Dual Pathology Research Articles

Sight threatening diabetic retinopathy in patients with macular telangiectasia type 2

PurposeAlthough diabetes is highly prevalent in patients with macular telangiectasia type 2 (MacTel), progression to severe non-proliferative (NPDR) and proliferative diabetic retinopathy (PDR) is rarely reported. We report multimodal imaging features of sight-threatening diabetic retinopathy (STDR) in eyes with MacTel.MethodsRetrospective case series of seven participants of the MacTel Study at the Moorfields Eye Hospital NHS Foundation Trust study site and one patient from the Institute of Retina and Vitreous of Londrina, Brazil. Sight threatening diabetic retinopathy was defined as severe NPDR, PDR or diabetic macular edema.ResultsWe report imaging features of 16 eyes of eight patients (7/8, 87.5% female) with diagnoses of MacTel and type 2 diabetes mellitus with STDR. Mean (SD) age was 56 (8.3) years. Patients were followed-up for a mean time of 9.1 (4.7) years. A total of 10/16 (62.5%) eyes showed PDR and 2/16 (12.5%) eyes presented a macular epiretinal neovascularization.ConclusionsPeople with diabetes mellitus and MacTel may not be protected from STDR as previously reported. Although the two diseases rarely co-exist, regular monitoring for diabetic retinopathy progression is recommended according to baseline retinopathy severity grades in line with established international guidelines. The presence of MacTel may not modify extended screening intervals, but there is no current evidence. The limited case series in the literature support treatment for complications and should follow the standard of care for either condition. Due to dual pathology, reactivation may be difficult to diagnose on standard imaging and multimodal imaging is recommended.

Comorbidity of dual pathology and behavioral disorders in adolescence

Comorbidity of dual pathology and behavioral disorders in adolescence

Screening for Occult Transthyretin Amyloidosis in Patients with Severe Aortic Stenosis and Amyloid Red Flags

Aims: The optimal strategy to identify transthyretin-type cardiac amyloidosis (ATTR-CA) in patients with aortic stenosis (AS) is still unclear. This study aimed to investigate if targeted screening for ATTR-CA in patients with severe AS and amyloid red flags is associated with higher detection rates. Methods: The study prospectively enrolled patients ≥65 years with severe AS. Patients who fulfilled ≥1 major (carpal tunnel syndrome (CTS), ruptured biceps tendon, spinal stenosis, N-terminal pro B-type natriuretic peptide ≥1000 pg/mL, cardiac troponin >99th percentile) or ≥2 minor criteria (diastolic dysfunction ≥2 grade/lateral e’ <10 cm/s, atrial fibrillation, atrioventricular conduction disease/pacemaker) received bone scintigraphy and biochemical analysis for light chain amyloidosis. Hypertensive patients (>140/90 mmHg) and those with interventricular septal thickness (IVSd) ≤13 mm were excluded. Results: Overall, 264 patients were screened, of whom 85 were included in the analysis. Tracer uptake Perugini grade ≥1 was detected in nine patients (11%). An endomyocardial biopsy was additionally performed in four of nine patients, yielding a prevalence of 7% (n = 6). All patients with dual AS-ATTR were male. Syncope was more commonly reported in AS-ATTR patients (50% vs. 6%, p = 0.010), who also tended to have more severe hypertrophy (IVSd of 18 vs. 16 mm, p = 0.075). Pericardial effusion and CTS were more common in patients with dual pathology (67% vs. 8%, p < 0.001, and 83% vs. 24%, p = 0.003, respectively). Conclusion: Targeted screening for ATTR-CA in patients with AS and amyloid red flags does not yield higher detection rates than those reported previously in all comers with AS.

Persistence of Kii amyotrophic lateral sclerosis after the 2000s and its characteristic aging-related tau astrogliopathy.

Kii amyotrophic lateral sclerosis (ALS) is a unique disease that occurs in the southern portion of the Kii Peninsula and exhibits a dual pathology of TAR DNA-binding protein of 43 kDa (TDP-43) proteinopathy and tauopathy. The incidence of ALS in this region was very high in the 1960s, briefly decreased through the 1980s, but began increasing again after 2000 with a change of high-concentration geographic foci. It is unclear, however, whether the unique pathological features have changed along with the incidence changes. This study analyzed postmortem specimens from neuropathologically confirmed Kii ALS cases from the 1970s (n = 4) and those after 1999 (n = 12) from the southern Kii Peninsula or outside of the area. Our results confirm the continued occurrence of Kii ALS after 2000 in the southern Kii Peninsula and the preservation of disease-specific neuronal tau pathology, including the widespread occurrence throughout the brain and spinal cord, sparse neuropil threads, and predominance in superficial layers. Furthermore, we assessed the glial tau pathology of Kii and non-Kii ALS in accordance with the aging-related tau astrogliopathy classification method for the first time and detected a unique brainstem predominant appearance of gray matter aging-related tau astrogliopathy in Kii ALS cases, which may provide clues to pathogenetic mechanisms.

Incidental diagnosis of microfilariae in urine in a case of prostatic carcinoma: A case report with a cytohistological correlation

Filariasis is an endemic parasitic infection commonly found in the tropics and subtropics, such as India. Microfilariae have been reported in various cytological samples, but they are rare to find in urine samples. The presence of microfilariae in urine can be incidental or associated with other malignancies. The cytological examination can help diagnose such cases. Clinically, it may present unusually as achylous hematuria and a urinary bladder mass lesion, mimicking bladder cancer. There have been a few reported cases of microfilariae in urine along with prostatic malignancy, and the present case highlights the same. Here, we report a treated case of metastatic prostatic carcinoma presenting as a bladder mass in a 61-year-old male, who was diagnosed with microfilariasis in urine cytology. This case is presented not only for its dual pathology or rare occurrence but also to emphasize that an incidental finding can help in treating it medically with no surgical intervention.

Proliferative verrucous leukoplakia/multifocal leukoplakia in patients with and without oral submucous fibrosis.

Oral submucous fibrosis (OSF) and proliferative verrucous leukoplakia (PVL) are established as oral potentially malignant disorders. Dual pathology of the two conditions is not commonly encountered in clinical practice. This study aims to present a case series of multifocal leukoplakia in patients with and without OSF to outline the clinical behavior and challenges in the management of this high-risk group in clinical practice. We retrospectively analyzed cases of six Indian patients (four with OSF) managed over a period of 5.5 to 13 years at the Government Dental College, Nagpur. Patient data consisting of age, gender, medical history, habits, clinical findings, and biopsy reports were recorded at the initial visit. During follow-up visits, the clinicopathological data were reassessed. When surgical intervention failed to arrest the disease or when surgery was contraindicated metronomic therapy with Folitrax 15 mg once a week and Celecoxib 100mg twice daily was initiated. All patients developed PVL after the initial pathology diagnosis of OSF or oral leukoplakia. Initial lesions were either homogenous or non-homogenous leukoplakia. All patients developed multiple recurrences, regional or systemic metastasis. Despite thorough interventions, the patients died of, or with the disease. The occurrence of two or more oral potentially malignant disorders poses challenges in patient management and possibly presents a higher risk of malignant transformation. More clinical trials are necessary to assess the benefits of metronomic therapy for patients diagnosed with aggressive PVL concurrently found with OSF.

Mesial temporal lobe epilepsy and hippocampal sclerosis associated with BRAFV600E mutant neurons in the Cornu Ammonis: an uncertain pathogenesis and a diagnostic challenge.

Mesial temporal lobe epilepsy (MTLE) is a common cause of seizures, and hippocampal sclerosis (HS) is the predominant subtype. BRAFV600E mutations in MTLE-HS have only been reported infrequently. Herein, we illustrate the neurologic, radiological, and histopathological details of a patient with MTLE-HS and BRAFV600E mutant neurons. A 31-year-old male with medically refractory epilepsy presented with magnetic resonance imaging (MRI) and electroencephalography (EEG) findings typical of mesial temporal sclerosis without a mass lesion. The surgical specimens showed ILAE Type 1 HS with neurons immunopositive for BRAFV600E mutant protein distributed along the Cornu Ammonis (CA) curvature. Instead of the normal mostly perpendicular orientation of pyramidal neurons relative to the hippocampal surface, the BRAF mutant neurons were often oriented in a parallel manner. On CD34 immunostaining, sparse clusters or nodules of CD34+ stellate cells and single immunopositive stellate cells were identified. BRAFV600E or CD34 immunopositive cells were less than 1 % of total cells. The patient responded well to surgery with no further seizures after 2 years and occasional auras. Hippocampal BRAF mutant non-expansive lesion (HBNL) has been used to describe such lesions with preserved cytoarchitecture and without overt tumor mass. Others may argue for the dual pathology of HS with early ganglioglioma. Whether pre-neoplastic lesions or early tumors, these cases are important for understanding early glioneuronal tumorigenesis and suggest that BRAFV600E studies should be routinely performed on MTLE-HS cases in the setting of clinical trials. With next-generation sequencing, a FANCL deletion was detected in almost half of the alleles in our case, suggesting that many of the histologically normal-appearing cells of the hippocampus contain this alteration. FANCL mutations can result in cytogenetic anomalies and defective DNA repair and therefore may underlie the development of a low frequency BRAF alteration.

Cardiac Amyloidosis and Valvular Heart Disease.

Growing interest has accrued in the co-existence of cardiac amyloidosis and valvular heart disease. Amyloid infiltration from either transthyretin (ATTR) or of light chain (AL) origin may affect any structure of the heart, including the valves. The recent literature has mainly focused on aortic stenosis and cardiac amyloidosis, improving our understanding of the epidemiology, diagnosis, treatment and prognosis of this dual pathology. Despite being of high clinical relevance, data on mitral/tricuspid regurgitation and cardiac amyloidosis are rather scarce and mostly limited to case reports and small cases series. It is the aim of this review article to summarize the current evidence of concomitant valvular heart disease and cardiac amyloidosis by including studies on epidemiology, diagnostic approaches, screening possibilities, therapeutic management, and prognostic implications.

Occult Filariasis in a Case of Lymphocytic Thyroiditis Diagnosed on Fine Needle Aspiration Cytology: An Unusual Finding of Dual Pathology

Filariasis is a common public health problem in Southeast Asia. The two species of worms most commonly associated with this disease are Wuchereria bancrofti and Brugia malayi. Cases of microfilaraemia have also been reported from atypical sites in the past. None of the previously reported cases of microfilaria in the thyroid gland have described occult filariasis against a background of lymphocytic thyroiditis. The authors present a case of incidental microfilaria in a case of lymphocytic thyroiditis, diagnosed on fine needle aspiration cytology of thyroid swelling in a female, a coexistence of dual pathology. There has been no case in literature where filariasis was reported against a background of lymphocytic thyroiditis. Peripheral blood examination also did not show any evidence of filariasis.

Depletion of microglia with CSF1R inhibitor prevents tau aggregation in the mouse model Thy1P301S

AbstractBackgroundNeuroinflammation and microglia proliferation are central in Alzheimer’s disease pathology. However, the role of microglia in the accumulation and spreading of plaques and tau tangles is not yet well understood.MethodIn this study, we depleted the microglia population in the brain of Alzheimer’s disease (APP PS1) tauopathy (Thy1P301S) and dual pathology (APPPS1 Thy1P301S) mice models using a colony stimulating factor 1 receptor (CSF1R) inhibitor to achieve microglia ablation. Consequences of compound treatment on brain pathology were analyzed.ResultReduced number of microglia cells in the brain was successfully achieved in the mouse model Thy1P301S. In a chronic treatment study of 3 months, mice treated with the CSF1R inhibitor showed a significant decrease in tau aggregation and deposition compared to the control group.ConclusionHere we show that inhibition of microglia proliferation induces attenuation of tau pathology. This work demonstrates that intervention on microglia is a potential therapeutic approach in Alzheimer’s disease.

Predictors of short-term response and the role of heavy alcohol use in treatment of depression

BackgroundDepression and alcohol use disorders frequently co-occur. However, research on psychosocial interventions for treating this dual pathology is limited. The Ostrobothnian Depression Study (ODS) aimed to increase the systematic use of evidence-based methods, particularly among patients with comorbid depression and substance use in a naturalistic setting. This is a secondary analysis of the ODS study. The aim of the present study was to explore the predictors of a response to treatment during the first six months of the ODS intervention with a specific focus on the role of comorbid heavy alcohol use.MethodsThe study sample (n = 242) comprised psychiatric specialist care patients with depression (Beck Depression Inventory score ≥ 17) at baseline. Patients with a baseline Alcohol Use Disorders Identification Test (AUDIT) score > 10 (n = 99) were assigned to the AUD (Alcohol Use Disorder) group in this study. The ODS intervention comprised behavioral activation (BA) for all and additional motivational interviewing (MI) for those in AUD group. The predictors of response to treatment (minimum of 50% reduction in depressive symptoms) during the first six months were analyzed with logistic regression models.ResultsIn the total sample at six months (n = 150), predictors of response to treatment were more severe depression (OR 1.10, CI 1.02–1.18), larger amounts of alcohol consumed (OR = 1.16, CI 1.03–1.31) and antipsychotic medication “not in use” (OR = 0.17, CI 0.07–0.44). In the non-AUD group (n = 100), more severe depression (OR 1.12, CI 1.01–1.25) and antipsychotics “not in use” (OR 0.20, CI 0.06–0.67) also predicted a positive response. Among AUD group patients (n = 50), larger amounts of alcohol consumed (OR 1.54, CI 1.04–2.27) and antipsychotic medication “not in use” (OR 0.12, CI 0.02–0.60) predicted a response to the treatment intervention.ConclusionsThe severity of symptoms and comorbid disorders were found to predict better treatment response, suggesting that the intervention was more effective in patients with severe symptoms. Patients with depression should be treated effectively regardless of having concomitant AUD. The results of this study suggest that BA combined with MI should be one of the treatment options for this dual pathology.Trial registrationClinicalTrials.gov Identifier NCT02520271 (11/08/2015).

Tumour-to-tumour metastasis to the parathyroid causing dual pathology hypercalcaemia

Tumour-to-tumour metastasis to the parathyroid causing dual pathology hypercalcaemia

Liver Disease and Sickle Cell Disease: Auto-Immune Hepatitis more than a Coincidence; A Systematic Review of the Literature.

In patients with SCD, chronic liver damage is a common manifestation. More than 50% of SCD patients have elevated liver enzymes. Common underlying aetiologies include sickle cell hepatic crisis, viral hepatitis, sickle cell intrahepatic cholestasis and hepatic sequestration in the acute setting, and cholelithiasis and iron overload in the chronic setting. Autoimmune hepatitis (AIH) is a rare disease that appears to occur more commonly in the sickle cell disease (SCD) population than in the general population. There are many schools of thought as to why this is the case, including the phosphatidylserine hypothesis, the heme inflammatory hypothesis, the complement generation hypothesis, and the transfusion alloimmunization hypothesis. Due to the natural history of the two illnesses, SCD is almost always diagnosed first in cases of dual pathology. Symptoms such as jaundice, fatigue, and abdominal pain are common in SCD, as are abnormal liver function tests (LFTs). These abnormalities, attributed to the other more frequent liver involvements in SCD, can lead to delays in AIH diagnosis in this population. Corticosteroids, sometimes with other immunosuppressive agents, such as azathioprine, are the cornerstone of acute AIH treatment. However, corticosteroid use in the SCD population has been shown to carry an increased risk of vaso-occlusive crises, providing a treatment dilemma. The following is a review of AIH in the SCD population, where we explore the pathophysiology behind the association between the two disorders, discuss an approach to investigating abnormal LFTs in SCD, and examine treatment options in this population with co-existing diseases.

Application value of multimodal MRI combined with PET metabolic parameters in temporal lobe epilepsy with dual pathology

ObjectivesTo investigate the application value of multimodal MRI combined with PET metabolic parameters in detecting temporal lobe epilepsy (TLE) with dual pathology (DP) and the prediction effect of post-surgical outcomes in these patients. MethodsWe retrospectively reviewed 50 patients with TLE-DP who underwent surgery at our hospital between January 2016 and December 2021 and collected the demographics, clinical characteristics, video-electroencephalography (v-EEG), neuroimaging, and surgical data. Seizure outcome data were collected during a regular follow-up of at least 12 months and were graded using Engel scores. Fisher's exact test was used to compare the differences in DP detection rates of various diagnostic modalities. Univariate and multivariate analyses were performed to explore the prognostic factors for predicting seizure outcomes post-surgery. ResultsOf the 50 patients, 20 were males. The median age was 30, the median age at first seizure was 14, and the median duration was ten years. Voxel-based morphometry-PET statistical parametric mapping-PET/MRI (VBM-PSPM-PET/MRI) had the highest detection rate, followed by PET/MRI, VBM analysis, and PET-SPM. Regardless of follow-up duration, v-EEG, PET, image post-processing methods, and VBM-PSPM-PET/MRI statistically correlated with seizure outcomes using the log-rank test in the Kaplan-Meier analysis. Multivariate analysis showed that VBM-PSPM-PET/MRI was an independent predictor of TLE-DP (hazard ratio (HR) = 15.674, 95 % CI = 0.002–0.122, P < 0.00 1). ConclusionsOur study illustrates that VBM-PSPM-PET/MRI has the highest detection value in patients with TLE-DP and can provide independent prognostic information for patients who undergo surgery. This approach has the most substantial potential for the selection of candidates for patients who undergo surgical treatment and for prognostic stratification.

APOE-ε4 and BIN1 increase risk of Alzheimer’s disease pathology but not specifically of Lewy body pathology

Lewy body (LB) pathology commonly occurs in individuals with Alzheimer’s disease (AD) pathology. However, it remains unclear which genetic risk factors underlie AD pathology, LB pathology, or AD-LB co-pathology. Notably, whether APOE-ε4 affects risk of LB pathology independently from AD pathology is controversial. We adapted criteria from the literature to classify 4,985 subjects from the National Alzheimer’s Coordinating Center (NACC) and the Rush University Medical Center as AD-LB co-pathology (AD+LB+), sole AD pathology (AD+LB–), sole LB pathology (AD–LB+), or no pathology (AD–LB–). We performed a meta-analysis of a genome-wide association study (GWAS) per subpopulation (NACC/Rush) for each disease phenotype compared to the control group (AD–LB–), and compared the AD+LB+ to AD+LB– groups. APOE-ε4 was significantly associated with risk of AD+LB– and AD+LB+ compared to AD–LB–. However, APOE-ε4 was not associated with risk of AD–LB+ compared to AD–LB– or risk of AD+LB+ compared to AD+LB–. Associations at the BIN1 locus exhibited qualitatively similar results. These results suggest that APOE-ε4 is a risk factor for AD pathology, but not for LB pathology when decoupled from AD pathology. The same holds for BIN1 risk variants. These findings, in the largest AD-LB neuropathology GWAS to date, distinguish the genetic risk factors for sole and dual AD-LB pathology phenotypes. Our GWAS meta-analysis summary statistics, derived from phenotypes based on postmortem pathologic evaluation, may provide more accurate disease-specific polygenic risk scores compared to GWAS based on clinical diagnoses, which are likely confounded by undetected dual pathology and clinical misdiagnoses of dementia type.

Contralateral hippocampal sclerosis following functional hemispherectomy in children: A report of three cases

PurposeHippocampal Sclerosis (HS) may co-exist with temporal or extratemporal lesions (dual pathology) in children and is usually ipsilateral to the radiological lesion. Here were report three cases with extensive hemispheric cortical malformation and drug resistant epilepsy who had persistent seizures after functional hemispherectomy (FH) and developed contralateral HS after the surgery. MethodsThis retrospective study enrolled children who underwent FH and developed contralateral HS after surgery. Their clinical, EEG, radiological and pathological data were reviewed and summarized. ResultsNinety-five children underwent FH during the study period; Three cases (3.2%) were eligible. They all had unilateral extensive hemispheric cortical malformation who underwent FH between 3 and 5 months of age with no clinical, EEG or radiological suggestion for involvement of contralateral hemisphere prior to FH. All three patients had persisting seizures after FH. Contralateral HS was detected between 2.2 to 3.7 years after FH in all three cases. Two of the patients showed pathogenic variants in GATOR1 pathway genes. ConclusionsThe genesis of contralateral HS in the reported patients remains unexplained. The presence and distribution of “second-hit” somatic mutations may play an important role in governing the seizure outcomes of epilepsy surgery in patients with apparently unilateral malformations of cortical development.

A unique association? A narcolepsy type 1 case comorbid with Primary Biliary Cholangitis

The aim of the study was to present a woman affected of a narcolepsy with cataplexy (narcolepsy type 1) comorbid with an asymptomatic Primary Biliary Cholangitis (PBC). The HLA haplotype was DRB1*15:01, DQA1*01:02, DQB1*06:02. The allele DQB1*06:02 has been considered until now protective for PBC and dual pathology has not been published.We think the important clinical message of the Case would be of continuing to monitor adults with narcolepsy type 1 for late complications that may be associated with other autoimmune conditions. Clinicians should be aware of the relationship between Narcolepsy and PBC. This highlights the need for screening and management in these individuals.

Breast Carcinoma and Tuberculosis in Axillary Lymph Nodes: A Case Report

The coexistence of tuberculosis with axillary lymph node metastases in breast carcinoma is rare. Axillary lymph node metastasis is the most important factor in the staging of breast carcinoma, this can mimic or complicate the staging of a malignant disease. Dual organ pathology can lead to interpretation difficulties and inappropriate treatment of tuberculosis as well as breast carcinoma. We report an observation of infiltrating carcinoma of the non-specific type of the breast in woman aged 39, where tuberculosis was found in the axillary lymph nodes in addition to metastases. The possible and simultaneous occurrence of breast carcinoma and tuberculosis should be mentioned in order to avoid difficulties of interpretation and allow adequate management of axillary tuberculous lymphadenitis and breast carcinoma.

Transthyretin cardiac amyloidosis in patients with severe aortic stenosis undergoing transcatheter aortic valve replacement: experience of a single center.

Even if prevalent among patients with severe aortic stenosis (AS), the clinical suspicion for transthyretin cardiac amyloidosis (ATTR-CA) remains difficult in this subset. We report our single center experience on ATTR-CA detection among TAVR candidates to provide insights on the prevalence and clinical features of dual pathology as compared to lone AS. Consecutive severe AS patients undergoing transcatheter aortic valve replacement (TAVR) evaluation at a single center were prospectively included. Those with suspected ATTR-CA based on clinical assessment underwent 99m Tc-3,3-diphosphono-1,2-propanodicarboxylic acid (DPD) bone scintigraphy. The RAISE score, a novel screening tool with high sensitivity for ATTR-CA in AS, was retrospectively calculated to rule-out ATTR-CA in the remaining patients. Patients were categorized as follow: "ATTR-CA+": patients with confirmed ATTR-CA at DPD bone scintigraphy; "ATTR-CA-": patients with negative DPD bone scintigraphy or a negative RAISE score; "ATTR-CA indeterminate": patients not undergoing ATTR-CA assessment with a positive RAISE score. The characteristics of ATTR-CA+ and ATTR-CA- patients were compared. Of 107 included patients, ATTR-CA suspicion was posed in 13 patients and confirmed in six. Patients were categorized as follow: 6 (5.6%) ATTR-CA+, 79 (73.8%) ATTR-CA-, 22 (20.6%) ATTR-CA indeterminate. Excluding ATTR-CA indeterminate patients, the prevalence of ATTR-CA was 7.1% (95% CI 2.6-14.7%). As compared to ATTR-CA - patients, ATTR-CA + patients were older, had higher procedural risk and more extensive myocardial and renal damage. They had higher left ventricle mass index and lower ECG voltages, translating into a lower voltage to mass ratio. Moreover, we describe for the first time bifascicular block as an ECG feature highly specific of patients with dual pathology (50.0% vs. 2.7%, P<0.001). Of note, pericardial effusion was rarely found in patients with lone AS (16.7% vs. 1.2%, P=0.027). No difference in procedural outcomes was observed between groups. Among severe AS patients, ATTR-CA is prevalent and presents with phenotypic features that may aid to differentiate it from lone AS. A clinical approach based on routine search of amyloidosis features might lead to selective DPD bone scintigraphy with a satisfactory positive predictive value.

COMORBIDITY OF MULTIPLE SCLEROSIS AND EPILEPSY: MORE QUESTIONS OR ANSWERS?

The literature data of the last three decades on the problem of comorbidity of multiple sclerosis (MS) and epilepsy have been analyzed, such as issues of pathogenesis, clinical course, prognosis, and treatment of this dual pathology. Epileptic seizures occur in 2–3% to 5.9% of patients with MS, which is 3–6 times more common than in the general population. The incidence of epilepsy raises with increasing duration and severity of MS, with its progressive course, and also depends on the effect of drugs for the treatment of MS. There is no unanimity in the literature on the age and gender characteristics of the occurrence of epileptic seizures in MS. Probable mechanisms of MS comorbidity and epilepsy are analyzed. Data on certain common pathophysiology of MS and epilepsy and the concept according to which the model of epilepsy in MS is considered as a network disease are presented. Data on clinical manifestations and diagnosis of comorbid MS with epilepsy are presented. Epileptic seizures can occur at any stage of MS: before the clinical manifestations, at the onset of the disease, in the late stages, or can indicate exacerbation of MS. Types of epileptic seizures with a dual diagnosis (MS + epilepsy) are diverse. The majority of patients (up to 87.5%) have focal seizures (aware or unaware) or focal seizures to bilateral tonic-clonic, and a small share of patients have seizures of unknown origin. Most researchers believe that patients with MS and epilepsy have a more severe MS course and a worse long-term prognosis. The main directions of MS treatment and the impact of such treatment on the development of epileptic seizures are highlighted. Data on the effect of some disease-modifying drugs for the treatment of MS on the course of epilepsy and, on the other hand, on the impact of some antiseizure medications on the course of MS are presented. It is concluded that patients with MS have individual profiles and inter-individual variability of epileptogenicity. The principles of treatment of epileptic seizures/epilepsy in patients with MS are proposed.