Causes of alterations to level of consciousness

Author(s):  
Tina Moore
2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Manon Carrière ◽  
Helena Cassol ◽  
Charlène Aubinet ◽  
Rajanikant Panda ◽  
Aurore Thibaut ◽  
...  

Abstract Auditory localization (i.e. turning the head and/or the eyes towards an auditory stimulus) is often part of the clinical evaluation of patients recovering from coma. The objective of this study is to determine whether auditory localization could be considered as a new sign of minimally conscious state, using a multimodal approach. The presence of auditory localization and the clinical outcome at 2 years of follow-up were evaluated in 186 patients with severe brain injury, including 64 with unresponsive wakefulness syndrome, 28 in minimally conscious state minus, 71 in minimally conscious state plus and 23 who emerged from the minimally conscious state. Brain metabolism, functional connectivity and graph theory measures were investigated by means of 18F-fluorodeoxyglucose positron emission tomography, functional MRI and high-density electroencephalography in two subgroups of unresponsive patients, with and without auditory localization. These two subgroups were also compared to a subgroup of patients in minimally conscious state minus. Auditory localization was observed in 13% of unresponsive patients, 46% of patients in minimally conscious state minus, 62% of patients in minimally conscious state plus and 78% of patients who emerged from the minimally conscious state. The probability to observe an auditory localization increased along with the level of consciousness, and the presence of auditory localization could predict the level of consciousness. Patients with auditory localization had higher survival rates (at 2-year follow-up) than those without localization. Differences in brain function were found between unresponsive patients with and without auditory localization. Higher connectivity in unresponsive patients with auditory localization was measured between the fronto-parietal network and secondary visual areas, and in the alpha band electroencephalography network. Moreover, patients in minimally conscious state minus significantly differed from unresponsive patients without auditory localization in terms of brain metabolism and alpha network centrality, whereas no difference was found with unresponsive patients who presented auditory localization. Our multimodal findings suggest differences in brain function between unresponsive patients with and without auditory localization, which support our hypothesis that auditory localization should be considered as a new sign of minimally conscious state. Unresponsive patients showing auditory localization should therefore no longer be considered unresponsive but minimally conscious. This would have crucial consequences on these patients’ lives as it would directly impact the therapeutic orientation or end-of-life decisions usually taken based on the diagnosis.


2021 ◽  
Vol 14 (5) ◽  
pp. e240647
Author(s):  
Blair Wallace ◽  
Daniel Edwardes ◽  
Christian Subbe ◽  
Muhammed Murtaza

A 40-year-old patient was admitted through the acute medical take with pleuritic chest pain and rigours. He had a medical history of opiate dependence and was receiving 60 mg of methadone once daily. He was diagnosed with a community-acquired pneumonia and treated with amoxicillin and clarithromycin. After administration of only two concomitant doses of methadone and oral clarithromycin, he developed an opioid toxidrome with type-2 respiratory failure, a decreased level of consciousness and pinpoint pupils. The patient was treated with naloxone and his symptoms improved. Retrospectively, it was suspected that an interaction between clarithromycin and methadone might have contributed to the toxidrome. Respiratory failure has not been previously prescribed for this combination of medication and is of high importance for physicians and pharmacists around the world.


2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Chikanori Tsutsumi ◽  
Toshiya Abe ◽  
Tomohiko Shinkawa ◽  
Hideyuki Watanabe ◽  
Kazuyoshi Nishihara ◽  
...  

Abstract Background Wernicke’s encephalopathy (WE) is an acute neuropsychiatric disorder resulting from thiamine (vitamin B1) deficiency, frequently associated with chronic alcoholism and total parenteral nutrition without thiamine. However, only a few reports have focused on the relationship between WE and subtotal stomach-preserving pancreatoduodenectomy (SSPPD). Case presentation A 71-year-old woman underwent SSPPD for an adenocarcinoma of the ampulla of Vater. Although there had been no evidence of recurrence, the patient was treated with antibiotics for cholangitis at 12 and 31 months, respectively, post-surgery. Thereafter, the patient presented with vomiting and disorientation 33 months after surgery. Although she was admitted and underwent closer inspection by a neurologist and a psychiatrist, the exact cause of these syndromes remained unknown. The psychiatrist measured thiamine concentration to examine the cause of disorientation. After 6 days, her level of consciousness worsened. Magnetic resonance imaging of the head showed symmetrically multiple abnormal hyperintense signals on fluid-attenuated inversion-recovery and diffusion weighted image, compatible with WE. An administration of intravenous thiamine was immediately initiated. After 8 days of the measurement of the thiamine level, the patient’s serum thiamine level was found to be 6 µg/mL (reference range, 24–66 µg/mL). Accordingly, the patient was diagnosed with WE. Shortly after starting the treatment, blood thiamine value reached above normal range with significant improvement of her confusional state. However, short-term memory and ataxia remained. Conclusions Development of WE after SSPPD is uncommon. However, to prevent an after-effect, the possibility of development of WE after SSPPD should be recognized.


Author(s):  
Janel O. Nadeau ◽  
Jiming Fang ◽  
Moira K. Kapral ◽  
Frank L. Silver ◽  
Michael D. Hill

ABSTRACT:Background:An estimated 20-25% of all strokes occur during sleep and these patients wake up with their deficits. This study evaluated outcomes among patients who woke up with stroke compared to those who were awake at stroke onset.Methods:Using data from the Registry of the Canadian Stroke Network Phases 1 and 2, we compared demographics, clinical data and six-month outcomes between patients with stroke-on-awakening versus stroke-while-awake. Strokes of all types (ischemic stroke, transient ischemic attack, intracerebral hemorrhage and subarachnoid hemorrhage) were included. Standard descriptive statistics, multivariable logistic regression and general linear modeling were applied to the data to compare variables.Results:Among 2,585 stroke patients, 349 (13.5%) woke up with stroke and 2,236 (86.5%) did not. Patients with stroke-on-awakening were more likely to have higher blood pressure and to suffer ischemic stroke, but stroke severity, measured by level of consciousness, did not differ. Mortality both at discharge and at six-month follow-up did not differ between the two cohorts. However, patients with stroke-on-awakening were less likely to return home, and their median Stroke Impact Scale-16 scores were 7.0 points lower compared to those with stroke-while-awake.Conclusions:There are minor demographic and clinical differences between patients with stroke-on-awakening and stroke-while-awake. Functional outcomes are slightly worse among patients with stroke-on-awakening, an effect which was driven by poor outcomes among patients with subarachnoid hemorrhage.


CJEM ◽  
2012 ◽  
Vol 14 (03) ◽  
pp. 193-197 ◽  
Author(s):  
Mathew B. Kiberd ◽  
Samuel F. Minor

ABSTRACT Tricyclic antidepressant (TCA) overdose is a leading cause of death among intentional overdoses. Intravenous lipid emulsion therapy is an emerging antidote for local anesthetic toxicity, and there is animal evidence that lipid therapy may be efficacious in TCA overdose. Furthermore, case reports in humans have described the use of lipid therapy to reverse the toxicity of other lipophilic drugs. Here we report a 25-year-old female presenting with coma and hemodynamic instability following intentional ingestion of amitriptyline. She had multiple episodes of pulseless wide-complex tachycardia despite conventional treatment with chest compressions, cardioversion, lidocaine, epinephrine, norepinephrine, magnesium sulphate, sodium bicarbonate, activated charcoal, and whole bowel irrigation. Twenty percent lipid emulsion was administered intravenously (an initial 150 mL bolus, followed by an infusion at 16 mL/h and a second bolus of 40 mL) over 39 hours (total dose 814 mL) yet resulted in no dramatic changes in hemodynamics or level of consciousness. However, there was a decrease in the frequency of wide-complex tachycardia during the lipid emulsion infusion and a recurrence of wide-complex tachycardia shortly after the infusion was stopped. The patient was discharged from the intensive care unit 11 days later with no lasting physiologic sequelae.


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