Endoscopic Fenestration of Enlarging Symptomatic Thalamic Cysts: Twin Cases.

Encephalopathy is a heterogeneous clinical syndrome with numerous neurological and systemic etiologies. We report the case of a 67-year-old man, a chronic ethanol consumer, admitted with a one-week history of confusional syndrome. Initial laboratory tests revealed severe hypercalcemia, acute kidney injury, mild anemia, and hyperproteinemia. Serum ammonia levels were within normal limits, reducing the likelihood of hepatic encephalopathy despite the patient's chronic ethanol use. Cerebral imaging excluded acute cerebrovascular events, while abdominal ultrasound demonstrated splenomegaly and normal-sized kidneys. Serum protein electrophoresis and immunofixation identified a monoclonal IgG-kappa component, strongly suggestive of multiple myeloma. The patient's neurocognitive symptoms improved rapidly following systemic corticosteroid therapy and fluid-electrolyte rebalancing, confirming hypercalcemia as the primary mechanism of encephalopathy. Hypercalcemic encephalopathy as an initial manifestation of multiple myeloma is exceedingly rare. This case highlights the diagnostic complexity in elderly patients with multiple potential contributors to altered mental status, including chronic ethanol exposure and renal dysfunction. The presence of normal renal dimensions, unexplained hypercalcemia, and a monoclonal component should prompt evaluation for plasma cell malignancy. Early recognition of hypercalcemia-induced encephalopathy and prompt investigation for underlying hematologic malignancy are essential to prevent irreversible organ damage and to ensure timely initiation of specific therapy.

Mild traumatic brain injury (mTBI), including concussion, is common and has received a great deal of attention, but terminology and diagnosis can be confusing. Postconcussive symptoms (PCS) are well-described in the setting of concussion and isolated mTBI, but the individual symptoms are nonspecific and may be present in patients with extracranial injuries without TBI. The time course of PCS has not been well-characterized in patients with extracranial trauma, either with or without concomitant mTBI. We hypothesized that patients with mTBI with moderate/severe extracranial trauma would experience a unique, more severe and longer-lasting pattern of PCS with more negative impact on quality of life (QOL) when compared with similar trauma patients without mTBI. Prospective multicenter study (2018-2024) of patients aged 5 to 17 with extracranial Injury Severity Score >8, excluding moderate/severe TBI. Patients with and without mTBI (GCS 13-15, alteration of mental status or other signs/symptoms of TBI) were included. Patients were assessed at 1 week, 3 weeks, and 3 months with the Rivermead PCS Inventory and PedsQL QOL assessments. One hundred thirty-four patients were included: 53 (40%) had mTBI. Adolescent mTBI patients had significantly higher PCS Inventory scores than non-mTBI adolescents at T1 and T2. Symptoms persisted in >25% of both groups at T3. The QOL was impacted by the PCS burden. Although attrition compromised the statistical power of the study, many patients with moderate/severe extracranial trauma have a significant PCS burden at 3 months postinjury. Those with mTBI have a greater symptom burden and unique symptomatology compared with those without mTBI. Attention to diagnosis and treatment of mTBI and support and anticipatory guidance for all pediatric moderate/severe trauma patients is warranted. (J Trauma Acute Care Surg 2026;00:000-000. Copyright © 2026 Wolters Kluwer Health, Inc. All rights reserved.). Therapeutic/Care Management; Level IV.

The Warden procedure effectively corrects partial anomalous pulmonary venous connection (PAPVC) draining into the superior vena cava (SVC), yet superior vena cava obstruction remains a serious potential complication. This report describes a rare case of acute prosthetic graft thrombosis in the SVC following Warden procedure, presenting primarily with rapid neurological deterioration and initially lacking typical signs of superior vena cava syndrome. A 51-year-old female patient underwent a Warden procedure with autologous pericardial tube reconstruction of the superior vena cava. Postoperatively, her central venous pressure (CVP) progressively increased from 12 mmHg to a peak of 28 mmHg. Concurrently, her level of consciousness deteriorated from mild coma to deep coma with brainstem reflex suppression. Emergency cranial CT revealed no hemorrhage or significant edema. The combination of elevated CVP and deteriorating neurological function suggested acute SVC obstruction, prompting emergency exploration. Intraoperatively, extensive thrombosis within the autologous pericardial graft was confirmed. After replacement with a large-bore bovine pericardial graft, venous return was restored. The patient regained consciousness 8h after the second surgery with no neurological sequelae. Acute superior vena cava (SVC) obstruction can directly cause severe neurological dysfunction due to impaired cerebral venous return and reduced cerebral perfusion pressure. During the perioperative period, even in the absence of facial/neck edema or positive cranial CT findings, immediate investigation of superior vena cava anastomotic patency is warranted upon detection of abnormally elevated central venous pressure (CVP) accompanied by altered mental status.

Sialorrhea, or excessive drooling, is a distressing side effect of certain antipsychotic medications, including aripiprazole, clozapine, and olanzapine. We present the case of a 53-year-old female with bipolar I disorder who presented with altered mental status, dysphagia, a 2-day history of excessive drooling, and acute hypoxic respiratory failure. Despite being alert and responsive, she required intubation due to the inability to manage oral secretions. At the time, she had been taking aripiprazole 20mg once daily and lithium 450mg twice daily for about three months for bipolar 1 disorder, which were continued inpatient. Aripiprazole was discontinued on the third day of hospitalization. Standard treatments for sialorrhea, including anticholinergics such as scopolamine, glycopyrrolate, and sublingual atropine, were ineffective. Substantial improvement only occurred after the initiation of dexmedetomidine, an alpha-2 adrenergic agonist, on day nine, leading to decreased oral secretions and successful extubation. The patient was transitioned to oral clonidine, another alpha-2 adrenergic agonist, and remained extubated for the rest of her hospital stay. Upon further improvement, she was discharged on glycopyrrolate, a 3-day taper of clonidine, and trazodone, with bipolar I disorder management switched to valproic acid monotherapy. This case highlights the potential role of alpha-2 adrenergic agonists in managing refractory aripiprazole-induced sialorrhea, offering a viable alternative when traditional anticholinergic therapies are ineffective.

Hepatic encephalopathy (HE) is a frequent and life-threatening neurological complication of acute liver failure (ALF) encountered in the intensive care unit and remains a major determinant of short-term mortality and long-term neurological outcomes. Increasing evidence indicates that HE in ALF is primarily driven by hyperammonemia, with synergistic contributions from systemic inflammation, cerebral hemodynamic dysregulation, metabolic failure, and osmotic imbalance. These interacting mechanisms promote astrocytic swelling, disruption of the blood-brain barrier, cerebral edema, and intracranial hypertension. In patients with ALF, early recognition of cerebral involvement and systematic exclusion of alternative causes of altered mental status are essential. Given the dynamic and heterogeneous neurological manifestations of HE, reliance on isolated clinical, biochemical, or radiological parameters is insufficient. Multimodal neuromonitoring-integrating neurological examination, ammonia kinetics, cerebral hemodynamic assessment, and neuroimaging-allows more accurate assessment of cerebral injury and supports timely, targeted intervention. This review summarizes current evidence on the pathophysiology of HE in ALF with a focus on mechanisms relevant to intensive care practice. We highlight evidence-based strategies for cerebral protection, including early and sustained control of hyperammonemia with continuous renal replacement therapy, optimization of cerebral perfusion and osmotic balance, selective use of plasma exchange, and structured neurocritical care. An integrated management framework is proposed to guide prognostication and inform timely decisions regarding advanced liver support and liver transplantation in the ICU setting.

A previously healthy 23-year-old man developed acute-onset fever, headache, and a rapidly deteriorating altered mental status, occurring 11 days after the resolution of self-limiting respiratory symptoms. The cerebrospinal fluid and brain MRI findings were consistent with meningoencephalitis. A recent M. pneumoniae infection was confirmed using nasopharyngeal PCR and serological testing. Despite appropriate antimicrobial therapy, his neurological deterioration progressed. The addition of steroids and intravenous immunoglobulin resulted in a rapid and complete neurological recovery. This case underscores the immune-mediated pathogenesis of M. pneumoniae-associated meningoencephalitis, particularly in cases with a delayed neurological onset following respiratory prodromes. Clinicians should therefore consider early immunotherapy in conjunction with antibiotics, even in adult populations.

Delirium is an acute encephalopathic syndrome that is highly prevalent in critically ill adult patients. The occurrence of delirium carries serious negative implications for patient outcomes and is a frightening and distressing experience for patients. The significance of delirium occurrence as an indicator of acute illness severity and clinical deterioration is well recognised. This is reflected in the inclusion of altered mental status in a number of national illness severity scoring systems. An awareness and understanding of delirium in the critically ill adult is therefore of relevance to all adult nurses. This article provides an overview of delirium in the critically ill adult patient, discussing current knowledge and recommended practice across key areas. These include the definition and classification of delirium; the implications of delirium for patient outcomes and experience; the aetiology and pathophysiology of delirium; delirium assessment tools used with critically ill patients and recommended approaches to prevention and management. The article will enable practitioners to develop a current understanding of key areas relating to delirium in the critically ill adult patient and encourage a reflective approach to considering the implications for practice.

Targeted Delirium Screening in At-risk Older Adults in the Emergency Department Improves Screening Rates

Associations between systemic vasculitis and hospitalization outcomes in adults with acute ischemic stroke: An analysis of the US National Inpatient Sample, 2006-2020.

Neutral-pH, low-glucose degradation product peritoneal dialysis (PD) solutions are widely used because of their favorable biocompatibility. These solutions are typically packaged in dual-chamber bags and must be mixed immediately before use. Although the mixing procedure is simple, improper preparation may occur, particularly in patients with cognitive impairment, potentially resulting in unintended electrolyte exposure. We report a case of severe hyponatremia with altered mental status associated with inadvertent infusion of an unmixed neutral-pH PD solution in an elderly patient undergoing automated peritoneal dialysis (APD). A man in his eighth decade with diabetic nephropathy and progressive cognitive decline presented with somnolence and severe hyponatremia after a dual-chamber PD bag with an unopened septum was connected. Based on the clinical course and the finding that a PD solution bag with an unopened inter-chamber septum had been connected, hyponatremia due to exposure to an unmixed dialysate compartment was diagnosed. Management consisted of immediate discontinuation of the improperly prepared dialysate and correction using appropriately mixed PD solutions, without administration of hypertonic saline. Serum sodium levels improved gradually without neurological complications, accompanied by recovery of mental status. This case highlights a rare but serious complication related to improper preparation of dual-chamber PD solutions. Increased awareness of this risk and careful monitoring of vulnerable patients, particularly those with cognitive impairment, are essential to ensure safe home PD therapy.

ABSTRACTHepatitis A virus (HAV) and hepatitis E virus (HEV) are common causes of acute viral hepatitis in developing countries where inadequate sanitation and contaminated water supplies facilitate fecal–oral transmission. Although both infections are usually self‐limiting, co‐infection may result in atypical presentations and pose diagnostic challenges. We report the case of a previously healthy 14‐year‐old girl who presented with a 5‐day history of nausea, vomiting, and anorexia, followed by sudden‐onset jaundice and dark urine. She denied fever, abdominal pain, pruritus, bleeding manifestations, or altered mental status. Physical examination revealed marked icterus without hepatosplenomegaly or stigmata of chronic liver disease. Laboratory investigations demonstrated significant hyperbilirubinemia and elevated liver transaminases. Serological testing confirmed acute HAV and HEV co‐infection with positive anti‐HAV IgM and anti‐HEV IgM antibodies. Abdominal ultrasonography showed a normal‐sized liver with altered echogenicity and a characteristic “starry sky” appearance, along with gallbladder wall thickening without calculi or sludge. The patient received supportive treatment, including intravenous fluids, antiemetics, and symptomatic care. Her clinical condition improved steadily, with resolution of symptoms and progressive normalization of liver function tests during hospitalization. She was discharged in stable condition and remained asymptomatic at 14‐day follow‐up, with complete biochemical and radiological recovery. This case highlights that HAV–HEV co‐infection can present with isolated jaundice and minimal systemic symptoms despite significant hepatic involvement. Recognition of characteristic imaging findings and timely serological evaluation can facilitate early diagnosis. Favorable outcomes can be achieved with supportive management, while prevention through vaccination, safe drinking water, and improved hygiene remains essential in endemic regions.

Major complications after reduction malarplasty are uncommon and generally non-life-threatening, but intracranial infectious complications associated with this procedure have not been reported. This paper presents a fatal case of postoperative meningitis to highlight this potential risk. A 35-year-old woman presented with an altered mental status ~2 weeks after undergoing revisional reduction malarplasty. The imaging and laboratory findings were suggestive of bacterial meningitis with intracranial involvement. Although surgical details were unavailable, postoperative craniofacial imaging indicated the possibility of dural violation by the fixation hardware, which may have served as a direct conduit for infection. This case shows that reduction malarplasty, though generally safe, can lead to fatal intracranial infections, albeit rare. Careful surgical planning and accurate fixation are crucial for preventing inadvertent dural penetration, and early recognition of neurologic symptoms is essential to improve the outcomes.

The influence of mild traumatic brain injury on attentional Bias: Preliminary evidence.

West Nile virus neuroinvasive disease (WNND) most commonly presents as meningitis, encephalitis, or acute flaccid paralysis, with variable neuroimaging findings. While MRI abnormalities classically involve deep gray matter and brainstem structures, hemorrhagic manifestations are rarely reported. We report a 77-year-old woman who presented with rapidly progressive altered mental status following a brief febrile prodrome. Cerebrospinal fluid studies demonstrated a lymphocytic pleocytosis consistent with aseptic meningitis. Brain MRI revealed an acute lacunar infarct and diffuse cerebral microhemorrhages initially concerning for cerebral amyloid angiopathy. During hospitalization, she developed livedo reticularis-like peripheral skin changes prompting evaluation for autoimmune or vasculitic etiologies. Extensive infectious and autoimmune testing was ultimately notable for positive serum and CSF West Nile virus serologies, confirming neuroinvasive WNV infection. Despite transient neurologic improvement, her clinical course deteriorated, and she died following transition to comfort-focused care. This case highlights diffuse cerebral microhemorrhages as a potential finding in WNND, although their attribution remains uncertain. These findings may reflect underlying neurovascular inflammatory injury related to WNV or may represent coincident pathology and can mimic other small-vessel or autoimmune pathologies, complicating early diagnostic evaluation. Recognition of this expanded radiographic and clinical spectrum may aid timely diagnosis of WNND in patients with atypical presentations.

BackgroundBlunt cerebrovascular injury (BCVI) is a serious complication of blunt trauma with high rates of morbidity and mortality. There is evidence to support universal screening, but this raises concerns about cost, radiation exposure, and system burden. This study examined the connection between clinical factors at initial presentation and BCVI risk to identify opportunities to improve imaging utilization.MethodsWe analyzed patients with blunt injury from the North Carolina Trauma Registry (2016-2021). Blunt cerebrovascular injury was identified using ICD-10 codes. Clinical risk factors evaluated were low Glasgow Coma Score (GCS), significant supraclavicular injury (above-the-clavicle (ATC) injury), and trauma activation level. Logistic regression was used to identify predictors of BCVI.ResultsAmong 198 211 blunt trauma patients, 1336 (0.70%) were diagnosed with BCVI. The highest prevalence was among patients with both a low GCS and significant ATC injury (4.0%), followed by those with only ATC injury (1.5%). Only two cases (0.001%) occurred in patients with neither indicator. The adjusted odds ratios for BCVI were 3.0 (95% CI: 2.6-3.5) for low GCS and 2.8 (95% CI: 2.4-3.2) for level 1 trauma activation. Above-the-clavicle injury was nearly a perfect predictor of BCVI.ConclusionsPatients without altered mental status or significant injuries above the clavicle had an extremely low risk of BCVI. Although liberal screening strategies remain important to prevent missed injuries, our findings suggest that a clearly defined low-risk subgroup may not require routine CTA screening. Prospective, multicenter validation of contemporary screening criteria is needed to refine risk stratification and optimize cross-sectional imaging utilization.Level of EvidenceLevel III, Prognostic/Epidemiological.

EEG reactivity (EEG-R) is currently classified as present, absent, or stimulus-induced rhythmic, periodic, or ictal discharges, per the American Clinical Neurophysiology Society's 2021 Critical Care EEG Terminology. However, our previous study suggested that there may be other forms of EEG-R that warrant distinction, potentially associated with different comorbidities and outcomes. We, therefore, aimed to define "typical" vs "atypical" EEG-R, referring to increased power of arrhythmic alpha/beta frequencies vs delta frequencies after stimulation, respectively, and to identify their associated comorbidities and outcomes. This was a retrospective single-center study, examining adult patients admitted between 2015 and 2022, who underwent continuous EEG (cEEG) as standard-of-care work-up for their illnesses. Univariate testing and logistic regression were performed. The primary patient outcome at hospital discharge was categorized by the modified Rankin Scale (0-2: good; 3-6: poor). The primary independent variable was the presence of typical vs atypical EEG-R. Additional covariates included age, presence of critical illness, and acute intracranial and nonintracranial pathologies. A total of 238 patients with typical EEG-R (median age 54 years, female 50%) and 322 with atypical EEG-R (median age 60 years, female 50%) were identified. Patients with typical EEG-R more commonly underwent cEEG for spell capture of non-neurological episodes (20% vs 0%, Δ20%, 95% CI 15-25, p < 0.0001) or primary seizures (13% vs 2%, Δ11%, 95% CI 7-16, p < 0.0001). Patients with atypical EEG-R were more critically ill (88% vs 32%, Δ56%, 95% CI 49-63, p < 0.0001) with more intracranial (69% vs 45%, Δ24%, 95% CI 15-32, p < 0.0001) and nonintracranial pathologies (92% vs 38%, Δ54%, 95% CI 48-61, p < 0.0001) and concomitant altered mental status (47% vs 30%, Δ17%, 95% CI 9-25, p < 0.0001). These patients were hospitalized longer (median 24.0 vs 7.0 days, Hodges-Lehmann estimator 14 days, 95% CI 12-17, p < 0.0001) with higher rates of poor outcomes (74% vs 22%, Δ52%, 95% CI 45-59, p < 0.0001). In the logistic regression model, the inverse association between atypical EEG-R and good outcome remained significant after adjusting for other covariates (odds ratio 0.20, 95% CI 0.11-0.34, p < 0.0001). Granular, frequency-based assessments of EEG-R, such as the differentiation between typical vs atypical EEG-R, may provide further insight into the potential outcomes of patients with altered states of consciousness. Limitations of this study include the single-center retrospective nature.

Subacute Encephalopathy with Seizures in Alcoholics (SESA) is a rare neurological syndrome characterized by altered mental status, periodic EEG discharges, and neuroimaging abnormalities, typically occurring in individuals with chronic alcohol use. Its progression to status epilepticus (SE), including refractory and super-refractory forms, is poorly documented. We present a super-refractory status epilepticus (SRSE) case in a patient with confirmed SESA and conduct a systematic review of the literature to explore the relationship between SESA and SE. A systematic literature review was performed using MEDLINE (accessed through PubMed), Scopus, EMBASE and Google Scholar, in accordance with the PRISMA guidelines. Data were extracted on demographics, EEG and imaging findings, treatment approaches, and outcomes. Our patient developed SRSE in the setting of chronic hepatic dysfunction. The patients responded to a combination of propofol and ketamine and obtained long-term seizure control with vagus nerve stimulation (VNS). Type 3 oligoclonal bands were detected in the CSF, although it is considered a non-specific marker of neuroinflammation. The literature review identified 7 cases of SE in SESA, with variable clinical presentations. While levetiracetam and valproic acid were the most employed treatments, benzodiazepines were notably absent from first-line protocols. Phenytoin and lacosamide resulted as favorable alternatives. SE in the context of SESA requires tailored therapeutic strategies due to hepatic comorbidities and diagnostic ambiguity with NCSE. Our report supports the cautious use of propofol and ketamine in SRSE, as well as the efficacy of VNS in long-term seizure control.

Inability to answer questions: a pragmatic red flag in altered mental status.

A 21‐year‐old woman was admitted to our emergency department following a 3‐h loss of consciousness after intentional ingestion of multiple psychotropic medications. Initial management included gastric lavage, catharsis, intravenous fluid resuscitation, diuresis, and hemoperfusion to enhance toxin elimination. Shortly after admission, she developed rapid respiratory deterioration, high fever, limb tremors, and tachycardia. Emergency endotracheal intubation and mechanical ventilation were initiated, along with sedation and active cooling measures. A comprehensive workup—including complete blood count, procalcitonin (PCT), blood, urine, and sputum cultures, and chest CT—was performed to exclude infectious etiologies. After ruling out other potential causes, a diagnosis of serotonin syndrome was related to quetiapine fumarate overdose. With aggressive supportive care and enhanced drug clearance, the patient gradually regained consciousness, achieved hemodynamic stability, and was successfully weaned from mechanical ventilation before being discharged without neurological sequelae. Clinicians should maintain a high index of suspicion for serotonin syndrome in patients with quetiapine overdose who present with altered mental status, autonomic instability, hyperthermia, and neuromuscular abnormalities. Early recognition and prompt symptomatic intervention are critical to improving clinical outcomes.