. The pathognomonic triad of symptoms is: fever, focal back pain aggravated on palpation and progressive neurological deficit. Early diagnosis is crucial since treatment may prevent neurological sequelae but should they appear, cannot warrant their subsidence. The correct diagnosis requires radiological studies, preferably MRI. The management involves surgical drainage of pus and long-standing treatment with antibiotics. The operative procedure aims for decompression of neural elements, meticulous evacuation of both pus and inflammatory granuloma, and obtaining samples for Gram stain and culture assessment. Mortality rate reaches 16%. Factors that influence prognosis in a negative way are: comorbidities, multiple spinal surgical procedures, empyema located in thoracic segment, MRSA infection.
An intracranial empyema is a sub- or epidural collection of pus. Subdural empyema comes frequently as a sequela of ENT infections, meningitis or neurosurgical procedures, and rarely as a result of hematogenous spread, whereas epidural one usually coexists with osteomyelitic flap in patients after surgery. A typical clinical picture consists of fever, meningeal irritation, symptoms of raised intracranial pressure including somnolence or coma, neurological deficit and seizures. Establishing the diagnosis requires radiological studies, preferably MRI including diffusion weighted images. Surgical treatment allows drainage of pus and obtaining samples for Gram stain and culture assessment. Craniectomy relieves raised intracranial pressure. Up-to-date there has been no randomised controlled clinical trial comparing three applicable methods of surgery: burr hole aspiration, craniotomy and craniectomy. Currently, the average mortality rate in subdural empyema is 10–20%, however, it does not exceed 5% in patients in good general condition on admission, reaching up to 75% in unconscious ones. Delayed diagnosis and treatment brings about a significant risk of permanent neurological deficit. Possible complications involve: herniation, ischaemic stroke, venous sinus thrombosis, cranial osteomyelitis, cerebral abscess, septic shock, hydrocephalus and epilepsy. The last-named has been reported in as many as 42% of patients after subdural empyema.
The aetiology of multiple sclerosis remains incompletely understood. In patients occurs both demyelination, inflammation, axonal damage and oligodendrocytes degeneration. The changes affect both white and grey matter, and also has been shown in normal appearing grey and white matter. However, it is well established that the immune system directly participates in the destruction of myelin and nervous cells and numerous abnormalities on the cellular and humoral response both in blood and cerebrospinal fluid were found in multiple sclerosis patients. The mechanisms leading to damage of the central nervous system are multifactorial. T lymphocytes play the key role, but B lymphocytes, macrophages and microglial cells are also included. Moreover, neurotoxic agents and metabolic disorders may lead to a direct damage of the central nervous system. The paper presents results of recent studies on the immunopathogenesis of multiple sclerosis and the various stages leading to damage to the central nervous system are discussed: the role of the activation of lymphocytes and antigen presenting cells both in blood and in the central nervous system, pass through the blood–brain barrier, the role of T cells and their respective subpopulations (Th1, Th2, and Th17), the importance of B cells, antibodies and the complement system and the mechanisms of demyelination and axonal damage. At the same time are discussed how drugs used in multiple sclerosis therapy affect different stages of the multiple sclerosis aetiopathogenesis, taking into account also the drugs which are at the clinical trials.
Multiple sclerosis (MS) is a common chronic neurological disorder of the central nervous system that leads to progressive disability. The disease usually affects people between 20 and 40 years of age, with women being affected twice as often. Despite many years of research, very little is known about its pathogenesis. There are four distinct clinical presentations, of which the most common are the relapsing-remitting, the secondary progressive and primary progressive courses. The pathogenesis of MS is a complicated process, involving the disruption of the blood–brain and blood–cerebrospinal fluid barriers, secondary hyperplasia of the astroglia, inflammation, and neurodegeneration in a broad sense, among others. The inflammatory process involving various subpopulations of inflammatory cells plays a major role in the development of the disease, especially in its early stages. Previous studies have indicated that the tumour necrosis factor alpha (TNF-α), a proinflammatory cytokine, is particularly involved in the process. Aim of the study: To assess levels of TNF-α in the plasma of patients suffering from MS both undergoing a relapse and in remission, to correlate its concentration with clinical parameters, and to determine whether TNF-α could potentially serve as a marker of MS progression. The relationship between plasma concentrations of TNF-α and the number of leukocytes and subpopulations was analyzed in an attempt to identify major sources of TNF-α in the plasma in MS patients. Material and methods: Thirty-seven MS patients formed study groups (20 in the relapse group, 17 in the remission group). Thirty healthy volunteers formed the control group. Four millilitres of venous blood were collected from each participant. The blood was centrifuged (5000 rpm, 20 min, 23ºC) until the plasma layer could be separated and stored at –80ºC until the testing. TNF-α concentrations were determined using the ELISA method. Results and conclusions: The preliminary results did not show a statistically significant increase in TNF-α levels in the plasma of MS patients, both in the relapse and the remission groups. A positive correlation was found between the clinical severity of MS (measured by the EDSS score) and TNF-α levels in remission and relapse groups. However, it was not statistically significant. In a subgroup of patients in remission with low plasma levels of TNF-α (<1 pg/ml), higher TNF-α concentrations correlated with greater disability (EDSS score). WBC counts were statistically significantly higher in patients undergoing a relapse compared to the joint group of MS patients in relapse and in remission. Preliminary findings of small studies indicate that TNF-α plasma concentrations could potentially reflect the activity of underlying pathological processes in MS. Further studies on larger groups of patients are necessary to confirm the hypothesis as well as in order to correlate TNF-α concentrations in blood and the cerebrospinal fluid.
Melkersson–Rosenthal syndrome is traditionally defined as a triad of syndromes including recurrent facial nerve palsy, oedematous changes within face and a geographic tongue. Aetiology of the disease is not definitely confirmed. Probably it is multifactorial with marked influence of autoimmune response of delayed hypersensitivity type. It is also claimed that infections, systemic disorders as well as trauma may be relevant. The genetic predisposition cannot be excluded. Cases with full clinical presentation are relatively rare, the incomplete cases are problematic for establishing diagnosis and treatment despite the fact that case report of the syndrome are more numerous nowadays. The article presents a case of patient with a recurrent facial nerve palsy and scrotal tongue, in whom the diagnosis was established after 18 years after the first sign occurred. There was a differential diagnostics conduced and the final diagnosis of incomplete Melkersson–Rosenthal syndrome was established. Standard therapeutic strategy was introduced but satisfactory results were not obtained. This case report highlights the diversity of clinical manifestation of the syndrome effecting from a sequence of their appearance, the variability of therapeutic theories, lack of standardized guidelines for therapeutic strategies and importance of collaboration between doctors of different specialties to elucidate this rare diagnosis.
Freezing of gait is the episodic gait disturbance common in Parkinson’s disease, often leading to falls and patient’s activity reduction. Physical rehabilitation should be an integral part of the treatment of Parkinson’s disease because of its different course, reaction to pharmacological treatment and progression. Especially in the case of the dominant gait and posture disorders, with stronger bradykinesia and freezing episodes special attention should be paid to gait training and the usage of techniques and equipment which helps the patient to overcome freezing and reduce its severity. Thanks to the early rehabilitation patients longer retain the ability to walk independently. This work aims to present possibilities of using different methods and equipment in the rehabilitation of patient with Parkinson’s disease. Due to the impairment of the functioning mechanism of the generation of internal stimuli the external signals are of particular importance as well as cognitive strategies, among which we can distinguish acoustic stimuli, visual and tactile, on which the widespread method of Frenkel is based on. Not without significance are also external aids such as canes, walkers and crutches recommended for patients with less efficiency.