Molecular, Electrophysiological, and Ultrasonographic Differences in Selected Immune-Mediated Neuropathies with Therapeutic Implications.

The spectrum of immune-mediated neuropathies is broad and the different subtypes are still being researched. With the numerous subtypes of immune-mediated neuropathies, establishing the appropriate diagnosis in normal clinical practice is challenging. The treatment of these disorders is also troublesome. The authors have undertaken a literature review of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), Guillain-Barre syndrome (GBS) and multifocal motor neuropathy (MMN). The molecular, electrophysiological and ultrasound features of these autoimmune polyneuropathies are analyzed, highlighting the differences in diagnosis and ultimately treatment. The immune dysfunction can lead to damage to the peripheral nervous system. In practice, it is suspected that these disorders are caused by autoimmunity to proteins located in the node of Ranvier or myelin components of peripheral nerves, although disease-associated autoantibodies have not been identified for all disorders. The electrophysiological presence of conduction blocks is another important factor characterizing separate subgroups of treatment-naive motor neuropathies, including multifocal CIDP (synonyms: multifocal demyelinating neuropathy with persistent conduction block), which differs from multifocal motor neuropathy with conduction block (MMN) in both responses to treatment modalities and electrophysiological features. Ultrasound is a reliable method for diagnosing immune-mediated neuropathies, particularly when alternative diagnostic examinations yield inconclusive results. In overall terms, the management of these disorders includes immunotherapy such as corticosteroids, intravenous immunoglobulin or plasma exchange. Improvements in clinical criteria and the development of more disease-specific immunotherapies should expand the therapeutic possibilities for these debilitating diseases.

Pathology of Initial Axon Segments in Chronic Inflammatory Demyelinating Polyradiculoneuropathy and Related Disorders.

The diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is based on a combination of clinical, electrodiagnostic and laboratory features. The different entities of the disease include chronic immune sensory polyradiculopathy (CISP) and autoimmune nodopathies. It is debatable whether CIDP occurring in the course of other conditions, i.e., monoclonal IgG or IgA gammopathy, should be treated as a separate disease entity from idiopathic CIDP. This study aims to evaluate the molecular differences of the nodes of Ranvier and the initial axon segment (AIS) and juxtaparanode region (JXP) as the potential cause of phenotypic variation of CIDP while also seeking new pathomechanisms since JXP is sequestered behind the paranode and autoantibodies may not access the site easily. The authors initially present the structure of the different parts of the neuron and its functional significance, then discuss the problem of whether damage to the juxtaparanodal region, Schwann cells and axons could cause CIDP or if these damages should be separated as separate disease entities. In particular, AIS's importance for modulating neural excitability and carrying out transport along the axon is highlighted. The disclosure of specific pathomechanisms, including novel target antigens, in the heterogeneous CIDP syndrome is important for diagnosing and treating these patients.

Regulation of microRNA Expression in Sleep Disorders in Patients with Epilepsy.

The effects of epilepsy on sleep and the activating effects of sleep on seizures are well documented in the literature. To date, many sleep-related and awake-associated epilepsy syndromes have been described. The relationship between sleep and epilepsy has led to the recognition of polysomnographic testing as an important diagnostic tool in the diagnosis of epilepsy. The authors analyzed the available medical database in search of other markers that assess correlations between epilepsy and sleep. Studies pointing to microRNAs, whose abnormal expression may be common to epilepsy and sleep disorders, are promising. In recent years, the role of microRNAs in the pathogenesis of epilepsy and sleep disorders has been increasingly emphasized. MicroRNAs are a family of single-stranded, non-coding, endogenous regulatory molecules formed from double-stranded precursors. They are typically composed of 21-23 nucleotides, and their main role involves post-transcriptional downregulation of expression of numerous genes. Learning more about the role of microRNAs in the pathogenesis of sleep disorder epilepsy may result in its use as a biomarker in these disorders and application in therapy.

Pathophysiology of the Different Clinical Phenotypes of Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP).

Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common form of autoimmune polyneuropathy. It is a chronic disease and may be monophasic, progressive or recurrent with exacerbations and incomplete remissions, causing accumulating disability. In recent years, there has been rapid progress in understanding the background of CIDP, which allowed us to distinguish specific phenotypes of this disease. This in turn allowed us to better understand the mechanism of response or non-response to various forms of therapy. On the basis of a review of the relevant literature, the authors present the current state of knowledge concerning the pathophysiology of the different clinical phenotypes of CIDP as well as ongoing research in this field, with reference to key points of immune-mediated processes involved in the background of CIDP.

Acute cerebral venous thrombosis - still an underdiagnosed pathology in emergency computed tomography of the brain.

PURPOSE: Acute cerebral venous thrombosis (CVT) is a rare condition that can lead to a serious clinical state; thus, prompt diagnosis and treatment are mandatory. Head computed tomography (CT) plays a crucial role in the initial prompt diagnosis in the emergency setting. The aim of the study was to retrospectively analyse emergency head CT studies and the rate of incorrect diagnoses and main sources of pitfalls. MATERIAL AND METHODS: Retrospective analysis of 31 emergency CT studies (22 without contrast, 19F/12M, age range: 4-94 years) of patients with confirmed acute CVT. RESULTS: Thrombosed dural sinuses were found in 24/31 (77.4%) cases, thrombosed veins in 7/31 (22.6%) cases, no lesions within vessels in 2/31 (6.5%) cases. Haemorrhagic brain lesions were found in 9/31 (29%) cases, hypodense oedema in 6/31 (19.6%) cases, brain swelling in 1/31 (3.2%) cases, and no parenchymal lesions were revealed in 15/31 (48.4%) cases. Correct diagnosis of CVT was established in 15 cases (48.4%); however, it was incorrect in 16 cases (51.6%). Incorrect cases consist of 4 groups: 1 - with both vascular and parenchymal lesions that were overlooked (50%), 2 - with vascular lesions only, which were either overlooked, misinterpreted, or covered by artefacts (31.3%,), 3 - with parenchymal lesions only, which were misinterpreted (12.5%), and 4 - with no lesions present in the emergency head CT (6.2%). CONCLUSIONS: The high rate of incorrect diagnoses of acute CVT based on emergency head CT requires constant training of radiologists and their close cooperation with clinicians because a delayed diagnosis may be lethal to the patient.

Abnormality of multimodal evoked potentials in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).

INTRODUCTION: Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an autoimmune disease of the peripheral nervous system, sometimes including the central nervous system. The aim of the study was the assessment of the prevalence of central sensory impairment and its reliance on peripheral nerve damage in patients with CIDP. MATERIAL AND METHODS: Multimodal (visual-VEP, brainstem auditory-BAEP, somatosensory-SEP) evoked potentials (EPs) were studied in 24 patients diagnosed with CIDP. The results were compared with neurographic parameters of sensory responses. The control group consisted of 35 healthy volunteers selected with respect to age and sex. RESULTS: Mean latency of most components of EP were considerably prolonged in patients compared with the control group. There were no correlations between the P100 VEP latency and the peripheral sensory parameters. Statistically significant negative correlations were obtained between BAEP and SEP responses and the amplitude and sensory conduction velocity of peripheral nerves. The inter-latencies were also longer. CONCLUSIONS: The authors indicated to the possibility of central sensory involvement in patients with CIDP, especially based on the prolonged inter-latency of BAEPs with simultaneously confirmed root affection. The severity of central damage correlates with the degree of peripheral nerve impairment.

Seasonal variations in the occurrence of transient global amnesia (TGA).

BACKGROUND: Transient global amnesia (TGA) is a rare, benign condition characterised by a sudden deficit of anterograde and retrograde memory that usually lasts for a few hours and is not accompanied by other focal neurological symptoms or signs. Its aetiology is still unclear. Various events or activities may trigger TGA. Evidence of seasonal variations in the appearance of TGA is inconsistent. METHODS: We retrospectively analysed the medical history of 114 adult patients with diagnosed TGA, hospitalised at two neurology departments in Wroclaw from 2008 to 2014. We reviewed risk factors, trigger points, and occurrence in each month of the year in our patient population. RESULTS: Over this seven-year period, 114 patients were diagnosed with TGA. The annual occurrence ranged from 13 to 22 hospitalisations. The mean age of the patients was 64 years. There were 36 TGA events in men and 78 in women. TGA occurred most frequently in spring (36%) and summer (30%), with the incidence peaking during March. CONCLUSIONS: Our findings suggest that there is a relationship between the season of the year and the probability of TGA.

Visual and somatosensory phenomena following cerebral venous infarction.

BACKGROUND: The most frequent clinical presentation of occipital or visual tract lesion is hemianopsia or quadrantanopsia. However, damage to the primary or secondary visual cortex can also manifest as visual hallucinations (photopsiae or complex phenomena). We report visual and somatosensory phenomena following cerebral venous infarction based on a study of a patient with a history of recent head injury. CASE PRESENTATION: We report a 61-year-old man with a history of recent head injury presented with a headache of two weeks duration. He was complaining of transient visual abnormalities, which he described as impaired ability to recognize faces, dark spots moving in the visual field and distorted contours of an objects. Clinical examination showed a balance disorder with no evidence of visual deficit. During further observation the patient started to experience more complex visual and sensory phenomena of: waving of the ceiling, clouds that he could form and feel, he had an impression of incorrect sizes of given objects, he could see a nonexistent pack of cigarettes and the character from the arcade game Pac-Man "eating" an existing drip stand. CONCLUSIONS: The patient mentioned above possessing simple and complex visual and somatosensory hallucinations and illusions in the course of venous stroke. A possible mechanism involves irritation of cortical centers responsible for visual processing.

The Usefulness of the TOAST Classification and Prognostic Significance of Pyramidal Symptoms During the Acute Phase of Cerebellar Ischemic Stroke.

Cerebellar stroke is a rare condition with very nonspecific clinical features. The symptoms in the acute phase could imitate acute peripheral vestibular disorders or a brainstem lesion. The aim of this study was to assess the usefulness of the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification in cerebellar stroke and the impact of clinical features on the prognosis. We retrospectively analyzed 107 patients with diagnosed ischemic cerebellar infarction. We studied the clinical features and compared them based on the location of the ischemic lesion and its distribution in the posterior interior cerebellar artery (PICA), superior cerebellar artery (SCA), and anterior inferior cerebellar artery (AICA) territories. According to the TOAST classification, stroke was more prevalent in atrial fibrillation (26/107) and when the lesion was in the PICA territory (39/107). Pyramidal signs occurred in 29/107 of patients and were more prevalent when the lesion was distributed in more than two vascular regions (p = 0.00640). Mortality was higher among patients with ischemic lesion caused by cardiac sources (p = 0.00094) and with pyramidal signs (p = 0.00640). The TOAST classification is less useful in assessing supratentorial ischemic infarcts. Cardioembolic etiology, location of the ischemic lesion, and pyramidal signs support a negative prognosis.

Visual Snow Syndrome in Patient with Migraine: Case Report and Literature Review.

Visual snow syndrome (VSS) is a rarely diagnosed neurological phenomenon. It is a visual disorder characterised by the presence of numerous white, black, or translucent dots in the visual field, resembling the 'snow' of an analogue TV set experiencing reception interference. According to The International Classification of Headache Disorders, 3rd edition, visual snow is defined as a pattern of continuous small dots across the visual field lasting >3 months and accompanied by at least two of the following four additional symptoms: palinopsia, increased entoptic phenomena, photophobia, and nyctalopia. These complaints are not consistent with a typical migraine with visual aura and cannot be better explained by another disorder. The authors present the case of a 39-year-old woman who was diagnosed with VSS. The symptoms appeared after a migraine attack and had not alleviated. The patient reported a sensation of constant 'TV screen snow'. A neurological examination found no signs of focal damage to the nervous system. The results of the ophthalmological examination, MRI of the brain with contrast, MRI of the eye sockets, and EEG were normal. VSS is a phenomenon that is still not fully understood, different from migraine aura and associated with a number of additional symptoms. VSS is very difficult to treat. In this case, a lot of drugs were used without improvement. Further research must be conducted to determine the best treatment options for these patients.

MuSK Myasthenia Gravis-Potential Pathomechanisms and Treatment Directed against Specific Targets.

Myasthenia gravis (MG) is an autoimmune disease in which autoantibodies target structures within the neuromuscular junction, affecting neuromuscular transmission. Muscle-specific tyrosine kinase receptor-associated MG (MuSK-MG) is a rare, often more severe, subtype of the disease with different pathogenesis and specific clinical features. It is characterized by a more severe clinical course, more frequent complications, and often inadequate response to treatment. Here, we review the current state of knowledge about potential pathomechanisms of the MuSK-MG and their therapeutic implications as well as ongoing research in this field, with reference to key points of immune-mediated processes involved in the background of myasthenia gravis.

Central nervous system involvement in chronic inflammatory demyelinating polyradiculoneuropathy-MRS and DTI study.

Objective: The current research aimed to analyze the alterations within the motor cortex and pyramidal pathways and their association with the degree of damage within the peripheral nerve fibers in patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). To achieve that goal, we investigated the microstructural changes within the pyramidal white matter tracts using diffusion tensor imaging (DTI) parameters, evaluated metabolic alterations in both precentral gyri using magnetic resonance spectroscopy (MRS) ratios, and correlated them with the neurographic findings in patients with CIDP. Methods: The spectroscopic ratios of NAA/Cr, Cho/Cr, and mI/Cr from both precentral gyri and the values of fractional anisotropy (FA), axial diffusivity (AD), and mean diffusivity (MD) from both of the corticospinal tracts were correlated with the results of neurological and neurographic findings. The comparison of DTI parameters between the patients and controls was performed using Student's t-test or the Mann-Whitney U test. Due to the lack of normal distribution of most variables, Spearman's Rho rank coefficient was used to test all correlations. All analyses were performed at a significant level of alpha = 0.05 using STATISTICA 13.3. Results: Compared to the control group (CG), the patient group showed significantly lower ratios of NAA/Cr (1.66 ± 0.11 vs. 1.61 ± 0.15; p = 0.022), higher ratios of ml/Cr in the right precentral gyrus (0.57 ± 0.15 vs. 0.61 ± 0.08; p = 0.005), and higher levels of Cho/Cr within the left precentral gyrus (0.83 ± 0.09 vs. 0.88 ± 0.14, p = 0.012). The DTI parameters of MD from the right CST and AD from the right and left CSTs showed a strong positive correlation (0.52-0.53) with the sural sensory nerve action potential (SNAP) latency of the right sural nerve. There were no other significant correlations between other DTI and MRS parameters and neurographic results. Significance: In our study, significant metabolic alterations were found in the precentral gyri in patients with CIDP without clinical symptoms of central nervous system involvement. The revealed changes reflected neuronal loss or dysfunction, myelin degradation, and increased gliosis. Our results suggest coexisting CNS damage in these patients and may provide a new insight into the still unknown pathomechanism of CIDP.

Motor fiber function in spinal muscular atrophy-analysis of conduction velocity distribution.

Objectives: The motor neuron survival protein, which is deficient in spinal muscular atrophy (SMA), performs numerous cellular functions. Currently, SMA is believed to be a multi-organ disease, including lesion of various structures of the central and peripheral nervous systems. Motor nerve damage, especially in milder SMA types, is controversial. This prompted the conduct of the electrophysiological studies in adults with SMA types 2 and 3 presented in this paper. Methods: The study group consisted of 44 adult patients with SMA types 2 and 3. All patients underwent neurological examination with Hammersmith Functional Motor Scale-Expanded (HFMSE) assessment. Standard electrophysiological studies in the ulnar nerve and conduction velocity distribution (CVD) tests were performed in all patients and controls. Results: A prolongation of the distal latency and lowering of the motor potential amplitude with no changes in CVD were found in the whole patient group. There were no dependencies on the number of gene copies. Patients with low HFSME value had slower standard conduction velocity, CVD in upper and median quartiles, and narrower CVD spread; in milder SMA, CVD spread was greater than in controls. Interpretation: The significant reduction in motor response amplitude in SMA seems to be primarily related to motor neuron loss and directly proportional to its severity. The coexisting rearrangement in the peripheral nerve structure is present in SMA, and this could be partially caused by a coexisting demyelinating process. Nerve remodeling mainly affects large fibers and occurs in more severe SMA types with significant disability.

Validity and reliability of the Polish version of the Michigan Neuropathy Screening Instrument.

BACKGROUND: Diabetic sensorimotor polyneuropathy is an important risk factor for foot ulceration and amputation. Thus, patients with diabetes should be screened for this disorder according to local guidelines. An obstacle to the diagnosis of this disease may be the lack of unified diagnostic criteria due to the lack of properly validated scales used for assessment. AIM: To validate both sections (A and B) of the Michigan Neuropathy Screening Instrument (MNSI) in Polish (PL) patients with diabetes. METHODS: A cross-sectional study using a test (A1, B1) and re-test (A2, B2) formula was performed in 80 patients with diabetes. The gold standard used for neuropathy detection was a nerve conduction study (NCS) which was performed in all participants. Reliability of the MNSI-PL was assessed using the Cronbach's alpha, Kuder-Richardson formula 20 (KR-20), split-half reliability, the Gottman split-half tests, and correlation between first and second half was accessed. Stability was assessed using an intraclass correlation coefficient (ICC). For external validation, we used simple linear correlation, binomial regression, and agreement between two different tools using a Bland-Altman plot analysis. RESULTS: The scale was internally consistent (Cronbach's alpha for the full scale: 0.81 for A and 0.87 for B). MNSI-PL scores in test/retest showed high stability (ICC = 0.73 for A and ICC = 0.97 for B). The statistically important correlations between MNSI-PL and NCS were found for B1, B2, and A1 (P < 0.005). The cut-off points of ≥ 3 for section A (sensitivity of 90%-100%; specificity of 33%-40%) and ≥ 2 for section B (sensitivity of 81%-84%; specificity of 60%-70%) were obtained during neuropathy detection. CONCLUSION: The MNSI-PL is a reliable and valid instrument in screening for diabetic neuropathy.

miR-31-5p as a Potential Circulating Biomarker and Tracer of Clinical Improvement for Chronic Inflammatory Demyelinating Polyneuropathy.

Background: MicroRNAs are endogenous, small noncoding RNA molecules that play a pivotal role in the regulation of gene expression. MicroRNAs are involved in many biological processes such as proliferation, cell differentiation, neovascularization, and apoptosis. Studies on microRNA expression may contribute to a better understanding of the pathomechanism of chronic inflammatory demyelinating polyneuropathy (CIDP) and consequently enable the development of new therapeutic measures using antisense miRNAs (antagomirs). In this study, we evaluated the level of miR-31-5p in the serum of patients with CIDP and its correlation with the miR-31-5p level and clinical presentation and electrophysiological and biochemical parameters. Methods: The study group consisted of 48 patients, mean age 61.60 ± 11.76, who fulfilled the diagnostic criteria of a typical variant of CIDP. The expression of miR-31-5p in patient serum probes was investigated by droplet digital PCR. The results were correlated with neurophysiological findings and the patient's clinical and biochemical parameters. Results: The mean copy number of miRNA-31 in 100 µl serum was 1288.64 ± 2001.02 in the CIDP group of patients, while in the control group, it was 3743.09 ± 4026.90. There was a significant positive correlation (0.426) between IgIV treatment duration and miR-31-5p expression. Patients without IgIV treatment showed significantly lower levels of miR-31 compared to the treated group (259.44 ± 304.02 vs. 1559.48 ± 2168.45; p = 0.002). The group of patients with body weight > 80 kg showed statistically significantly lower levels of miRNA-31-5p than the patients with lower body weight (934.37 ± 1739.66 vs. 1784.62 ± 2271.62, respectively; p = 0.014). Similarly, the patients with elevated cerebrospinal fluid (CSF) protein levels had significantly higher miRNA-31-5p expression than those with normal protein levels (1393.93 ± 1932.27 vs. 987.38 ± 2364.10, respectively; p = 0.044). Conclusion: The results may support the hypothesis that miR-31-5p is strongly involved in the autoimmune process in CIDP. The positive correlation between higher miR-31-5p levels and duration of IVIg treatment may be an additional factor explaining the efficacy of prolonged IVIg therapy in CIDP.

Isolated arteritis misdiagnosed as bilateral orbital tumors in a patient with acute ischemic stroke.

Vasculitis is a heterogeneous group of disorders characterized by multifocal segmental inflammation of the small and medium vessels of the central nervous system. The predominant symptoms of cerebral vasculitis are stroke, headache, and encephalopathy. Additional symptoms include seizures, cranial nerve palsies, and myelopathy. Imaging techniques play a crucial role in identifying the diagnosis of vasculitis and demonstrating brain involvement. An 89-year-old woman with permanent atrial fibrillation developed an embolic stroke. In treatment, intravenous thrombolysis and thrombectomy with complete antegrade reperfusion of the left middle cerebral artery was used, without the clinical effectiveness. Brain MRI revealed bilateral oval lesions in medial parts of the orbits, which were initially misinterpreted as orbital tumors. Final diagnosis confirmed thickened arterial walls as orbital changes due to inflammatory arteritis. Ten days later, follow-up MRI was performed and showed complete regression of the orbital masses. Primary central nervous system vasculitis, manifesting as acute ischemic stroke, may be reversible with early systemic thrombolytic treatment.

Is Fecal Calprotectin an Applicable Biomarker of Gut Immune System Activation in Chronic Inflammatory Demyelinating Polyneuropathy? - A Pilot Study.

Introduction: Chronic inflammatory demyelinating polyneuropathy (CIDP) is a complex autoimmune disease caused by dysregulated response to not fully recognized antigens. Some association between CIDP and inflammatory bowel disease (IBD) has been reported, but the exact pathophysiological links of these disorders are not well understood. Aim of the Study: To evaluate fecal calprotectin as a biomarker of gut inflammation in CIDP patients without IBD. Methods: Fifteen patients with CIDP and 15 healthy controls were included in the study. The CIDP diagnosis was based on the EFNS/PNS criteria. The occurrence of bowel symptoms was assessed based on a questionnaire. The quantitative evaluation of fecal calprotectin level was performed by the ELISA test. Results: The fecal calprotectin level (µg/g) expressed as median along with the lower and upper quartiles [25Q-75Q] was significantly higher in CIDP patients compared to the controls: 26.6 [17.5-109.0] vs 15.6 [7.1-24.1], p = 0.0066. Abnormal fecal calprotectin level (>50 µg/g) was found in 33% of all CIDP patients and in none of the control subjects. The patients with abnormal fecal calprotectin level did not differ from the rest of the study group regarding the neurological status. The most common bowel symptoms reported by CIDP patients included constipation (33%), feeling of incomplete evacuation (33%), bloating (27%), and alternating bowel movement pattern (27%). Conclusion: In one-third of CIDP patients the signs of gut immune system activation have been observed. This finding may be associated with CIDP pathogenesis and induction of autoimmune response as well as concomitant dysautonomia with gastrointestinal symptoms.

Monogenic Causes of Strokes.

Strokes are the main cause of death and long-term disability worldwide. A stroke is a heterogeneous multi-factorial condition, caused by a combination of environmental and genetic factors. Monogenic disorders account for about 1% to 5% of all stroke cases. The most common single-gene diseases connected with strokes are cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) Fabry disease, mitochondrial myopathy, encephalopathy, lactacidosis, and stroke (MELAS) and a lot of single-gene diseases associated particularly with cerebral small-vessel disease, such as COL4A1 syndrome, cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL), and Hereditary endotheliopathy with retinopathy, nephropathy, and stroke (HERNS). In this article the clinical phenotype for the most important single-gene disorders associated with strokes are presented. The monogenic causes of a stroke are rare, but early diagnosis is important in order to provide appropriate therapy when available.

Predictive factors in post-stroke epilepsy: Retrospective analysis.

BACKGROUND: Cerebrovascular disease is an important cause of epilepsy. The incidence may significantly vary (from 2.3% to 43%). Post-stroke seizures occur within 2 weeks of stroke onset (as early-onset seizures) or 2 weeks after a stroke (as late-onset seizures). OBJECTIVES: To retrospectively evaluate and differentiate predictive factors for post-stroke seizures. MATERIAL AND METHODS: We retrospectively analyzed the medical histories of 164 adult patients diagnosed with post-stroke seizures but no epilepsy recognized prior to the stroke who were hospitalized at the Neurology Clinic of Wroclaw Medical University between 2012 and 2018. The seizures were classified according to the criteria of the International League Against Epilepsy (ILAE) from 2017. The relevant demographic data, type of stroke (ischemic/hemorrhagic), time of occurrence of seizures in relation to the type of stroke, score on the modified Rankin Scale, presence of cardiovascular risk factors, electroencephalography (EEG) recording, and antiepileptic treatment (AED) were collected. In the case of ischemic stroke (IS), the size of the stroke lesion was rated on the ASPECTS scale. RESULTS: The study involved 164 patients (average age = 68.83 years), including 86 men (average age = 66.2 years). In 20 out of 164 patients, the seizures were associated with hemorrhagic stroke (HS); in 144 out of 164 patients, the post-stroke epilepsy was associated with IS. Generalized tonic-clonic seizures occurred in 101 out of 164 patients, focal aware seizures occurred in 19 out of 164 patients and focal impaired-awareness seizures occurred in 44 out of 164 patients. CONCLUSIONS: Our study has confirmed that generalized seizures occur mostly after an IS and are late complications of it. Early-onset seizures occur mostly after HS associated with severe disability. Seizures are more likely to happen due to the cortical location of the stroke. There is a shift from generalized to focal seizures with an increase in the extent of IS as evaluated using the ASPECTS scale.