BACKGROUND: Over the last decade, there has been an emerging trend of recreational misuse of several drugs and inhaled solvent including ethyl chloride. This case report follows CARE guidelines and highlights, with supporting video, the neurological features of ethyl chloride intoxication.
METHODS: A 48-year-old man was seen for the sudden occurrence of an unsteady gait with dizziness. His only medical history was a chronic and treated HIV infection without any complications. Clinical examination revealed a cerebellar syndrome associated with impairment of short-term memory. Biological and radiological workups were normal. After several days, the patient recalled ethyl chloride inhalation. He fully recovered after being discharged from hospital.
CONCLUSIONS: Clinicians should recognise the clinical features and neurological manifestations of ethyl chloride intoxication due to the potential fatal cardiovascular complications of this intoxication.

An 85-year-old man was diagnosed with hepatocellular carcinoma (HCC) and was initially treated with transarterial chemoembolization (TACE) and sorafenib. He was then switched to nivolumab and ipilimumab in view of sorafenib intolerance and disease progression. Subsequently, he developed dysphagia and generalized dyspnea culminating in hypercapnic respiratory failure requiring intubation. After an extensive workup, the etiology of his fluctuating respiratory issues was narrowed down to a likely neuromuscular process. Although antibodies to acetylcholine receptors (anti-AChR Ab) were negative, he was treated with high-dose steroids due to clinical concern for Immune Checkpoint Inhibitor (ICI) neurotoxicity. His recovery post immune suppression and absence of recurrence after ICI cessation suggested the possibility of this being an ICI neurotoxicity manifesting with myasthenic symptoms. Incidentally, he also had evidence of aseptic meningitis on cerebrospinal fluid analysis further strengthening this diagnosis. This case illustrates the importance of early recognition of ICI toxicity which will in turn lead to initiating treatments sooner and also decreasing the length of illness.

BACKGROUND: Chronic nitrous oxide (N2O) use causes inactivation of vitamin B12, resulting in neurological and psychiatric symptoms. This case series presents all N2O-related presentations to the emergency department at Royal Perth Hospital between June 2019 and June 2021, alongside the costs of these admissions.
METHODS: Twenty-two patients were identified; 68% (n = 15) were male. The median age was 22.4 years (interquartile range [IQR], 20-30). Median daily number of N2O bulbs inhaled was 150 (IQR, 64-300) with a median duration of use of 9 months (IQR, 3-12). Presentations included ataxia, paraesthesia and falls (n = 18), urinary retention (n = 3) and psychotic symptoms (n = 2). Fourteen patients had severe symptoms prompting a magnetic resonance imaging of brain and spine, confirming 12 cases of subacute combined degeneration of the spinal cord. All patients had IMI vitamin B12 therapy, while 14 had oral methionine therapy. The median length of admission was 4 days (IQR 1-23 days). The median cost of admission per day for patients where costs were accessible (n = 7) was $2061 (IQR, $1903-$2860).
CONCLUSIONS: A case series of symptomatic chronic N2O use with severe neurological sequelae and significant costs associated per admission. Triangulation of emergency department and Ecstasy and Related Drugs Reporting System data helped prompt a swift public health response, including mandatory warning labels, limits to transaction amounts and legislative changes to the Medicines and Poisons Act to make it illegal for sale if there is a suspicion that it will be abused.

Toxic leukoencephalopathy (TL) refers to damage to the brain white matter following exposure to toxic agents. Multiple agents are incriminated in this condition, including chemotherapy drugs. 5-Fluorouracil, widely used in oncology, is responsible for neurotoxicity in less than 5% of cases. We report the case of a 54-year-old male patient who presented with neurological symptoms following 5-FU-based chemotherapy for gastric adenocarcinoma, and whose MRI scan revealed signs suggestive of toxic leukoencephalopathy. We also report on the evolution of the abnormalities described on his MRI after 1 year.

Polymyxin-induced neuromuscular blockade is a rare but potentially fatal condition, with majority of cases that were reported between 1962 and 1973. We describe a patient who developed hypercapnic respiratory failure after initiation of polymyxin for multi-drug resistant Escherichia Coli bacteremia, due to polymyxin-induced neuromuscular dysfunction. After cessation of polymyxin, he regained full strength, had complete resolution of ptosis, and was successfully extubated. In light of the renewed use of polymyxin in this era of antimicrobial-resistance, this case aims to raise awareness about this rare but life-threatening condition, which is easily reversible with early recognition and prompt discontinuation of the drug.

Carbamazepine remains a first-line antiepileptic medication for the treatment of partial seizures. Despite its widespread use, carbamazepine has significant neurotoxicity and hypersensitivity reactions. We report a case of a patient post-kidney transplant who was on regular carbamazepine for childhood epilepsy and developed nystagmus, diplopia and a broad-base gait after receiving diltiazem. Understanding of the interaction between diltiazem and carbamazepine is necessary to prevent the neurotoxic effects.

BACKGROUND: S-lon® (S) is a locally produced polyvinyl chloride-based solvent cement. It is a clear, slightly viscous liquid. Other constituents include 1-cyclohexanone, 3-butanone, and 1-acetone. It is used ubiquitously for building construction in Sri Lanka. Although the clinical effects of the compound have not yet been ascertained, the constituents have been implicated in neurotoxicity, respiratory tract, eye and skin irritation, and delayed liver and renal injury.
METHODS: A 42-year-old South Asian male presented following self-ingestion of S. His vital parameters were stable and initially managed symptomatically. A few hours later, he developed central nervous system depression and stridor requiring elective intubation. Examination of the upper airway revealed inflammation and edema. He was sedated and ventilated, and intravenous dexamethasone was administered. Attempts at removal of the nasogastric tube after extubation on day 3 failed. The patient had to be reintubated and sedated owing to extreme agitation not responding to routine doses of sedatives. The nasogastric tube had been amalgamated after reacting with S, forming a solid clump, later found after removal. The posterior pharynx and nasopharynx were packed and later removed before extubation. The patient made a full recovery and was transferred to the ward on day 5.
CONCLUSIONS: Ingestion of a sufficient quantity of S could result in gut absorption with central nervous system depression, coma, and even death. No antidote is available for toxicity, and management is largely supportive. As witnessed in our patient, chemical laryngitis and upper airway inflammation may lead to upper airway obstruction. Chemical reactions with medical equipment may lead to unforeseen outcomes.

UNASSIGNED: Capecitabine has rarely been associated with neurotoxicity. Cerebellar ataxia, multifocal leukoencephalopathy, and sensorimotor peripheral neuropathy have been reported in the literature. A case of 6th nerve palsy associated with capecitabine has also been described. This article reports the first case of capecitabine-related 4th nerve palsy.
UNASSIGNED: A 72-year-old Caucasian woman was referred by the Oncology Department because she had been complaining of binocular diplopia for 6 months. The symptoms started 1 month after the introduction of capecitabine. A diagnosis of right 4th nerve palsy was made using the Parks three-step test and the Hess test. Neuroimaging analysis was negative. A slow but progressive deterioration of function was confirmed during a year of follow-up. On suspicion of a chemotherapy-related palsy, capecitabine was discontinued and switched to vinorelbine. Subsequent improvement of the clinical picture was confirmed within 2 months.
UNASSIGNED: The recognition of chemotherapy-related neurotoxicity is of paramount importance in the management of oncology patients. Once secondary invasion of the brain or the orbit by the tumor itself is ruled out, it must be suspected to prevent further deterioration.

Chemotherapy and radiotherapy are widely used in the treatment of central nervous system tumors and acute lymphocytic leukemia even in the pediatric population. However, such treatments run the risk of a broad spectrum of cognitive and neurological deficits. Even though the correlation with cognitive decline is still not clear, neuroradiological defects linked to white matter injury and vasculopathies may be identified. Thanks to the use of 7T MRI it is possible to better define the vascular pattern of the brain lesions with the added advantage of identifying their characteristics and anatomical localization, which, however, are not evident with a conventional brain scan. Moreover, the use of Quantitative Susceptibility Mapping (QSM) makes it possible to discriminate between calcium deposits on vessels (chemo-radiation-induced) and hemoglobin deposition in radio-induced cavernomas, speculating, as a result, about the pathophysiology of iatrogenic brain damage. We describe the case of a 9 year-old boy with a T-type acute lymphoid leukemia who had previously been treated with polychemotherapy and high-dose RT. To better define the child\'s neuroradiological pattern, 7T MRI and QSM were performed in addition to conventional imaging examinations. Our case report suggests the potential usefulness of a QSM study to distinguish radio-induced vascular malformations from mineralizing microangiopathy.

UNASSIGNED: The central nervous system (CNS) is the most common site of extramedullary invasion in acute lymphoblastic leukemia (ALL), and involvement of the CNS is often associated with relapse, refractory disease, and poor prognosis. Chimeric antigen receptor-T (CAR-T) cell therapy, a promising modality in cancer immunotherapy, has demonstrated significant advantages in the treatment of hematological malignancies. However, due to associated adverse reactions such as nervous system toxicity, the safety and efficacy of CAR-T cell therapy in treating CNSL remains controversial, with limited reports available.
UNASSIGNED: Here, we present the case of a patient with confirmed B-ALL who experienced relapse in both bone marrow (BM) and cerebrospinal fluid (CSF) despite multiple cycles of chemotherapy and intrathecal injections. The infusion of autologous CD19 CAR-T cells resulted in complete remission (CR) in both BM and CSF for 40 days. However, the patient later experienced a relapse in the bone marrow. Subsequently, allogeneic CD19 CAR-T cells derived from her brother were infused, leading to another achievement of CR in BM. Significantly, only grade 1 cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) events were detected during the treatment period and showed improvement with symptomatic management. During subsequent follow-up, the patient achieved a disease-free survival of 5 months and was successfully bridged to hematopoietic stem cell transplantation.
UNASSIGNED: Our study provides support for the argument that CNS involvement should not be deemed an absolute contraindication to CAR-T cell therapy. With the implementation of suitable management and treatment strategies, CAR-T therapy can proficiently target tumor cells within the CNS. This treatment option may be particularly beneficial for relapsed or refractory patients, as well as those with central nervous system involvement who have shown limited response to conventional therapies. Additionally, CAR-T cell therapy may serve as a valuable bridge to allogeneic hematopoietic stem cell transplantation (allo-HSCT) in these patients.