Potentiated fractalkine signaling axis affects neuroinflammation in 1,2-dichloroethane- intoxicated mice via divergent modulating ways on microglial hyperactivation.

Granularity of EEG reactivity in response to stimulation: "Atypical" reactivity in non-sedated and sedated patients.

Introduction Diisopropylcarbodiimide is a peptide coupler commonly used in biotechnology. Dermal and respiratory effects, due to irritant and sensitizing properties, have been reported in exposed workers and experimental studies. Neurological toxicity, as demonstrated in animal studies, has not been reported in humans. We describe three male workers who experienced dermal, respiratory, and neurological sequelae after accidental exposure to diisopropylcarbodiimide, a volatile liquid product. Methods Clinical data were collected retrospectively through review of medical files and follow-up interviews. Each worker underwent a symptom-guided clinical evaluation, including dermatological, respiratory, neurological, and neuropsychological assessment. Follow-up extended up to three years, depending on the case. Results Three workers were occupationally exposed to diisopropylcarbodiimide by inhalation and dermal contact due to a leaking barrel. All experienced similar clinical courses after the incident, including the development not only of contact dermatitis and occupational asthma, but also neurological effects (persistent headaches, neuropathic pain and paraesthesia in hands/feet, fatigue and cognitive impairment, compatible with chronic toxic encephalopathy). They also developed sleep disturbances, including new-onset obstructive sleep apnoea syndrome. Discussion The consistency of these presentations across patients, the close temporal association to a brief exposure to diisopropylcarbodiimide, and evidence from animal studies suggest a possible causal relationship. Conclusions Three workers experienced contact dermatitis, occupational asthma, severe neurological sequelae, as well as new-onset obstructive sleep apnoea syndrome after occupational exposure to diisopropylcarbodiimide. The close temporal association to a single presumably high-level exposure suggests a possible causal relationship. To prevent such health consequences, workers with potential exposure to peptide couplers must be made aware of their hazards and adequately protected.

Methyl acetic acid methyl ester (MAME), a colorless, transparent, low-toxicity chemical with an aromatic odor, is widely used in the textile industry as a liquid substance. When absorbed through inhalation, ingestion, or skin contact, MAME is metabolized into methanol, potentially causing methanol-like poisoning symptoms. Clinical manifestations vary significantly among individuals, commonly presenting as metabolic acidosis, toxic encephalopathy, optic nerve damage, and even death, all associated with accumulation of formate in the body. This study reports two cases of acute MAME poisoning from August to December 2024. Both patients had confirmed occupational exposure to MAME and exhibited acute optic nerve and retinal damage, diagnosed as occupational acute severe MAME poisoning.

Background: Hepatic encephalopathy (HE) is a severe neuropsychiatric complication of advanced liver disease, driven primarily by ammonia accumulation due to impaired hepatic detoxification and portosystemic shunting. Lactulose is a cornerstone therapy, while rifaximin serves as an effective adjunct for reducing recurrence and hospitalizations. Methods: We conducted a retrospective cohort study at Constanța Emergency County Hospital from January 2022 to March 2025, including 120 adult patients diagnosed with HE. Inclusion criteria were confirmed diagnosis of cirrhosis with clinical and/or biochemical evidence of HE. Patients with other primary neurological disorders or incomplete medical records were excluded. Data on demographics, comorbidities, laboratory results, and medications were collected. Statistical analyses were performed employing descriptive statistics, Friedman’s two-way ANOVA by ranks for medication use, and Cox proportional hazards regression to assess survival associations. Results: The mean age was 61.19 years, with high prevalence of anemia (mean hemoglobin: 9.35 g/dL) and thrombocytopenia (mean: 121.86 × 103/µL). Inflammatory markers were elevated (mean CRP: 36.95 mg/L; ESR: 55.83 mm/h), and INR averaged 1.86. Lactulose was administered to 63.3% of patients, rifaximin to 52.5%, with diuretics, pantoprazole, and albumin being frequently used. Friedman’s analysis ranked lactulose highest in usage frequency. Cox regression indicated no significant short-term survival difference associated with toxic encephalopathy or rifaximin use. Conclusion: In this cohort, lactulose remained the primary treatment for HE, often complemented by supportive pharmacotherapy. While rifaximin use was limited, the overall medication patterns reflected standard practice priorities in HE management.

Rationale:Mercury toxic encephalopathy is uncommonly encountered in clinical practice.Patient concerns:The aim of presenting this case is to increase the awareness of this disease, especially regarding its radiological presentation.Diagnoses:Toxic encephalopathy due to mercury.Interventions:The medical team administered sodium dimercaptopropane sulfonate as a mercury antagonist and treated with plasma purification and massive hydration to promote mercury excretion.Outcomes:Following admission, the patient underwent an magnetic resonance imaging (MRI) examination. The results revealed symmetrical alterations in the brain parenchyma (including both cerebrum and cerebellum), characterized by hypoperfusion on MRI perfusion imaging. The patient died after a series of lifesaving measures.Lessons:Mercury poisoning encephalopathy is a rare disorder for which currently established diagnostic criteria are lacking. On brain MRI scans, it manifests as symmetric cerebral edema, involving the parenchyma of both the cerebrum and cerebellum. It is important to question patients carefully about any history of exposure to mercury-containing drugs.

Toxic encephalopathy is a central nervous system disorder caused by endogenous or exogenous toxic substances. Granzyme B (GZMB), a key serine protease, plays a crucial role in immune regulation and the progression of various diseases. Abnormal expression of GZMB may contribute to the development and progression of toxic encephalopathy; however, its specific mechanisms remain unclear. This study aims to preliminarily explore the association between granzyme B and toxic encephalopathy through big data. This study retrieved the toxic encephalopathy dataset GSE253309 from the gene expression omnibus database. Differentially expressed genes were identified using the “limma” R package, followed by gene ontology and Kyoto encyclopedia of genes and genomes enrichment analyses. A protein–protein interaction network was constructed using the search tool for the retrieval of interacting genes (STRING) database, key hub genes were identified with Cytoscape software. A total of 994 differentially expressed genes were identified. Among them, GZMB was moderately overexpressed in toxic encephalopathy tissues (log2 fold change = 0.70, P = .00087), suggesting a potential disease association. and was enriched in the TGF-beta signaling pathway. Kyoto encyclopedia of genes and genomes enrichment analysis revealed that GZMB-related genes were involved in several pathways, notably the TGF-beta signaling pathway and apoptosis, both of which are implicated in immune regulation and neuronal injury. Protein–protein interaction network analysis confirmed GZMB as a hub gene potentially contributing to disease progression. Furthermore, β-escin sodium and methylprednisolone may modulate GZMB expression, thereby alleviating neuronal damage and improving outcomes in delayed encephalopathy after carbon monoxide poisoning. Elevated GZMB expression likely contributes to the pathogenesis and progression of toxic encephalopathy through multiple pathways, making it a potential disease biomarker and therapeutic target.

IntroductionDimethylacetamide (DMAC) is used as a solvent in the dye, leather, and acrylic manufacturing industries. However, it is associated with significant risks of liver and nerve damage. 4,4’-Diaminodiphenyl ether (4,4’-ODA) is a crucial precursor for synthesizing curing agents and dyes but can disrupt the methemoglobin reduction system, resulting in methemoglobinemia.MethodsThis paper reports an incident involving a plant pipeline leak on May 10, 2024, which primarily contained a DMAC solution and trace amounts of 4,4’-ODA. The patient’s occupational history, onset time of clinical symptoms, physical examination results, laboratory data, and treatment course were analyzed, and follow-up evaluation was performed to monitor the patient’s long-term health status.ResultsTwo patients exhibited clinical symptoms, including respiratory failure, methemoglobinemia, hemolytic anemia, and acute liver injury due to dermal and respiratory exposure. They were successfully treated and discharged. Notably, Patient 1 was diagnosed with toxic encephalopathy 16 days post-exposure, while Patient 2 developed peripheral neuropathy 58 days post-exposure.DiscussionThis study aimed to elucidate the clinical characteristics associated with this type of poisoning. Moreover, the incident calls for enhanced safety measures in industries using DMAC and 4,4’-ODA to prevent similar poisoning events.

The link between serum glucose-potassium ratio (GPR) and mortality in critically ill toxic encephalopathy (TE) patients is not well defined. This study has aimed to clarify the effect of GPR fluctuations on TE mortality. A total of 3,462 TE patients with TE requiring ICU care were selected from the Medical Information Mart Intensive Care (MIMIC-IV) database. Patients were categorized into three groups based on GPR tertiles: Tertile 1 (n = 1154, range 0.103-1.442), Tertile 2 (n = 1153, range 1.444-1.966), and Tertile 3 (n = 1155, range 1.967-12.937). The primary outcomes studied were 28-day and 90-day all-cause mortality (ACM). To analyze the relationship between GPR and outcomes, we employed Cox regression models adjusted for multiple covariates and restricted cubic splines to explore the potential non-linear association. The 3,462 - patient cohort had a mean age of 67.7 ± 16.6 years, with 58.2% male. The 28-day and 90-day ACM were 21.9% and 31.2%, respectively. Multivariate adjusted analysis showed no overall GPR-ACM correlation at 28 and 90 d. Regarding different groups, with T2 as the reference group (Ref), for 28-day ACM, the adjusted hazard ratio (HR) of the T1 was 1.20 (95% Confidence Interval [CI]: 1.00-1.44, p ≡ P = 0.049), and that of T3 group was 1.22 (95% CI: 1.01-1.47, P = 0.035). For 90 - day ACM, the adjusted HR of the T1 was 1.19 (95% CI: 1.02-1.39, P = 0.023), and the T3 was 1.20 (95% CI: 1.03-1.40). The correlation between the GPR lesvel and ACM was U-shaped association. The left and right - hand side effect sizes at the inflection point (1.65) were 0.472 (HR: 0.472, 95% CI 0.306-0.728, P < 0.001) and 1.127 (HR: 1.127, 95% CI 1.032-1.229, P = 0.0075). Sensitivity analysis was stable. Our findings have revealed a U-shaped relationship between GPR levels and ACM in critically ill patients with TE. Close attention should therefore be paid to this issue in order to improve patient care.

Introduction. In the contemporary world, the problem of poisoning caused by organophosphorus compounds (OPs) is of great concern, with the risk of exposure to OP nerve agents remaining a reality in military settings. Healthcare professionals can utilize clinical cases of OP intoxication to prepare for the treatment of affected individuals. This study aims to investigate the characteristics of poisoning in a patient who suffered from acute oral exposure to OPs. Description of the clinical case. The patient was discovered in a state of unconsciousness on the staircase, with a bottle of AgranTM insecticide nearby. It was estimated that the patient had ingested approximately 600 milligrams of the substance per kilogram of their body weight. The acetylcholinesterase (AChE) activity in their serum was significantly diminished, measuring at 12 units per liter. Furthermore, the patient was also exposed to another organophosphorus (OP) substance, cypermethrin, at an estimated dose of 50 milligrams per kilogram. Upon admission, the severity of the patient’s condition was attributed to a cholinomimetic syndrome, accompanied by acute respiratory failure of mixed origin, decompensated mixed acidosis, and toxic encephalopathy. No abnormalities in neuromuscular conduction or transmission were observed. Timely etiological therapy with atropine and detoxification measures such as gastric lavage and hemosorption contributed to the normalization of the patient’s condition. Nonetheless, fourteen days following the exposure, there was a persistent and substantial reduction in the activity of serum cholinesterases and erythrocyte acetylcholinesterase. Conclusion. Consequently, it is reasonable to infer that acetylcholinesterase activity may not consistently correlate with the severity of OP intoxication in the prolonged post-toxic period. In the absence of comprehensive treatment for OP, extracorporeal detoxification emerges as a recommended approach. Limitations. In the performed study, the activity of erythrocyte AChE and serum butyrylcholinesterase was not evaluated, electromyography was not performed at the time of admission and during the start of treatment, the patient did not receive antidote therapy with cholinesterase reactivators.

Mercury possesses high toxicity and metal-dissolving properties, enabling it to form amalgam alloys with precious metals such as gold, silver, tin, and lead. The purification of target metals can be achieved through the volatilization process of heated amalgam. This report presents a case of toxic encephalopathy caused by acute mercury poisoning. The Department of Occupational Medicine and Toxicology at Beijing Chaoyang Hospital, affiliated with Capital Medical University, admitted and successfully treated a clinical case of toxic encephalopathy resulting from acute exposure to metallic mercury vapor. The nursing protocol and clinical outcomes are detailed herein. This paper conducts a retrospective analysis of clinical data to provide support for the prevention and control of mercury poisoning.

7018 Background: CAR-T cell therapy represents a notable advancement in treating relapsed/refractory (R/R) hematological malignancies. Adverse events include CRS, infections, and neurological and cardiac complications. While there are reports from major academic institutions on the adverse effects of CAR-T therapy, we used data from the National Inpatient Sample (NIS) to gather national estimates of complications related to CAR-T therapy. Methods: A retrospective study was conducted to analyze patients who underwent CAR-T cell therapy by utilizing appropriate ICD-10-PCS procedure codes (XW033C3, XW043C3, XW23346, XW24346, XW23376, and XW24376) from NIS 2019 to 2021. Data regarding infections, toxic encephalopathy (a surrogate for neurological toxicity), and adverse cardiac events were extracted using relevant ICD-10-CM diagnostic codes. Patients experiencing various grades of CRS were identified through specific ICD-10 codes available in 2021 (Grades 1-5: D89.831-D89.835). Results: This study analyzed 6515 patients who underwent CAR-T cell therapy from January 2019 to December 2021. Among them, 60.7% were male. 74.6% were Caucasian, 11.7% were Asian and 6.7% were African American. 49.8% of patients had private insurance, 36.2% had Medicare, and 8.6% had Medicaid. 6.8% of patients were diagnosed with pneumonia, while sepsis occurred in 7.4% of patients and 3% experienced septic shock. 19.4% of patients experienced cardiac arrhythmias, and major cardiovascular events were recorded in 4.7% of the cohort. Acute myocardial infarction and stroke were documented in 0.6 and 1.2% of patients, respectively. Toxic encephalopathy was reported in 19.7% of patients. Among 2235 patients identified to have received CAR-T in 2021, 59.7% developed CRS. Grade 1 and grade 2 CRS were reported in 32% and 21% of patients, respectively, while grade 3 and grade 4 reactions were noted in 4.7% and 2% of patients, with no cases of grade 5 identified. The mean total cost of hospitalization was 308,364$, and the mean length of hospital stay was 19.5 days. The overall in-hospital mortality rate was 3.4%. Conclusions: Our study describes real-world outcomes from a large dataset of CAR-T patients. Infections pose a significant challenge with CAR-T therapy, highlighting the importance of early detection and timely antimicrobial treatment. CRS is common, with a 60% incidence, similar to previous clinical trials (55%). Immediate management is crucial for addressing CRS toxicity. Adverse neurological and cardiovascular incidents are often reported, emphasizing the need for meticulous monitoring and coordinating multidisciplinary care plans. The financial burdens also bear mentioning: CAR-T therapy costs significantly higher than autologous stem cell transplants. Further studies to address these issues are warranted.

e24121 Background: Bispecific antibodies have revolutionized cancer treatment but are associated with a distinct toxicity profile. This study explores real-world outcomes, highlighting demographic trends, treatment complications, and clinical predictors of adverse events using National Inpatient Sample data from 2018 to 2021. Methods: A retrospective analysis was conducted on 61,890 patients treated with bispecific antibodies across U.S. hospitals. Data on comorbidities, complications, and outcomes were stratified by year, patient demographics, and hospital characteristics. Logistic regression determined associations between clinical factors and adverse events, with results expressed as odds ratios (ORs) and confidence intervals (CIs). Results: Neutropenia emerged as the most frequent complication (14.32 OR in 2021, p &lt; 0.001), followed by thrombocytopenia and anemia. Tumor lysis syndrome (TLS) showed a rising trend, peaking in 2021 (OR: 58.58, p &lt; 0.001). Protective factors included elective admissions and female gender, while advanced age, anemia, and CKD increased the likelihood of complications. Toxic encephalopathy, though less common, peaked at 413 cases in 2020, reflecting potential neurotoxic effects of therapy. Urban teaching hospitals accounted for most admissions (95%), and routine discharge was achieved in 76% of cases. Conclusions: The findings emphasize the need for vigilant monitoring of hematologic and systemic complications, especially TLS and neutropenia, in patients receiving bispecific antibodies. Targeted management protocols for older adults and individuals with preexisting anemia or CKD may mitigate treatment-related risks.

e23053 Background: The adoption of bispecific antibodies has transformed cancer therapeutics, but concerns regarding their toxicity profiles and clinical outcomes remain. This study examines patient demographics, hospitalization trends, and treatment-related complications in a nationally representative inpatient cohort from 2018–2021. Methods: Using the National Inpatient Sample, data from 61,890 patients receiving bispecific antibody treatments were analyzed. Outcomes included discharge patterns, length of stay, and mortality, along with complications such as neutropenia, thrombocytopenia, tumor lysis syndrome (TLS), and toxic encephalopathy. Statistical models identified predictors of adverse events, with subgroup analyses by demographics and comorbidities. Results: Neutropenia was the most common complication (peak 2,515 cases in 2021), with strong associations noted across all years (2019: OR: 13.84, 2021: OR: 14.32, p &lt; 0.001). TLS cases increased significantly, reaching an OR of 58.58 in 2021 (p &lt; 0.001). Anemia and thrombocytopenia remained prevalent but showed variable trends, while toxic encephalopathy peaked in 2020. Female gender and elective admissions were protective across complications, while older age, anemia, and CKD emerged as significant risk factors. The South represented the largest regional population (35%), and most admissions occurred in urban teaching hospitals (95%). Conclusions: Bispecific antibody therapies are associated with substantial hematologic and systemic toxicities, requiring tailored management strategies. Increased risk in older patients and those with preexisting conditions highlights the need for personalized care. These findings inform future research and clinical guidelines to optimize safety and efficacy in bispecific antibody treatments.

Screening of toxic-metabolic encephalopathy with and without epileptic seizure with density spectral array.

Intravenous thrombolysis is an established treatment to improve functional outcomes in acute ischemic stroke. However, various acute central nervous system dysfunctions can mimic stroke, where thrombolytic therapy may provide no benefit and carries potential risks. The ability to accurately distinguish stroke mimics vs stroke by telemedicine evaluation is uncertain. This study aims to identify clinical predictors of stroke mimics in patients evaluated via telemedicine for suspected ischemic stroke and treated with thrombolytics. We conducted a retrospective observational study of patients treated with thrombolytics for suspected acute ischemic stroke via telemedicine at Southern Illinois Healthcare between 2017 and 2024. Data on demographics, past medical history, clinical presentation, National Institutes of Health Stroke Scale (NIHSS), stroke metrics, and laboratory values were collected. Final diagnoses were categorized as cerebrovascular disease (CD), including acute ischemic stroke and transient ischemic attack, and stroke mimic (SM). Outcomes included hospital length of stay (LOS) and discharge disposition. Of 171 patients treated with thrombolytics via telemedicine, 128 (75%) were diagnosed with CD, and 43 (25%) were SM, with toxic-metabolic encephalopathy being the most common mimic (40%, n = 17). Adjusted forward logistic regression showed age (OR: 0.957, 95% CI: 0.931-0.984, P = .002) and NIHSS (OR: 1.098, 95% CI: 1.032-1.168, P = .003) remained independently associated with SM. The predictive TeleStroke Mimic was score performed with c-statistic of 0.61. SM had shorter median LOS (3 [2-3] vs 3 [2-6], P < .01) and higher rate of discharge home (86% vs 55%, P < .01). In our population, younger age and higher NIHSS were associated with higher odds of SM diagnosis in patients treated with telemedicine-administered thrombolytics. These variables are insufficient to reliably identify a subgroup of patients evaluated via telemedicine for whom thrombolytics could be withheld. The poor performance of Telestroke Mimic score highlights the need for improved predictive tools. Until larger studies are conducted, telemedicine-administered thrombolytics should adhere to current in-person guidelines.

Diquat is the third most widely used herbicidal biocide globally, following glyphosate and paraquat, with toxicity lower than paraquat. In the United States, diquat poisoning is predominantly linked to occupational exposure (8%–44%), with a low mortality rate (&lt;1%–3%). In China, however, diquat use has increased only recently, following the ban on paraquat, leading to limited awareness and a significantly higher fatality rate compared to developed countries. Diquat primarily affects the liver and kidneys, but it can also damage the central nervous and respiratory systems. We report three cases admitted to our hospital, each involving severe central nervous system injury following accidental diquat ingestion. These patients exhibited characteristic clinical and imaging findings associated with diquat-induced brain injury. This case series provides valuable insights and may guide prevention and management strategies for similar poisoning cases in the future.

BackgroundNarcotization with the home-made, artisanal psychostimulant - "Jeff" can be considered especially dangerous for the population of Georgia due to the availability, cheapness, simple technology, as well as the strongest narcogenic and toxic effects of the medications required for its manufacturing. Toxic (ephedronic) encephalopathy is characterized by development of severe, almost irreversible neurological disorders, affective disorders, and cognitive impairment (3-4). Consequently, the above-mentioned will be resulted in a disability of home-made psychostimulant consumers and significant reduction in their quality of life. The social drama of the disease arises from the fact that "ephedronic parkinsonism" appeared to be the cause of severe disability in young people, even at a strong remission from drug addiction. The situation is especially complicated by the fact that modern narcology has no known specific treatment for addiction caused by the use of drugs containing ephedrone and potassium permanganate.Aim and objectivesBased on the above, the aim of the study conducted was describing the neurological disorders in the users of the home-made psychostimulants of ephedrone group and evaluating the effectiveness of Thiogamma in their treatment.Methods60 in-patients of the Narcological Clinic - "Neogene" were involved in the study; prerequisite for study involvement was - a diagnosis: mental and behavioral disorders associated with ephedrone use; withdrawal state. Toxic encephalopathy; age - 20-65 years; gender - male. Patients were selected and diagnosed for the study according to ICD-10 criteria. The study was conducted applying bioethical principles, based on informed consent. The main study group (group I) consisted of 45 patients and the control group (group II) of 15 patients, respectively. The study was anonymous and confidential. In the patients (at both inpatient and outpatient treatment) of the main study group (Group I), Thiogamma drug (alpha-lipoic acid, meglumine salt) (1,2,5,6,7) with a daily dose of 600 mg was added to the standard treatment for one month.The patients (at both inpatient and outpatient treatment) in the control group (Group II) were treated with placebo drug along with standard treatment for the same period. Clinico-neurological disorders of the patients were evaluated before and after administering a one-month therapy course. Neurological examination and Unified Parkinson Disease Rating Scale - UPDSR - were used.Discussion and ConclusionBased on the study materials it can be reported that the users of home-made ephedron group psychostimulants ("Jeff"), had neurological disorders, mainly manifested with the symptoms of Parkinson’ s disease; dystonia, postural instability, pseudobulbar and vegetative syndromes have been expressed.As a result of treatment, a decrease in the scores on the Unified Parkinson Disease Rating Scale - UPDSR (improved condition) was observed in patients of both study groups, however, the latter was more expressed in the patients of group I where Thiogamma (alpha-lipoic acid meglumine salt) drug was added to the standard treatment protocol. The above results indicate to the effectiveness of Thiogamma drug in the treatment of neurological disorders caused by consuming the home-made psychostimulants ("Jeff").

Canadian Association of Radiologists Central Nervous System Diagnostic Imaging Referral Guideline.

Background: Cocaine has been shown to cause cytotoxic neuronal damage, which has been implicated in cases of leukoencephalopathy. We present a case of cocaine-induced toxic encephalopathy resulting in predominant lesions to the gray matter on magnetic resonance imaging (MRI). Case Presentation: A 70-year-old female presented acutely with confusion, agitation, and disorientation. She was markedly hypertensive with other vital signs within normal range. On presentation to the emergency department, she was uncooperative and had an unsteady gait but showed no focal neurological deficits. Her lab work was positive for elevated cardiac troponins, elevated D-dimer, and a urine drug screen positive only for cocaine. Head computed tomography (CT) showed no hemorrhage and head CT angiogram showed no abnormalities and no significant vascular stenosis. Chest X-ray and CT showed diffuse ground glass opacities compatible with atypical pneumonia. Antibiotics were initiated to treat the pneumonia and antihypertensives were administered to manage her blood pressure. She was also given IV thiamine. Brain MRI showed restricted diffusion involving bilateral hippocampi, thalami, putamen, caudate, and right occipital lobe, findings suspicious for cytotoxic edema. After acute stabilization, the patient demonstrated profound anterograde and retrograde amnesia, which improved gradually over days to weeks. She was eventually discharged to a skilled nursing facility. Conclusion: To our knowledge, this is the first reported case of profound amnesia secondary to cocaine-induced toxic encephalopathy with bilateral hippocampal involvement. These symptoms correlate with the implicated neuroanatomical structures. This case demonstrates that cocaine may be implicated in toxic encephalopathy affecting the brain’s gray matter and highlights a unique presentation of these findings.