Therapeutic plasma exchange (TPE) is an extracorporeal blood purification technique, which removes large molecular weight particles such as autoantibodies from plasma. TPE is accepted by the American Society for Apheresis as first line treatment for some severe neuroimmune disorders. Double filtration plasmapheresis (DFPP) is a newer technique in which plasma is not entirely removed, only the antibodies, using special filters. High-dose intravenous immunoglobulins are an alternative treatment for these patients but are much more expensive. We reviewed medical records of 20 patients with severe neurological diseases requiring TPE or DFPP. We analyzed the indications, complications and efficacy of these procedures. After completing the procedures, neurological improvement was recorded in 80% of the patients, 5% had no improvement, and the mortality was 15%. The rate of neurological improvement was similar to other studies. None of the patients presented catheter related complications. Systemic complications were mild, transient and completely reversible.
The circle of Willis is a very important vascular mechanism of protecting against cerebral ischemia, especially when circulation within the main arteries irrigating the brain is somehow impeded. As result of congenital malformation arising early in embryonic development, the fetal-type posterior circle of Willis remains as such during the rest of one's life. Consequently, the posterior cerebral artery (PCA) becomes a branch of the internal carotid artery (ICA), rather than of the basilar artery (BA). Furthermore, the rest of collateral circulation, between the anterior and the posterior regions of the brain, is also negatively affected (e.g., leptomeningeal vessels). The anatomical variant represented by the artery of Percheron (AOP) has its origin on one of the PCAs, supplying singlehandedly both paramedian areas of the thalamus (right and left) and posterior regions of the midbrain. In the present study, we report a case of bilateral thalamic infarction with midbrain involvement, where the correct diagnosis was made retrospectively using computed tomography (CT) scan, magnetic resonance imaging (MRI), diffusionweighted imaging (DWI) and three-dimensional time-of-flight magnetic resonance angiography (3D TOF MRA).
Background. Stroke is one of the leading causes of mortality and morbidity worldwide. Despite extensive research, to this date there is no panel of biomarkers for the prevention and prognosis of ischemic stroke and there is still much incomplete and insufficiently researched information. Aim. We conducted a prospective, observational study between January and June 2020. The main objective of this study was to clarify the role of inflammation markers, i.e. neutrophil/ lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), high-sensitivity C – reactive protein (hsCRP) in ischemic stroke and whether there is or not a correlation between these markers and carotid stenosis. Study design. In the study we included 150 subjects divided in two groups: study group – 100 subjects and control group – 50 subjects. Methods. Data collected during the research (at the time of patient admission): 1) biological sample: 5 ml of peripheral blood were collected in a vial with clot activator and separating gel, from which the following laboratory tests were performed: hsCRP, neutrophils, lymphocytes, platelets. NLR and PLR were subsequently calculated as the ratio of neutrophils to lymphocytes, respectively platelets and lymphocytes), 2) paraclinical examinations: extracranial carotid Doppler ultrasound examination. Results. The results were impressive: high-sensitivity C reactive protein (hsCRP), neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR) were strongly, respectively moderately correlated with the severity of stroke (the severity being established with the NIHS (National Institute of Health Stroke) score. None of the inflammation markers included in the present study was correlated with carotid stenosis. Conclusion. hsCRP, NLR and PLR may potentially be prognostic markers for ischemic stroke, being of major help in preventing its possible complications.
Guillain-Barre syndrome (GBS) is the most common cause of acute flaccid paralysis worldwide, having an incidence of about 1/100,000 across several studies in a number of countries. We present the case of a 60-year-old female patient, with known hypertension, admitted to our department for paresthesia and muscle weakness predominantly in the distal upper and lower limbs. Symptomatology had an acute onset after 14 days from influenza vaccine administration. Lumbar puncture revealed CSF glucose (91 mg/dl), CSF protein (0.508 g/l) and no pleocytosis. Electromyography supported the presumptive diagnosis of polyradiculoneuritis. The patient underwent three sessions of double filtration and the final diagnosis was Guillain-Barre polyradiculoneuritis secondary to influenza vaccination. Approximately 80% of patients with polyradiculoneuritis recover completely within a few months to one year; however, 5-10% of these patients experience one or more recurrences. It should be emphasized that acute-phase rehabilitation must start immediately and include an individualized program of gentle strengthening, and manual resistive and progressive resistive exercises. Key words: polyradiculoneuropathy, influenza vaccine, neurorehabilitation,
Twenty percent of strokes occurring in young patients are represented by posterior ischemic strokes. Acute basilar occlusion is a devastating, life-threatening condition, with the highest mortality in young patients. We present the case of a 33-year-old female patient, without vascular risk factors or oral contraceptive treatment, admitted to our department through the emergency ward for comatose state -Glasgow Coma Scale (GCS) 11 points, headaches, right-sided hemiparesis, dizziness and vomiting, with acute onset. CT angiography was performed, which showed left vertebral artery with no flow in the intradural section and absent flow in the basilar artery. After more than 12 hours from onset, endarterectomy was excluded; initiation of treatment with heparin 1000 IU/hour was decided. MRI performed after 24 hours revealed: subacute median and left paramedian pontine ischemic stroke, subacute stroke in the base of the left midbrain peduncle. The following diagnosis was established: pontine ischemic stroke caused by two autoimmune diseases: thrombophilia and antiphospholipid antibody syndrome. Our patient started rehabilitation very early and was discharged with the following neurological sequelae: tetraparesis with the predominance of left hemiparesis: 4/5 on the Medical Research Council strength scale (MRC) -right limbs, 3/5 on the Medical Research Council strength scale (MRC) -left limbs, and dysphagia for liquids.
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