Published information about fish botulism is scant. We review here the current literature on fish botulism. Freshwater fish are susceptible to botulism. Only anecdotal evidence exists about possible botulism cases in saltwater fish. With only a few exceptions, the etiology of all cases of fish botulism reported is Clostridium botulinum type E, although fish are sensitive to, and may carry, various C. botulinum types. Clinical signs of botulism in fish include loss of equilibrium and motion, abducted opercula, open mouths, dark pigmentation, and head up/tail down orientation in which attempts to swim result in breaching the surface of the water. Dark pigmentation is thought to be associated with acetylcholine imbalance in botulinum neurotoxin (BoNT)-affected fish. Rarely, but similar to the situation in other animal species, fish can recover from botulism. Fish botulism can cause secondary outbreaks of the disease in birds, as botulism-affected fish stand out from normal fish, and are selectively preyed upon by fish-eating birds, which thus become intoxicated by the BoNT present in sick fish. The source of BoNT in fish has not been definitively confirmed. Fish may ingest C. botulinum spores that then germinate in their digestive tract, but the possibility that fish ingest preformed BoNT from the environment (e.g., dead fish, shellfish, insects) cannot be ruled out. The presumptive diagnosis of botulism in fish is established based on clinical signs, and as in other species, confirmation should be based on detection of BoNT in intestinal content, liver, and/or serum of affected fish.

OBJECTIVE: Analysis of demographic, clinical, laboratory, electrophysiological and neuroimaging data and pathogenetic therapy of pediatric patients with chronic inflammatory demyelinating polyneuropathy (CIDP).
METHODS: Patients (n=30) were observed in a separate structural unit of the Russian Children\'s Clinical Hospital of the Russian National Research Medical University named after. N.I. Pirogova Ministry of Health of the Russian Federation in the period from 2006 to 2023. The examination was carried out in accordance with the recommendations of the Joint Task Force of the European Federation of Neurological Societies and the Peripheral Nerve Society on the Management of CIDP (2021). All patients received immunotherapy, including intravenous immunoglobulin (IVIG) (n=1), IVIG and glucocorticosteroids (GCS) (n=17, 56.7%), IVIG+GCS+plasmapheresis (n=12, 40.0%). Alternative therapy included cyclophosphamide (n=1), cyclophosphamide followed by mycophenolate mofetil (n=1), rituximab (n=2, 6.6%), azathioprine (n=3), mycophenolate mofetil (n=2, 6.6%).
RESULTS: In all patients, there was a significant difference between scores on the MRCss and INCAT functional scales before and after treatment. At the moment, 11/30 (36.6%) patients are in clinical remission and are not receiving pathogenetic therapy. The median duration of remission is 48 months (30-84). The longest remission (84 months) was observed in a patient with the onset of CIDP at the age of 1 year 7 months.
CONCLUSIONS: Early diagnosis of CIDP is important, since the disease is potentially curable; early administration of pathogenetic therapy provides a long-term favorable prognosis.
UNASSIGNED: Анализ демографических, клинических, лабораторных, электрофизиологических и нейровизуализационных данных и результатов патогенетической терапии пациентов детского возраста с хронической воспалительной демиелинизирующей полинейропатией (ХВДП).
UNASSIGNED: Пациенты (n=30) наблюдались в ОСП «Российская детская клиническая больница ФГАОУ ВО «РНИМУ им. Н.И. Пирогова» Минздрава России в период с 2006 по 2023 г. Обследование проведено в соответствии с рекомендациями Объединенной целевой группы Европейской федерации неврологических обществ и Общества периферических нервов по ведению ХВДП (2021 г.). Все пациенты получали иммунотерапию, включая внутривенный иммуноглобулин (ВВИГ) (n=1), ВВИГ и глюкокортикостероиды (ГКС) (n=17, 56,7%), ВВИГ, ГКС и плазмаферез (n=12, 40,0%). Альтернативная терапия включала циклофосфан (n=1), циклофосфан с последующим переходом на микофенолата мофетил (n=1), ритуксимаб (n=2, 6,6%), азатиоприн (n=3), микофенолата мофетил (n=2, 6,6%).
UNASSIGNED: У всех пациентов наблюдалась достоверная разница между оценками по функциональным шкалам MRCss и INCAT до лечения и после него. На данный момент 11/30 (36,6%) пациентов находятся в клинической ремиссии и не получают патогенетическую терапию. Медиана длительности ремиссии 48 (30—84) мес. Наиболее длительная ремиссия (84 мес) отмечена у пациента с дебютом ХВДП в возрасте 1 года 7 мес.
UNASSIGNED: Ранняя диагностика ХВДП является актуальной, поскольку заболевание потенциально курабельно, раннее назначение патогенетической терапии обеспечивает долгосрочный благоприятный прогноз.

Guillain-Barré syndrome (GBS) is an immune-mediated disease of the peripheral nervous system that can occur in both children and adults. The classic presentation of GBS is characterized by progressive symmetrical, ascending muscle weakness. Patients with GBS require meticulous monitoring due to the risk of bulbar syndrome, respiratory failure and autonomic dysfunction, which can be life-threatening. Early diagnosis and timely prescription of pathogenetic therapy for GBS are particularly important, especially in young children. Meanwhile, the spectrum of disorders covered by GBS has expanded significantly; its eponym is now designate any variant of acute dysimmune polyneuropathy, and its atypical forms pose a serious diagnostic problem for clinicians. This review article provides an analysis of the data available in the medical literature on GBS in children and discusses the tactics for diagnosing and managing patients with GBS, taking into account the Russian and European clinical recommendations.
Синдром Гийена—Барре (СГБ) — иммуноопосредованное заболевание периферической нервной системы, встречающееся как у детей, так и у взрослых. Основным проявлением СГБ является симметричная прогрессирующая и восходящая мышечная слабость. Пациенты с СГБ имеют высокий риск развития бульбарного синдрома, дыхательной недостаточности и вегетативной дисфункции, создающих угрозу жизни пациенту. Ранняя диагностика и своевременное назначение патогенетической терапии при СГБ исключительно актуальны. Спектр расстройств, охватываемых рубрикой СГБ, значительно расширился, его эпоним стал применяться для обозначения любого варианта острой дизиммунной полинейропатии, а его атипичные формы представляют серьезную диагностическую проблему. В статье приведен анализ имеющихся данных о СГБ у детей, обсуждается тактика диагностики и ведения пациентов с СГБ с учетом отечественных и зарубежных клинических рекомендаций.

BACKGROUND: West Nile Virus is a single-stranded Ribonucleic Acid arbovirus of the Flaviviridae family that is transmitted to humans by Culex species mosquitoes. West Nile Virus infection is asymptomatic in the majority of affected people. Of those who develop symptoms, the usual manifestation is a febrile syndrome, while only 1% develop neurological symptoms due to a neuroinvasive form of infection, including encephalitis, meningitis, asymmetrical flaccid paralysis, or a combination of all these features. Parsonage-Turner syndrome is a rare disorder characterized by sudden painful symptoms and subsequent paralysis, involving a shoulder or one of the upper limbs due to post-infective brachial plexopathy. The etiology is unknown, although it can be considered a multifactorial process: a predisposing factor, such as viral infection or strenuous upper-extremity exercise, can trigger an immune-mediated process localized in the brachial plexus.
METHODS: In late summer, a 79-year-old male Italian patient was admitted to the emergency department for acute right upper limb weakness and high fever, without any mental status impairment, pain, sensory alterations, or signs of meningeal irritation. Laboratory tests confirmed acute West Nile Virus infection, expressed as a unilateral upper limb flaccid paralysis. After a few days, the patient reported an acute pain in the right upper limb scarcely responsive to nonsteroidal anti-inflammatory drug therapy and a subsequent wider distribution of flaccid paralysis. After multiple examinations, Parsonage-Turner syndrome could be suspected. Patient was treated with steroids and reported an improvement of clinical condition after 2 months, with complete pain remission but partial strength recovery in the affected limb.
CONCLUSIONS: West Nile Virus disease has a broad spectrum of neurological manifestations, among which the most common are signs of meningeal irritation or cognitive impairment. We report an unusual presentation of neuroinvasive West Nile Virus infection with arm weakness as expression of unilateral viral neuritis, followed by a post-infective brachial plexopathy consistent with Parsonage-Turner syndrome diagnosis. We diagnosed Parsonage-Turner syndrome after excluding the most common causes of atraumatic acute upper limb pain, through a challenging differential diagnosis in a patient with several comorbidities.

Hypernatremia (serum sodium>160 meq/L) present with diverse neurological manifestations, ranging from flaccid paralysis to impaired cognition, encephalopathy, and even deep coma. Osmotic demyelination refers to changes in brain cells because of an acute change in plasma osmolality. It is further divided into two types, i.e., central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM). Patients with EPM, besides spasticity, may also present with other movement disorders such as catatonia, parkinsonism, and dystonia. We present a case of a postpartum woman bought to the emergency department by her relatives in an unconscious state. In view of poor sensorium (Glasgow coma scale < 7), she was intubated and received mechanical ventilatory support. On admission, computed tomography ofthebrain was normal, and the patient was transferred to the intensive care unit (ICU) for further management. The preliminary work-up in the ICU showed hypernatremia (serum sodium of 182 mEq/L) with hyper-osmolality (359 mOsm/kgH2O). She was managed as per the ICU protocol for hypernatremia. During her ICU stay, her sensorium improved, but she developed flaccid paralysis and was quadriplegic. Thus, a tracheostomy was performed, and she was weaned from the ventilator. After ventilator weaning, she was transferred to the ward for further rehabilitation. During rehabilitation, the patient was able to sit and takefoodorally.To date, only a few cases are reported in postpartum women with acute severe hypernatremia caused by high-grade fever and loss of body fluids leading to extra-pontine demyelination and flaccid paralysis. This case highlightsthat prompt recognition and appropriate intervention can improve the outcomes in these patients.

BACKGROUND: Japanese encephalitis is an arthropod-borne zoonotic flavivirus infection endemic to tropical and subtropical Asia. A minority of infections leads to a symptomatic course, but affected patients often develop life-threatening encephalitis with severe sequelae.
METHODS: Myelitis with flaccid paralysis is a rare complication of Japanese Encephalitis, which-according to our literature search-was reported in 27 cases, some of which were published as case reports and others as case series. Overall, there is a broad clinical spectrum with typically asymmetric manifestation and partly severe motor sequelae and partly mild courses. Lower limb paralysis appears to be more frequent than upper limb paralysis. An encephalitic component is not apparent in all cases CASE PRESENTATION: We herein add the case of a 29 year-old female who developed encephalitis and myelitis with flaccid paralysis during a long-time stay in Indonesia. Diagnostic workup in Indonesia did not clearly reveal an underlying cause. Upon clinical stabilization, the patient was evacuated to her home country Germany, where further diagnostics confirmed Japanese encephalitis virus as the causative agent. The patient has partly recovered, but still suffers from residual paralysis of the upper limb.
CONCLUSIONS: Flaccid paralysis is a rare, and likely underdiagnosed complication of Japanese encephalitis, which, to the best of our knowledge, has never been diagnosed outside endemic areas before.

Guillain-Barré syndrome is the most common cause of flaccid paralysis, with multiple known clinical variants. Autonomic dysfunction, although frequently reported in the clinical course, is often overlooked in the pediatric population and is usually not the initial presenting symptom in this age group CASE PRESENTATION: We present the case of a previously healthy 17-year-old who arrived at the Emergency Department complaining of gastrointestinal symptoms associated with lipothymia. An initial electrocardiogram (ECG) showed sustained sinus bradycardia subsequently associated with arterial hypertension. Structural and inflammatory cardiac pathology were ruled out, as well as auriculoventricular conduction block and posterior reversible encephalopathy syndrome. On the ninth day after initial symptoms, the patient presented sensory and motor nerve disturbances with the cerebrospinal fluid analysis showing a clear albumin-cytologic dissociation, consistent with an atypical presentation of GBS with autonomic dysfunction. Immunoglobulin therapy was administered, developing subsequent aseptic meningitis, that required discontinuation of previous therapy and treatment with plasmapheresis. Clinical improvement was achieved with full motor function recovery.
This case illustrates a Guillain-Barré syndrome variant in which autonomic dysfunction preceded neurologic deficit, a finding uncommon in children, emphasizing this as an important differential diagnosis for severe bradycardia in pediatric patients.

Guillain-Barré Syndrome (GBS) is currently the most frequent cause of acute flaccid paralysis on a global scale, being an autoimmune disorder wherein demyelination of the peripheral nerves occurs. Its main clinical features are a symmetrical ascending muscle weakness with reduced osteotendinous reflexes and variable sensory involvement. GBS most commonly occurs after an infection, especially viral (including COVID-19), but may also transpire after immunization with certain vaccines or in the development of specific malignancies. Immunoglobulins, plasmapheresis, and glucocorticoids represent the principal treatment modalities, however patients with severe disease progression may require supportive therapy in an intensive care unit. Due to its symptomology, which overlaps with numerous neurological and infectious illnesses, the diagnosis of GBS may often be misattributed to pathologies that are essentially different from this syndrome. Moreover, many of these require specific treatment methods distinct to those recommended for GBS, in lack of which the prognosis of the patient is drastically affected. Such diseases include exposure to toxins either environmental or foodborne, central nervous system infections, metabolic or serum ion alterations, demyelinating pathologies, or even conditions amenable to neurosurgical intervention. This extensive narrative review aims to systematically and comprehensively tackle the most notable and challenging differential diagnoses of GBS, emphasizing on the clinical discrepancies between the diseases, the appropriate paraclinical investigations, and suitable management indications.

Electrolyte abnormalities are an underrecognized cause of respiratory failure in the intensive care unit. One such abnormality is a relatively rare phenomenon of hypermagnesemia resulting in paralysis. A 73-year-old Caucasian male patient presented to the emergency department with diffuse abdominal pain of 2-day duration. He received magnesium citrate and gastrointestinal cocktail for his constipation after initial imaging showed constipation. In view of acute worsening, follow-up computed tomography of the abdomen was done, which showed free air in upper abdomen along with free fluid. Hence, he was taken for emergent laparotomy with repair of pyloric ulcer perforation with omental patch. Post procedure course was complicated by sepsis, acute kidney injury, and respiratory failure with hypoxemia and hypercapnia. On physical examination the patient had flaccid paralysis in all his extremities along with absent brain stem reflexes. Extensive workup including imaging of brain failed to reveal diagnosis. On postoperative day 1, the patient was noted to have magnesium level of 9.2 mg/dL (1.6-2.3 mg/dL), which was thought to be cause of flaccid paralysis and respiratory failure. In view of his acute oliguric kidney injury, he was initiated on intermittent hemodialysis, until his magnesium levels were back to its physiologic limits. His paralysis gradually improved over next 48 to 72 hours and he was liberated from ventilator successfully.

Background: Guillain-Barre syndrome is the most common cause of acute flaccid paralysis worldwide since the eradication of poliomyelitis. Severe cases may require intensive care and mechanical ventilation. Purpose: was to study pediatric patients with severe GBS requiring intensive care unit (ICU) admission, to assess their course and response to initial treatment modality plasma exchange (PE) or intravenous immunoglobulins (IVIg) and their final outcome. Methods: children with severe GBS who had either actual or impending respiratory failure, bulbar involvement or rapid progression of acute flaccid paralysis with trunk, upper limb and neck involvement within 24 h of the onset of weakness were enrolled. Results: 40 children were included. Following the initial treatment (33 subjects had 5 PE sessions each and IVIg in 7), 16 patients improved (40%), two died and 22 (55%) showed initial treatment failure. Axonal neuropathy, rapid progression and severe motor weakness significantly predicted poor response to therapy. At discharge, favorable outcomes (patient can walk unaided) were present in 22 cases (58%). Conclusion: Despite relatively low mortality, critically ill children with severe GBS have increased prevalence of axonal neuropathy and guarded response to initial therapy with PE or IVIg.