BACKGROUND: Argon gas poisoning is an often overlooked yet critical public health concern with the potential for severe and persistent neurological consequences. Current treatment protocols primarily focus on acute-phase management, but a comprehensive understanding of the long-term neurological effects remains incomplete.
METHODS: A 22-year-old male worker was found unconscious in the furnace room of an argon production facility. After regaining consciousness, he presented with symptoms of dizziness, headache, fatigue, and irritability. Neurological examination revealed impairments in both recent and remote memory, notably pronounced short-term memory deficits and reduced arithmetic skills.
METHODS: Argon gas poisoning, hypoxic encephalopathy, and mild hepatic and renal dysfunction.
METHODS: Upon admission, symptomatic supportive measures included oxygen therapy via nasal cannula (3 L/min), daily hyperbaric oxygen therapy (1.5 ATA, 60 minutes), oral neurotrophic methylcobalamin (0.5 mg, 3 times daily), and intravenous vitamin C infusion (2 g daily) to scavenge oxygen free radicals.
RESULTS: A 2-year telephone follow-up indicated persistent short-term memory impairment, particularly with memorizing numbers. In a memory test, he achieved a digit span forward of 5 but a digit span backward of 2, indicating impairment. Despite these challenges, his daily life and work performance remained largely unaffected.
CONCLUSIONS: This case offers valuable insights into the biological mechanisms underlying prolonged neurological sequelae following asphyxiating gas exposure, specifically the persistent impairment of hippocampal function.

This is the case of a 26-year-old male who developed Anton Babinski syndrome (ABS), quadriplegia, and delayed post-hypoxic leukoencephalopathy (DPHL) after an opioid overdose. He exhibited cortical blindness, visual anosognosia, and confabulation upon awakening. Several days later, he experienced acute psychosis and agitation. T2-FSE MRI revealed extensive supratentorial leukoencephalopathy involving both cerebral hemispheres, extending to the posterior corpus callosum due to cerebral anoxia. This case report will discuss different types of encephalopathy from opioid abuse, ABS, visual anosognosia, and confabulation\'s pathogenic mechanisms. It underscores the necessity of researching substance-induced neuropsychiatric disorders and their pathogenic mechanisms for effective treatments.

Delayed post-hypoxic encephalopathy can occur after an episode of anoxia or hypoxia. Symptoms include apathy, confusion, and neurological deficits. We describe a 47-year-old male patient who inhaled gas from a kitchen stove liquid petroleum gas cylinder. He was diagnosed with hypoxic ischaemic encephalopathy 12 hours after his emergency department admission. He received six sessions of hyperbaric oxygen treatment (HBOT) and was discharged in a healthy state after six days. Fifteen days later, he experienced weakness, loss of appetite, forgetfulness, depression, balance problems, and inability to perform self-care. One week later, he developed urinary and fecal incontinence and was diagnosed with post-hypoxic encephalopathy. After 45 days from the onset of symptoms, he was referred to the Underwater and Hyperbaric Medicine Department for HBOT. The patient exhibited poor self-care and slow speech rate, as well as ataxic gait and dysdiadochokinesia. Hyperbaric oxygen was administered for twenty-four sessions, which significantly improved the patient\'s neurological status with only hypoesthesia in the left hand remaining at the end of treatment. Hyperbaric oxygen has been reported as successful in treating some cases of delayed neurological sequelae following CO intoxication. It is possible that HBO therapy may also be effective in delayed post-hypoxic encephalopathy from other causes. This may be achieved through mechanisms such as transfer of functional mitochondria to the injury site, remyelination of damaged neurons, angiogenesis and neurogenesis, production of anti-inflammatory cytokines, and balancing of inflammatory and anti-inflammatory cytokines.

OBJECTIVE: Cerebral anoxia is the absence or near absence of oxygen in the brain\'s arterial blood supply. One cause of cerebral anoxia is acute cardiorespiratory failure, which, if left untreated, can lead to brain tissue necrosis, causing an anoxic brain injury (AnBI). AnBI causes a range of motor and cognitive deficits, though long-term (> 2.0 years) neuropsychological sequelae of AnBI are not well understood.
METHODS: A 66-year-old female presented for a neuropsychological evaluation 5.4 years status post myocardial infarction complicated by cardiac arrest requiring cardiopulmonary resuscitation (CPR) for one hour. The patient was comatose for two weeks and initially exhibited a 20-year- retrograde amnesia (RA). She reportedly reached a cognitive plateau approximately 2.5 years after the original insult. 4.9 years after the original insult, a new emergence of severe functional impairment was observed. Relevant medical history was significant for hypertension, hypocholesterolemia, and coronary artery disease. Neuroimaging revealed mild cortical atrophy and mild microvascular ischemia.
RESULTS: Her neurocognitive profile demonstrated impairments in all assessed cognitive domains. Her MMSE score declined 11 points in 2 months. Behavioral observations and assessment findings demonstrated features of Balint\'s Syndrome (e.g., optic apraxia, optic ataxia, simultanagnosia).
CONCLUSIONS: The patient\'s AnBI was severe, given multiple markers: CPR duration, coma length, and RA. Moreover, her decline in functional ability demonstrates that a resurgence of functional impairment 5.4 years status post a severe AnBI is possible, highlighting the importance of neuropsychological monitoring over time.

BACKGROUND: Bradycardia frequently occurs in heart-transplanted patients, mainly as a temporally restricted manifestation early after transplantation and often without symptoms. A high-degree atrioventricular block is mostly symptomatic through cerebral hypoxia induced through cerebral hypoperfusion. Only a few published cases show this specific electroencephalography result in this context. The purpose of this case is to bring attention to atypical manifestations of typical cardiac complications after heart transplantation and the importance of perseverance in the diagnostic.
METHODS: A Central European man in his 50s with history of heart transplantation 31 years previously was admitted to the internal medicine ward for short-lived recurrent episodes of generalized weakness with multiple falls but without loss of consciousness. During routine electroencephalography, the patient perceived this recurrent sensation. This episode coincided with a transient third-degree atrioventricular block followed 8-10 seconds later by a generalized slowing of the electroencephalography, reflecting cerebral hypoxia due to cerebral hypoperfusion. Holter monitoring confirmed the diagnosis. A pacemaker was implanted, consequently resolving the episodes.
CONCLUSIONS: This case report illustrates the pathophysiological central hypoxemic origin of episodes of generalized weakness caused by a high-degree atrioventricular block in a patient surviving 29 years after heart transplant. It highlights the benefit of electroencephalography as a diagnostic tool in well-selected patients.

UNASSIGNED: The association of COVID-19 with diabetes mellitus is bidirectional. In one direction, diabetes mellitus is associated with an increased risk of severe COVID-19. In the opposite direction, in patients with COVID-19 new-onset diabetes mellitus, severe diabetic ketoacidosis and severe metabolic complications have been described.
UNASSIGNED: This report describes two patients with diabetes mellitus who came to our hospital with ketoacidosis resulting from new-onset diabetes mellitus. We describe the clinical course and the management approach during the COVID-19 pandemic.
UNASSIGNED: COVID-19 is associated with metabolic complications such as severe diabetic ketoacidosis.
UNASSIGNED: La relación entre la enfermedad por el coronavirus de 2019 (COVID-19) secundaria a SARS-CoV-2 y la diabetes mellitus es bidireccional. Por un lado, la diabetes mellitus se asocia con un mayor riesgo de COVID-19 grave. Por otro lado, en pacientes con COVID-19 se han observado diabetes mellitus de nueva aparición con presentaciones de cetoacidosis diabética y complicaciones metabólicas graves de dicha presentación.
UNASSIGNED: En este informe, describimos a dos pacientes pediátricos con diabetes mellitus que acudieron a nuestro hospital con cetoacidosis diabética, de debut inicial. Describimos la evolución y el manejo clínico y terapéutico durante la pandemia de COVID-19.
UNASSIGNED: La infección por COVID-19 puede precipitar complicaciones como cetoacidosis diabética severa.

Paroxysmal sympathetic hyperactivity (PSH) is a clinical syndrome of episodic sympathetic hyperactivities following severe acquired brain injury. It is characterized by paroxysmal hyperthermia, tachycardia, hypertension, tachypnea, excessive diaphoresis, and specific posturing. Although the persistence of PSH increases the risk of several adverse events and worsens the prognosis, pharmacological treatments for PSH have not yet been clearly established. We report the valuable case of a 60-year-old man who developed PSH following hypoxic encephalopathy, which was effectively treated with a combination therapy of gabapentin and guanfacine. The present case suggests that combination therapy with gabapentin and guanfacine may be a therapeutic option for PSH.

Delayed Post Hypoxic Leukoencephalopathy (DPHL) is a syndrome that occurs after hypoxia, and can present with a variety of neuropsychiatric symptoms, including catatonia and paroxysmal sympathetic hyperactivity (PSH). The gold standard for the treatment of catatonia is electroconvulsive therapy (ECT). However, ECT can exacerbate the paroxysms of sympathetic hyperactivity and complicate recovery from DPHL. The treatment of PSH is not well established.
We present a case of a patient with multiple opiate overdoses who presented with altered mental status. He was diagnosed with catatonia and subsequently treated with ECT. His clinical condition worsened, and a revised diagnosis of PSH was established. The patient\'s condition improved with medical management.
This case highlights the need to distinguish between these two related symptom clusters, as the incidence of DPHL and opioid overdose related neuropsychiatric problems increase. This distinction can greatly influence the course of treatment, and the need to consider alternative treatments.

暂无摘要。

A 76-year-old man suffering from chest pain was admitted to our hospital with a suspected acute myocardial infarction (AMI). Emergent coronary angiography revealed a totally occluded proximal left circumflex artery (LCX). During primary percutaneous coronary intervention, his blood pressure suddenly fell within seconds, and he developed pulseless electrical activity (PEA). Surprisingly, the 12-lead electrocardiogram (ECG) findings including the heart rate remained unchanged before and after the PEA, but a heart rate reduction and asystole occurred a few minutes after developing PEA. After tracheal intubation and mechanical assistance by venoarterial extracorporeal membrane oxygenation (VA-ECMO), the sudden onset of PEA appeared to be caused by cardiac tamponade due to a blowout-type left ventricular free wall rupture (BO-LVFWR) diagnosed by transthoracic echocardiography. While pericardiocentesis was performed and the drained blood was directly continuously perfused intravenously to keep the VA-ECMO flow, the patient was moved to the operation room. The surgical findings revealed a solitary BO-LVFWR due to a lateral AMI, and a direct closure was performed. Successful perioperative management, oral medication administration, and rehabilitation lead to the patient being transferred to a rehabilitation hospital without any serious cerebral damage. This case report suggested the detailed onset pattern of a BO-LVFWR followed by a rapid diagnosis by echocardiography and lifesaving treatment.