Dementia with non-convulsive seizures: a case report

Non-convulsive seizures (NCSs) are highly treatable, but appropriate management is usually delayed because of inaccurate diagnoses as a result of variable clinical presentations, including an altered mental state. It is difficult to detect NCSs in patients with dementia. We report a case of NCS superimposed on cognitive decline caused by Alzheimer’s dementia. The patient’s history was carefully recorded. An electroencephalogram was recorded with sphenoidal electrodes, which showed epileptiform discharges in the right mesial temporal lobe and focal, sharply contoured, slow wave activity in the left fronto-temporal area, suggesting an epileptic origin contributing to the patient’s cognitive decline. After treatment with antiepileptic drugs, the patient’s cognitive functioning gradually improved. An accurate diagnosis of NCS relies on performing a detailed inventory of a patient’s history, thorough physical and neurological examinations, and electroencephalogram recordings. In patients with cognitive decline, testing for NCS should always be included in the differential diagnosis of cognitive impairment, even in the case of dementia. Early administration of antiepileptic drug therapy is the mainstay treatment for reversing the condition and for preventing prolonged insults from neurological sequelae.

Acute and chronic toxicity of ethyl chloride insufflation in two patients

Objective: Inhalant abuse has been a source of increasing concern because of its easy accessibility and affordability. Anecdotal reports have previously described ethyl chloride as a potential cause of altered mental state and neurologic symptoms. Its use has been thought to be found most often in adolescents and among men who have sex with men. Common acute symptoms include confusion, dizziness, headache, nausea, and fatigue. We describe two cases of adult patients who presented to one general hospital emergency department with ethyl chloride toxicity. The first presented with acute delirium; the second with a picture of chronic neurological symptomatology. It is important that clinicians become familiar with ethyl chloride intoxication because of its prevalence and potential to present with varying acute and chronic symptomatology.

A Man With Flulike Symptoms and Hemorrhagic Brain Lesions

A 52-year-old man is admitted to a neurosciences intensive care unit during winter for management of seizures requiring mechanical ventilation. Two days earlier he reported cough and myalgia. He was found seated on the couch with altered mental state and was minimally responsive. Upon arrival to the emergency department he was febrile at 38.8 °C and tachycardic. Complete blood cell count showed leukocytosis (11.1×109 cells/L, neutrophilic predominance). Computed tomography of the head showed an area of hypodensity in the left temporal lobe. During computed tomography, the patient had generalized convulsions requiring lorazepam, fosphenytoin, and levetiracetam, followed by initiation of a continuous midazolam infusion before seizures were controlled. He was started on broad-spectrum antimicrobials, including acyclovir, and a lumbar puncture was performed. Cerebrospinal fluid protein concentration was 196 mg/dL, and he had 10 white blood cells/µL with lymphocyte predominance. There was no hypoglycorrhachia. After 24 hours, the patient was weaned from the midazolam infusion and maintained on levetiracetam monotherapy. He was extubated but remained encephalopathic. Magnetic resonance imaging performed the day after admission demonstrated numerous T2 hyperintense lesions throughout both cerebral hemispheres including both mesial temporal lobes and right thalamus. Nasopharyngeal polymerase chain reaction was positive for influenza virus A, which was later typed further and identified as pandemic 2009 H1N1 virus. A diagnosis of influenza-associated encephalopathy/encephalitis was made. The patient was treated with oseltamivir, as well as high-dose intravenous methylprednisolone. His encephalopathy gradually improved. Repeated imaging at 3-month follow-up showed resolution of the previously seen abnormalities. His neurologic examination was normal. Postinfectious or parainfectious autoimmunity syndromes refer to neurologic signs and symptoms that develop during or after an infection but are not thought to be caused by direct infection of the nervous system.

Neuroleptic Malignant Syndrome Associated with Rhabdomyolysis Induced by Antipsychotic Agents: A Rare Occurrence

Neuroleptic Malignant Syndrome (NMS) is a medical emergency of infrequent presentation in Emergency department, which is associated with the use of psychotropic agents, classical and atypical antipsychotics. We report a case involving a 56-year-old male patient diagnosed with schizophrenia and depression for 30 years, who had been receiving Amisulpride, Trifluoperazine, Clozapine, and Amitryptiline as part of his treatment. This patient presented with symptoms of NMS with fever, muscle rigidity, altered mental state, elevated CPK, Urea, and S. Creatinine levels. NMS may be responsible for serious rhabdomyolysis, acute respiratory distress syndrome, and disseminated intravascular coagulation. We hypothesize the occurrence of acute renal failure precipitated by NMS. His treatment included the withdrawal of all psychotropic agents, Bromocriptine, and other supportive measures.

Neuroleptic Malignant Syndrome Applied with Targeted Temperature Management

Neuroleptic malignant syndrome (NMS) is a life-threatening neurologic emergency associated with the use of dopamine receptor-antagonist properties or the rapid withdrawal of dopaminergic medications. NMS is characterized by refractory hyperpyrexia, altered mental state, dysautonomia, and rigor. If hyperpyrexia persists, it can result in multiorgan failure. Herein, we report a case of NMS occurring after metoclopramide administration in a patient with pontine hemorrhage, which was successfully treated with targeted temperature management using a surface cooling device.

#3125 Novel framework for neurocognitive COVID-19 assessment

BackgroundThe neurotrophic effects of Covid-19 are becoming increasingly recognized, with altered mental state now being the second most common presenting complaint insert numbers. A key question is whether this has long term consequences. Cognitive problems are commonly reported in patients 3 months after acute infection as part of the so called Long-Covid syndrome. However, the underlying cause is not well understood. Candidate explanations include legacy from encephalitis and stroke; however, other complications such as the sequelae, delirium, remain underexplored. Furthermore, little consideration has been given to functional cognitive disorders and the cognitive consequences of depression, anxiety and fatigue.AimsWe propose a structured approach to clinical assessment for clinicians reviewing late cognitive complaints after COVID 19.MethodsWe created our own unique framework for neurocognitive Covid assessment based upon a review of the literature.ResultsCovid status- Any positive test. If not review of core symptoms such as breathlessness, headache, anosmia, nasal obstruction, cough, myalgia, or gustatory dysfunction; duration, extent of exposure to Covid confirmed cases. Consider rapid antibody testing.Neuropsychiatric history- Part 1 symptoms at onset- in particular disruptions of consciousness and altered mental state. Acute memory impairment, anterograde/retrograde and with/without a temporal gradient. neurocognitive function. ITU admission and oxygen requirements.Part 2 Current cognitive and mental state- in addition to standard history seek evidence of internal inconsistency of memory symptoms and attentional dysregulation. Has social cognition and meta-cognition been affected. Note attribution bias i.e. no Im not depressed, I cant enjoy anything because of my symptomsBackground history- subtle suggestion of neurodegeneration and depression, anxiety and functional symptoms should be explored.MRI findings- signal changes in the medial temporal lobe, nonconfluent multifocal white matter hyperintense lesions, and isolated white matter microhemorrhages.Novel biomarkers IL-6, MCP-1, and IP-10.ConclusionCognitive symptoms are common after confirmed and assumed COVID exposure. We propose a framework for neuropsychiatric assessment and the use of adjuvant imaging and potential biomarkers.

Recurrent Altered Mental State Associated with Nonhepatic Hyperammonemia Presented in an Elderly Female Patient: Probable Late-Onset Urea Cycle Disorder

Altered mentality associated with hyperammonemia is usually diagnosed in patients with liver disease. Nonhepatic hyperammonemia may be present in critically ill patients or may be caused by high protein diets or certain drugs. Urea cycle disorders (UCDs) rarely present with altered mentality with hyperammonemia in adult patients. An 82-year-old female visited our hospital with complaints of abnormal behavior and confusion. Routine blood tests revealed elevated serum ammonia. Her mentality and serum ammonia level normalized after lactulose enema and she was discharged thereafter. However, she was later re-admitted because of recurrent altered mentality. Amino acid analysis revealed that serum levels of ornithine and glutamine increased significantly, whereas the levels of alanine and glutamic acid increased slightly, and the levels of arginine, lysine, and citrulline were normal, which were probably caused by reduced activity of the mitochondrial ornithine carrier-1. Although our patient was not diagnosed genetically, this case illustrates the under-recognized fact that UCD can occur in a senile age. Clinical suspicion of UCDs in patients with hyperammonemia is critical for early diagnosis and to prevent the significant neurologic sequelae.

Wernicke’s encephalopathy in women with hyperemesis gravidarum – Case series and literature review

Whilst nausea affects around 80% of pregnant women, hyperemesis gravidarum, an extreme form of the same, affects only 0.5% to 3%, but may lead to severe nutritional deficiency. Wernicke’s encephalopathy is an acute neuropsychiatric disorder which occurs due to thiamine deficiency and needs emergency treatment to prevent neurological morbidity and mortality. Wernicke’s encephalopathy is characterised by a clinical triad of oculomotor abnormalities, cerebellar dysfunction and altered mental state. Korsakoff’s psychosis is a chronic condition and consequence of Wernicke’s encephalopathy, resulting from its delayed treatment. Wernicke’s encephalopathy is a well-known complication of chronic alcohol abuse. Not many are aware of its association with hyperemesis gravidarum. Although it is a rare complication, if not diagnosed and treated promptly, it may result in permanent and irreversible neurological sequelae. The objective of our retrospective observational study was to analyse the clinical profile and outcome (short and long term) in a rare yet preventable complication of pregnancy.

Unexpected presentation of acute porphyria

Acute porphyrias are rarely reported in Southeast Asia. They may be underdiagnosed due to their clinical mimicry and lack of awareness among physicians. There is a common cognitive bias to gravitate towards common conditions. In this case report, a 28-year-old woman, who presented with seizures, rhabdomyolysis hyponatraemia and altered mental state, was initially diagnosed as amphetamine overdose. She had presented 3 days prior with abdominal pain, treated for acute cystitis and discharged. On readmission for seizures a day later, she was extensively worked up for altered mental state. Despite normalisation of serum sodium concentration and control of her seizures, she remained unwell. Further investigations later confirmed a diagnosis of acute porphyria. The aim of this case report is to highlight the non-specific nature of presentation of acute porphyria and the importance of considering it as a differential diagnosis in cases of abdominal pain with neuropsychiatric features.