Hashimoto\'s encephalopathy (HE) has been a poorly understood disease. It has been described in all age group, yet, there is no specific HE marker. Additionally, the treatment data in the available studies are frequently divergent and contradictory. Therefore, the aim of our systematic and critical review is to evaluate the diagnosis and treatment of HE in view of the latest findings. The databases browsed comprised PubMed, Scopus, and Google Scholar as well as Cochrane Library, and the search strategy included controlled vocabulary and keywords. A total of 2443 manuscripts were found, published since the beginning of HE research until February 2024. In order to determine validity of the data collected from studies, bias assessment was performed using RoB 2 tool. Ultimately, six studies were included in our study. HE should be considered in the differential diagnosis in patients with psychiatric and neurological symptoms. According to our findings, negative thyroid peroxidase antibodies (anti-TPOs) may represent a valuable parameter in ruling out HE. Nonetheless, this result cannot be used to confirm HE. Furthermore, the proposed anti NH2-terminal-α-enolase (anti-NAE) is non-specific for HE. The effectiveness of glucocorticoid therapy is 60.94%, although relapse occurs in 31.67% of patients following the treatment. Our review emphasizes the significance of conducting further large-scale research and the need to take into account the potential genetic factor.

Nodular regenerative hyperplasia (NRH) is a primary disease of the liver that may cause noncirrhotic portal hypertension. Common causes include autoimmune, hematologic, immune deficiency, and myeloproliferative disorders. Given the limited data regarding the development of NRH in contemporary immunosuppressive protocols and the occurrence of NRH post-liver transplantation, we systematically reviewed NRH as it pertains to liver transplantation. We performed a comprehensive search for NRH and transplantation. Nineteen studies were identified with relevant data for NRH as an indication for a liver transplant. Thirteen studies were identified with relevant data pertaining to NRH development after liver transplant. Pooled analysis revealed 0.9% of liver transplant recipients had NRH. A total of 113 patients identified with NRH underwent liver transplantation. Most series report transplants done after the failure of endoscopic banding and TIPS management of portal hypertension. Reported 5-year graft and patient survival ranged from 73%-78% and 73%-90%. The pooled incidence of NRH after liver transplant for all indications was 2.9% and caused complications of portal hypertension. Complications related to portal hypertension secondary to NRH are a rare indication for a liver transplant. NRH can develop at any time after liver transplantation often without an identifiable cause, which may lead to portal hypertension requiring treatment or even re-transplantation.

Cisplatin is a cancer therapy drug commonly used. It is well-known for its antineoplastic properties, as well as for its numerous adverse effects, particularly its neurotoxicity. Symptoms associated with a central nervous system injury are unusual but can present a diagnostic challenge. Here, we report a case of a 62-year-old patient who was diagnosed with undifferentiated nasopharyngeal carcinoma. Cisplatin-based chemotherapy was administrated. Five days following the second cycle of treatment, the patient presented neurological disorders. A full biological workup and brain imaging were requested and revealed no abnormalities. The diagnosis of cisplatin encephalopathy was then suspected. Twenty days after cessation of cisplatin therapy, the neurological symptoms began to improve. Based on our case and a review of the literature, cisplatin-induced encephalopathy remains unusual. Its diagnosis is based on a combination of clinical, biological, and radiological criteria and requires the exclusion of other etiologies for neurological disorders in a patient being treated for cancer. Treatment is symptomatic and depends on stopping cisplatin therapy. These neurological adverse effects are often transitory and disappear without major repercussions.

BACKGROUND: Posterior leukoencephalopathy syndrome (PRES) is a rare neurological disease possibly associated with the use of calcineurin inhibitors like cyclosporine A (CSA). Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) responsible for the outbreak of coronavirus disease 19 (COVID-19) can cause neurological manifestations. We described a case of CSA-related PRES whose diagnosis was difficult due to a concurrent infection with SARS-CoV-2.
METHODS: The 16-year-old patient was known to have corticosteroid-resistant nephrotic syndrome secondary to minimal change disease. CSA was introduced, and on the fifth day of treatment, the patient presented with seizures followed by fever. Biological and magnetic resonance imaging data were in favor of SARS-CoV-2 encephalitis. Relief of immunosuppression by discontinuation of CSA was decided and the patient was put on anticonvulsants. After being declared cured of COVID-19, which was without other clinical signs, the CSA was reintroduced but the patient presented with seizures the next day. This allowed the physicians to rectify the diagnosis and relate the seizures to a CSA-related PRES.
CONCLUSIONS: Infection with SARS-CoV-2 could be a differential diagnosis of a PRES related to calcineurin inhibitors.

A patient presenting to the emergency room with neurological symptoms is more commonly found to have manifestations of stroke, transient ischemic attack, or nervous system injury. Alcoholic Wernicke encephalopathy (WE) is also another common manifestation of neurological dysfunction; however, the prevalence of non-alcoholic WE is relatively uncommon. We discuss a 37-year-old male who presented to the ED with dysphagia, slurred speech, word-finding difficulty, and restricted extraocular movements from non-alcoholic WE in the setting of semaglutide use.

BACKGROUND: Malabsorption syndromes are known chronic complications of bariatric surgery. Therefore, it is recommended to take oral supplementation with multivitamins. Wernicke\'s encephalopathy represents an acute neuropsychiatric syndrome associated with alcoholism or severe malnutrition; sporadic cases of this potential complication related to bariatric surgery are described in the literature. We present a case of Wernicke\'s encephalopathy due to severe vitamin B1 deficiency after bariatric surgery.
METHODS: A 31-year-old woman with deaf-mutism from the age of 3 years old, operated 3 months before with a mini-gastric bypass for severe obesity, was transferred to our unit after accessing the emergency room. In the immediate medical history, there was the sudden and rapid decline in vision, leading to complete loss of vision, marked asthenia, and paresthesia in the four limbs. Considering the previous bariatric surgery, the diagnosis of non-alcoholic Wernicke\'s syndrome was suspected, for which IV therapy with Vitamin B1 was started at a dosage of 5 vials of 200 mg in 100 cc of saline solution (three times a day for the first 72 hours, subsequently 1 once/day). After 12 hours, there was an improvement in visual acuity, and the symptoms completely resolved within 48 hours. She was discharged with complete resolution of all symptoms after 1 month.
CONCLUSIONS: Initial vision loss without confusion or encephalopathy is one atypical presentation of Wernicke syndrome. Clinical suspicion must be high in case of alcoholism or post-bariatric surgery. Early recognition of atypical symptoms, including vision loss, and timely administration of therapy improves the prognosis of this potentially reversible but time-dependent neurological emergency.

Encephalopathy is part of the clinical triad of Susac syndrome, but a detailed understanding of the neurocognitive and neuropsychiatric profile of this condition is lacking. Existing literature indicates that cognitive deficits range in severity from subtle to profound. Executive function and short-term recall are affected frequently. Psychiatric manifestations may be absent or may include anxiety, mood disorders or psychosis. If psychiatric phenomena develop during the disease course, it can be hard to disentangle whether symptoms directly relate to the pathology of Susac syndrome or are secondary to treatment-related side effects. In this article, we review what is known about the cognitive and psychiatric morbidity of Susac syndrome and identify areas where knowledge is deficient. Importantly, we also provide a framework for future research, arguing that better phenotyping, understanding of pathophysiology, evaluation of treatments on cognitive and psychiatric outcomes, and longitudinal data capture are vital to improving patient outcomes.

BACKGROUND: Delirium is a common complication of older people in hospitals, rehabilitation and long-term facilities.
OBJECTIVE: To assess the worldwide use of validated delirium assessment tools and the presence of delirium management protocols.
METHODS: Secondary analysis of a worldwide one-day point prevalence study on World Delirium Awareness Day, 15 March 2023.
METHODS: Cross-sectional online survey including hospitals, rehabilitation and long-term facilities.
METHODS: Participating clinicians reported data on delirium, the presence of protocols, delirium assessments, delirium-awareness interventions, non-pharmacological and pharmacological interventions, and ward/unit-specific barriers.
RESULTS: Data from 44 countries, 1664 wards/units and 36 048 patients were analysed. Validated delirium assessments were used in 66.7% (n = 1110) of wards/units, 18.6% (n = 310) used personal judgement or no assessment, and 10% (n = 166) used other assessment methods. A delirium management protocol was reported in 66.8% (n = 1094) of wards/units. The presence of protocols for delirium management varied across continents, ranging from 21.6% (on 21/97 wards/units) in Africa to 90.4% (235/260) in Australia, similar to the use of validated delirium assessments with 29.6% (29/98) in Africa to 93.5% (116/124) in North America. Wards/units with a delirium management protocol [n = 1094/1664, 66.8%] were more likely to use a validated delirium test than those without a protocol [odds ratio 6.97 (95% confidence interval 5.289-9.185)]. The presence of a delirium protocol increased the chances for valid delirium assessment and, likely, evidence-based interventions.
CONCLUSIONS: Wards/units that reported the presence of delirium management protocols had a higher probability of using validated delirium assessments tools to assess for delirium.

Leucine aminoacyl tRNA-synthetase 1 (LARS1)-deficiency (infantile liver failure syndrome type 1 (ILFS1)) has a multisystemic phenotype including fever-associated acute liver failure (ALF), chronic neurologic abnormalities, and encephalopathic episodes. In order to better characterize encephalopathic episodes and MRI changes, 35 cranial MRIs from 13 individuals with LARS1 deficiency were systematically assessed and neurological phenotype was analyzed. All individuals had developmental delay and 10/13 had seizures. Encephalopathic episodes in 8/13 were typically associated with infections, presented with seizures and reduced consciousness, mostly accompanied by hepatic dysfunction, and recovery in 17/19 episodes. Encephalopathy without hepatic dysfunction occurred in one individual after liver transplantation. On MRI, 5/7 individuals with MRI during acute encephalopathy had deep gray matter and brainstem changes. Supratentorial cortex involvement (6/13) and cerebellar watershed injury (4/13) occurred with seizures and/or encephalopathy. Abnormal brainstem contour on sagittal images (8/13), atrophy (8/13), and myelination delay (8/13) were not clearly associated with encephalopathy. The pattern of deep gray matter and brainstem changes are apparently characteristic of encephalopathy in LARS1-deficiency, differing from patterns of hepatic encephalopathy or metabolic stroke in organic acidurias and mitochondrial diseases. While the pathomechanism remains unclear, fever and energy deficit during infections might be causative; thus, sufficient glucose and protein intake along with pro-active fever management is suggested. As severe episodes were observed during influenza infections, we strongly recommend seasonal vaccination.

In recent years, reports of health problems associated with nitrous oxide consumption have significantly increased. In Germany, nitrous oxide (N2O) is easily available in cartridges without legal restrictions. The main reason for its popularity in the party scene are the euphoric, psychedelic effects of the gas. In addition to severe and sometimes irreversible health problems associated with long-term use of nitrous oxide, e.g., anemia and nerve damage, life-threatening or fatal consequences of acute nitrous oxide consumption can also occur: accidents under the influence of nitrous oxide, pneumothorax, pneumopericardium and shock due to an explosive increase in airway pressure when inhaled directly from the cartridge. But the most common cause of severe complications is asphyxia as the gas is usually inhaled pure from large balloons and without oxygen. The resulting hypoxia during use may be perpetuated by the diffusion hypoxia that occurs during the reoxygenation period. Nitrous oxide as a cause in accidental or intoxication events is usually not detectable but can only be identified as a trigger based on the patient\'s history or the circumstances. Acute medical treatment is symptomatic.
UNASSIGNED: In den letzten Jahren haben Berichte über lachgaskonsumassoziierte Gesundheitsstörungen erheblich zugenommen. Lachgas (N2O) ist in Deutschland problemlos legal und nahezu ubiquitär in Kartuschen erhältlich. Grund für die Beliebtheit in der Partyszene sind v. a. die euphorisierend-psychedelischen Effekte des Gases. Neben ernsthaften und manchmal irreversiblen gesundheitlichen Problemen bei Langzeitanwendung (Blutbild- und Nervenschädigungen) ereignen sich immer wieder auch akutmedizinisch bedeutsame, lebensbedrohliche oder tödliche Folgen des Lachgaskonsums: Unfälle unter Lachgaseinfluss, Pneumothorax, Pneumoperikard und Schock durch explosionsartige Druckerhöhung in den Atemwegen bei Inhalation direkt aus der Kartusche, aber v. a. hypoxische Komplikationen, da das Gas meist pur und ohne Sauerstoffbeimengung aus großen Ballons inhaliert wird. Die während der Anwendung auftretende Hypoxie kann zudem durch die in der Abflutungsphase auftretende Diffusionshypoxie perpetuiert werden. Lachgas als Ursache ist bei Unfällen oder Intoxikationsgeschahen meist nicht nachweisbar, sondern nur anamnestisch oder durch die Umstände als Auslöser zu identifizieren. Die akutmedizinische Therapie ist symptomatisch.