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Copyright of Rechtsmedizin is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. Methods The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. Results The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3±10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. Conclusions The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3±10.1 mg/kg/hr.

Background Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. Methods The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. Results The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3±10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. Conclusions The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3±10.1 mg/kg/hr.

The two-component compound formed by codeine and cyclopentobarbital was produced using grinding techniques and through evaporation from alcoholic solutions. The cocrystal nature of this phase was established unequivocally through single crystal X-ray structure determination. The asymmetric unit contains one formula unit. In the cyclopentobarbital molecule, the cyclopentenyl ring is disordered over two positions related by a rotation of approximately 180° about its C—C bond to the pyrimidine ring. The two NH groups of the cyclopentobarbital molecule form N—H⋯N and N—H⋯O bonds to piperidine and hydroxyl groups, respectively, belonging to different codeine molecules. In addition, the hydroxyl and methoxy groups of neighboring codeine molecules are linked by O—H⋯O interactions, resulting in a H-bonded framework structure of codeine and cyclopentobarbital molecules. The cocrystal was also characterized using thermal analysis, X-ray powder diffraction and IR spectroscopy. [ABSTRACT FROM AUTHOR]

The two-component compound formed by codeine and cyclopentobarbital was produced using grinding techniques and through evaporation from alcoholic solutions. The cocrystal nature of this phase was established unequivocally through single crystal X-ray structure determination. The asymmetric unit contains one formula unit. In the cyclopentobarbital molecule, the cyclopentenyl ring is disordered over two positions related by a rotation of approximately 180° about its C—C bond to the pyrimidine ring. The two NH groups of the cyclopentobarbital molecule form N—H⋯N and N—H⋯O bonds to piperidine and hydroxyl groups, respectively, belonging to different codeine molecules. In addition, the hydroxyl and methoxy groups of neighboring codeine molecules are linked by O—H⋯O interactions, resulting in a H-bonded framework structure of codeine and cyclopentobarbital molecules. The cocrystal was also characterized using thermal analysis, X-ray powder diffraction and IR spectroscopy.

Copyright of Rechtsmedizin is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Enamine derivative barbiturate ligands were prepared from reaction of 5-formylbarbituric acid with the selected aryl amines in methanol. The copper(II) complexes were obtained from the treatment of the ligands with copper(II) acetate monohydrate in methanol. The synthesized compounds were characterized using different spectroscopic techniques such as ATR-IR and NMR. The biological activities of the prepared compounds were studied. Antioxidant activities of the compounds were evaluated using 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging method. Ligand 5-[[4-(phenyldiazenyl)phenylamino]methylene]pyrimidine-2,4,6(1H,3H,5H)-trione exhibited higher antioxidant capacity (IC50 of 1.13 ± 0.25 mM) than the other compounds. Larvicidal activities were performed to examine the efficiency of the compounds against Aedes aegypti. Complex bis[(2-phenoxyphenyl)(2,4,6-trioxotetrahydropyrimidin-5(2H)-ylidene)methyl]amidocopper(II) showed greater larvicidal activity (LC50 of 37.91 ppm) than other compounds. Results of the biological activities indicated that prepared compounds have promising antioxidant and larvicidal activities. [ABSTRACT FROM AUTHOR]

Background: Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. Methods: The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. Results: The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3 +10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. Conclusions: The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3 +10.1 mg/kg/hr.

New series of barbiturates linked to aryl hydrazone derivatives 4a-n were designed and synthesized. Briefly, aniline derivatives in the presence of HBF4 and NaNO2 convert to aryl diazonium tetrafluoroborate which is further attacked to barbituric acid derivatives in water. Finally, with tautomerization, the desired products were achieved. Next, compounds were evaluated as possible urease inhibitors and all the synthesized compounds (IC50 = 8.43 ± 0.14–10.91 ± 0.42 μM) were more potent than standard inhibitors hydroxyurea (IC50 = 100.00 ± 0.15 μM) and thiourea (IC50 = 23 ± 1.7 μM) against urease. It was shown that 4-bromo substitution on the phenyl ring of barbiturate improved the inhibitory potency. Furthermore, based on the molecular dynamic studies, compound 4g depicted noticeable interaction with the urease active site and mobile flap residues through the barbituric acid moiety by coordinating toward the metal bi-nickel center and the essential residues at the active site flap-like Cys592, His593, His594, respectively. These interactions cause interfering catalytic activity of the active site and reduce the flexibility of the mobile flap at the entrance of the active site channel, which significantly decreases the ureolytic activity of urease. [ABSTRACT FROM AUTHOR]

Background: Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. Methods: The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. Results: The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3 +10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. Conclusions: The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3 +10.1 mg/kg/hr.

Abstract Background Febrile status epilepticus is the most common form of status epilepticus in children. No previous reports compare the effectiveness of treatment strategies using fosphenytoin (fPHT) or phenobarbital (PB) and those using anesthetics as second-line anti-seizure medication for benzodiazepine-resistant convulsive status epilepticus (CSE). We aimed to examine the outcomes of various treatment strategies for febrile convulsive status epilepticus (FCSE) in a real-world setting while comparing the effects of different treatment protocols and their presence or absence. Methods This was a single-center historical cohort study that was divided into three periods. Patients who presented with febrile convulsive status epilepticus for ≥60 min even after the administration of at least one anticonvulsant were included. During period I (October 2002–December 2006), treatment was performed at the discretion of the attending physician, without a protocol. During period II (January 2007–February 2013), barbiturate coma therapy (BCT) was indicated for FCSE resistant to benzodiazepines. During period III (March 2013–April 2016), BCT was indicated for FCSE resistant to fPHT or PB. Results The rate of electroencephalogram monitoring was lower in period I than period II+III (11.5% vs. 85.7%, p

Abstract Objective Cholinergic‐induced status epilepticus (SE) is associated with a loss of synaptic gamma‐aminobutyric acid A receptors (GABAAR) and an increase in N‐methyl‐D‐aspartate receptors (NMDAR) and amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptors (AMPAR) that may contribute to pharmacoresistance when treatment with benzodiazepine antiseizure medication is delayed. The barbiturate phenobarbital enhances inhibitory neurotransmission by binding to a specific site in the GABAAR to increase the open state of the channel, decrease neuronal excitability, and reduce glutamate‐induced currents through AMPA/kainate receptors. We hypothesized that phenobarbital as an adjunct to midazolam would augment the amelioration of soman‐induced SE and associated neuropathological changes and that further protection would be provided by the addition of an NMDAR antagonist. Methods We investigated the efficacy of combining antiseizure medications to include a benzodiazepine and a barbiturate allosteric GABAAR modulator (midazolam and phenobarbital, respectively) to correct loss of inhibition, and ketamine to reduce excitation caused by increased synaptic localization of NMDAR and AMPAR, which are NMDA‐dependent. Rats implanted with transmitters to record electroencephalographic (EEG) activity were exposed to soman and treated with atropine sulfate and HI‐6 one min after exposure and with antiseizure medication(s) 40 minutes after seizure onset. Results The triple therapy combination of phenobarbital, midazolam, and ketamine administered at 40 minutes after seizure onset effectively prevented soman‐induced epileptogenesis and reduced neurodegeneration. In addition, dual therapy with phenobarbital and midazolam or ketamine was more effective than monotherapy (midazolam or phenobarbital) in reducing cholinergic‐induced toxicity. Significance Benzodiazepine efficacy is drastically reduced with time after seizure onset and inversely related to seizure duration. To overcome pharmacoresistance in severe benzodiazepine‐refractory cholinergic‐induced SE, simultaneous drug combination to include drugs that target both the loss of inhibition (eg, midazolam, phenobarbital) and the increased excitatory response (eg, ketamine) is more effective than benzodiazepine or barbiturate monotherapy.

Ultraviolet nonlinear optical (NLO) crystals are the key materials to realize the development of ultraviolet solid-state lasers. At present, NLO crystals mainly rely on borate crystals, but the existing NLO crystals could not meet the applications fully. While it is increasingly difficult to find new NLO crystals, so it is particularly urgent to develop new material systems. From the relationship between borate structures and optical and nonlinear optical properties, it can be known that borates which containing planar conjugated groups have the characteristics of large frequency doubling coefficient, suitable birefringence and short UV cut-off edge. Group with planar conjugated configuration is the core functional unit of borate NLO crystals. The study of expanding planar conjugated groups based on geometric configuration is an important idea for exploring new systems of UV nonlinear optical materials. Based on these, our team proposes to expand the exploration scope of UV NLO crystals by studying CO3, NO3, C(NH2)3 groups with planar triangular conjugated structures and HC3N3O3, H2C4N2O3 groups with planar six-member ring conjuated structures. The research results obtained by our team in the exploration of UV crystals of carbonate, nitrate, guanidine, cyanurate and barbiturate in recent years are mainly introduced in this paper. [ABSTRACT FROM AUTHOR]

Barbiturates and benzodiazepines are GABAA-receptor agonists and potent antiseizure medications. We reported that exposure of neonatal macaques to combination of phenobarbital and midazolam (Pb/M) for 24 h, at clinically relevant doses and plasma levels, causes widespread apoptosis affecting neurons and oligodendrocytes. Notably, the extent of injury was markedly more severe compared to shorter (8 h) exposure to these drugs. We also reported that, in the infant macaque, mild hypothermia ameliorates the apoptosis response to the anesthetic sevoflurane. These findings prompted us explore whether mild hypothermia might protect infant nonhuman primates from neuro- and gliotoxicity of Pb/M. Since human infants with seizures may receive combinations of benzodiazepines and barbiturates for days, we opted for 24 h treatment with Pb/M.Neonatal rhesus monkeys received phenobarbital intravenously, followed by midazolam infusion over 24 h under normothermia (T > 36.5 °C-37.5 °C; n = 4) or mild hypothermia (T = 35 °C-36.5 °C; n = 5). Medication doses and blood levels measured were comparable to those in human infants. Animals were euthanized at 36 h and brains examined immunohistochemically and stereologically.Treatment was well tolerated. Extensive degeneration of neurons and oligodendrocytes was seen at 36 h in both groups within neocortex, basal ganglia, hippocampus and brainstem. Mild hypothermia over 36 h (maintained until terminal perfusion) conferred no protection against the neurotoxic and gliotoxic effects of Pb/M. This is in marked contrast to our previous findings that mild hypothermia is protective in the context of a 5 h-long exposure to sevoflurane in infant macaques.These findings demonstrate that brain injury caused by prolonged exposure to Pb/M in the neonatal primate cannot be ameliorated by mild hypothermia.

The design and synthesis of three star‐shaped nonfullerene (NFA) acceptors, TPA‐2T‐INCN, TPA‐2T‐BAB, and TPA‐T‐INCN, based on a triphenylamine (TPA) core and linked through π‐conjugated thiophene (T) spacers to different terminal units (3‐oxo‐2,3‐dihydro‐1H‐inden‐1‐ylidene) malononitrile, INCN, and 1,3‐dimethylbarbituric acid, BAB), are reported. These materials are blended with the widely used poly(3‐hexylthiophene‐2,5‐diyl) (P3HT) donor polymer and tested in flexible organic photovoltaics (OPVs). The NFAs capped with the strong electron‐withdrawing INCN unit perform best in OPVs. Both P3HT:TPA‐T‐INCN and P3HT:TPA‐2T‐INCN blends also show the highest photoluminescence quenching efficiency (95.8% and 92.6%, respectively). Surprisingly, when reducing the number of T spacers from 2 to 1, the solubility of the NFAs in o‐dichlorobenzene increases, leading to easier processing during the OPV fabrication and better surface morphology. This explains the best performance of TPA‐T‐INCN‐based blends in OPVs, with a champion power conversion efficiency of 1.13%. [ABSTRACT FROM AUTHOR]

Deaths caused by barbiturate overdoses have increased in the past decade, especially as a result of suicide attempts. Pentobarbitone is a central nervous system depressant used for sedation and euthanasia in veterinary medicine. However, pentobarbitone analysis is not commonly available in the hospital setting; hence, its occurrence in overdoses is under-reported. Herein we describe a patient who ingested pentobarbitone obtained from the Internet with the purpose of ending his life. He became comatose and required ventilation for 6 days. While critically ill, the drug and a barbiturate test kit were found in his room at his residence. Toxicological analysis of the patient’s blood determined the presence of pentobarbitone at levels of 91, 56, and 19 mg/L at 11, 59, and 107 h after ingestion, respectively. With supportive care, the patient made a full recovery. He stated that he believed the liquid was to be pentobarbitone, and that he had received advice on its use from an online forum that he had found on a dark web marketplace. In this report, we highlight the process by which we facilitated pentobarbitone analysis with a rapid turnaround time, which helped to inform clinical management and raise awareness among clinicians. The access was made through the Prescription, Recreational and Illicit Substance Evaluation (PRISE) programme, which is a collaborative network among the New South Wales (NSW) Ministry of Health, NSW Poisons Information Centre (PIC), and NSW Health Pathology Forensic & Analytical Science Service (FASS).Key points • We report a patient with confirmed severe pentobarbitone toxicity who developed coma, respiratory failure, barbiturate related skin and vascular manifestations who required intensive care for 6 days.• The diagnosis of pentobarbitone poisoning can be missed as it is not routinely included in Australian standard hospital urine drug screens, and it may not cross-react with phenobarbitone testing which may be more readily available. • Timely access to comprehensive toxicology testing with rapid turnaround time assists diagnosis for unknown toxicity, and enhances case management and public health interventions. • The PRISE programme in Australia is a collaboration between multiple health functional units in NSW, Australia that provides timely access to extensive toxicology testing for severe and unusual toxicity from drugs or substance-related toxicities.

The study of supramolecular morphology is gaining significant attention. This may be attributed to the fact that nanostructures of aggregates have been found to significantly influence the photoelectronic properties of supramolecular materials. In this study, the self‐assembling behaviour of rod–coil molecules with barbiturate (Ba) or Hamilton wedge (Hw) units and the supramolecule Ba‐Hw was investigated. In chloroform solution, molecule Hw consisted of an oligo‐ethylene chain with degree of polymerization of 17 as well as biphenyl, phenyl and Hw units. Ba molecules incorporated octyloxy, biphenyl, phenyl and Ba groups that self‐organized into nanofibres with different diameters. Supramolecular amphiphile Hw‐Ba self‐aggregated into different sizes of nanosheet‐like aggregates. In a dimethylsulfoxide/H2O (1:19 v/v) mixed polar solvent, molecules Hw and Ba aggregated into twist‐shaped and nanosheet aggregates, while the supramolecular Hw‐Ba aggregated into larger‐size microtubes. Experimental results obtained for these molecular assemblies suggest that combining Ba and Hw units by employing hydrogen bonds is an effective strategy for forming amphiphilic supramolecules. Compared with the individual rod–coil molecules Ba and Hw, supramolecule Hw‐Ba has stronger π–π intermolecular forces due to the presence of more planar Hw‐Ba building blocks, which form various supramolecular assemblies with less curvature than the rigid and flexible surfaces of the original molecules. © 2021 Society of Industrial Chemistry. [ABSTRACT FROM AUTHOR]

Background: Febrile status epilepticus is the most common form of status epilepticus in children. No previous reports compare the effectiveness of treatment strategies using fosphenytoin (fPHT) or phenobarbital (PB) and those using anesthetics as second-line anti-seizure medication for benzodiazepine-resistant convulsive status epilepticus (CSE). We aimed to examine the outcomes of various treatment strategies for febrile convulsive status epilepticus (FCSE) in a real-world setting while comparing the effects of different treatment protocols and their presence or absence.Methods: This was a single-center historical cohort study that was divided into three periods. Patients who presented with febrile convulsive status epilepticus for ≥60 min even after the administration of at least one anticonvulsant were included. During period I (October 2002-December 2006), treatment was performed at the discretion of the attending physician, without a protocol. During period II (January 2007-February 2013), barbiturate coma therapy (BCT) was indicated for FCSE resistant to benzodiazepines. During period III (March 2013-April 2016), BCT was indicated for FCSE resistant to fPHT or PB.Results: The rate of electroencephalogram monitoring was lower in period I than period II+III (11.5% vs. 85.7%, p<0.01). Midazolam was administered by continuous infusion more often in period I than period II+III (84.6% vs. 25.0%, p<0.01), whereas fPHT was administered less often in period I than period II+III (0% vs. 27.4%, p<0.01). The rate of poor outcome, which was determined using the Pediatric Cerebral Performance Category scale, was higher in period I than period II+III (23.1% vs. 7.1%, p=0.03). The rate of poor outcome did not differ between periods II and III (4.2% vs. 11.1%, p=0.40).Conclusions: While the presence of a treatment protocol for FCSE in children may improve outcomes, a treatment protocol using fPHT or PB may not be associated with better outcomes. [ABSTRACT FROM AUTHOR]

Copyright of Adiyaman University Journal of Science & Technology / Adıyaman Üniversitesi Fen Bilimleri Dergisi is the property of Adiyaman University, Institute of Science / Adiyaman Universitesi Fen Bilimleri Enstitusu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: Cholinergic‐induced status epilepticus (SE) is associated with a loss of synaptic gamma‐aminobutyric acid A receptors (GABAAR) and an increase in N‐methyl‐D‐aspartate receptors (NMDAR) and amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptors (AMPAR) that may contribute to pharmacoresistance when treatment with benzodiazepine antiseizure medication is delayed. The barbiturate phenobarbital enhances inhibitory neurotransmission by binding to a specific site in the GABAAR to increase the open state of the channel, decrease neuronal excitability, and reduce glutamate‐induced currents through AMPA/kainate receptors. We hypothesized that phenobarbital as an adjunct to midazolam would augment the amelioration of soman‐induced SE and associated neuropathological changes and that further protection would be provided by the addition of an NMDAR antagonist. Methods: We investigated the efficacy of combining antiseizure medications to include a benzodiazepine and a barbiturate allosteric GABAAR modulator (midazolam and phenobarbital, respectively) to correct loss of inhibition, and ketamine to reduce excitation caused by increased synaptic localization of NMDAR and AMPAR, which are NMDA‐dependent. Rats implanted with transmitters to record electroencephalographic (EEG) activity were exposed to soman and treated with atropine sulfate and HI‐6 one min after exposure and with antiseizure medication(s) 40 minutes after seizure onset. Results: The triple therapy combination of phenobarbital, midazolam, and ketamine administered at 40 minutes after seizure onset effectively prevented soman‐induced epileptogenesis and reduced neurodegeneration. In addition, dual therapy with phenobarbital and midazolam or ketamine was more effective than monotherapy (midazolam or phenobarbital) in reducing cholinergic‐induced toxicity. Significance: Benzodiazepine efficacy is drastically reduced with time after seizure onset and inversely related to seizure duration. To overcome pharmacoresistance in severe benzodiazepine‐refractory cholinergic‐induced SE, simultaneous drug combination to include drugs that target both the loss of inhibition (eg, midazolam, phenobarbital) and the increased excitatory response (eg, ketamine) is more effective than benzodiazepine or barbiturate monotherapy. [ABSTRACT FROM AUTHOR]

Objective There is growing interest in the use of phenobarbital for alcohol withdrawal syndrome in critically ill patients, though experience in neurologically injured patients is limited. The purpose of this study was to compare the safety and effectiveness of phenobarbital-containing alcohol withdrawal regimens versus benzodiazepine monotherapy in the neurocritical care unit. Methods We conducted a retrospective cohort study of adult patients admitted to the neurocritical care unit from January 2014 through November 2021 who received pharmacologic treatment for alcohol withdrawal. Treatment groups were defined as benzodiazepine monotherapy versus phenobarbital alone or in combination with benzodiazepines. The primary outcome was the percentage of patients requiring intubation after receiving alcohol withdrawal treatment. Secondary outcomes included all-cause, in-hospital mortality, intensive care unit length of stay, discharge disposition, change in Glasgow Coma Scale (GCS) score, and the use of adjunctive agents. Results We analyzed data from 156 patients, with 77 (49%) in the benzodiazepine group and 79 (51%) in the phenobarbital combination group. The groups were well-balanced for baseline characteristics, though more males (67, 85%) were in the phenobarbital group. Only three (1.9%) patients received phenobarbital monotherapy, and the rest (153, 98.1%) received combination therapy. The percentage of patients requiring mechanical ventilation was significantly higher in the phenobarbital combination group compared to benzodiazepine monotherapy (39% (n=31) versus 13% (n=10); OR: 4.33, 95% CI: 1.94-9.66; p<0.001). The use of adjunctive propofol and dexmedetomidine was higher in the phenobarbital group (propofol 35% (n= 28) versus 9% (n=7) and dexmedetomidine 30% (n=24) versus 5% (n=4), respectively). Patients in the phenobarbital group also had lower GCS scores and higher Clinical Institute Withdrawal Assessment of Alcohol (CIWA-Ar) scores during their intensive care unit admission, possibly suggesting more severe alcohol withdrawal. There was no difference in intensive care unit length of stay, all-cause, in-hospital mortality, discharge disposition, or therapeutic adjuncts. Conclusions Combination therapy of phenobarbital plus benzodiazepines was associated with higher odds of requiring mechanical ventilation. Few patients received phenobarbital monotherapy. Additional studies are needed to better compare the effects of phenobarbital monotherapy versus benzodiazepines in neurocritical patients., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. University of Washington issued approval STUDY 00014298. The study (STUDY 00014298) was approved (14 February 2022) by the University of Washington Medical Center institutional review board (IRB), and a waiver of informed consent was in place. Animal subjects: All authors have confirmed that this study did not involve animal subjects or tissue. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: Abhijit V. Lele declare(s) personal fees from LifeCenter Northwest. Medical Advisor. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Norris et al.)

Deaths caused by barbiturate overdoses have increased in the past decade, especially as a result of suicide attempts. Pentobarbitone is a central nervous system depressant used for sedation and euthanasia in veterinary medicine. However, pentobarbitone analysis is not commonly available in the hospital setting; hence, its occurrence in overdoses is under-reported. Herein we describe a patient who ingested pentobarbitone obtained from the Internet with the purpose of ending his life. He became comatose and required ventilation for 6 days. While critically ill, the drug and a barbiturate test kit were found in his room at his residence. Toxicological analysis of the patient's blood determined the presence of pentobarbitone at levels of 91, 56, and 19 mg/L at 11, 59, and 107 h after ingestion, respectively. With supportive care, the patient made a full recovery. He stated that he believed the liquid was to be pentobarbitone, and that he had received advice on its use from an online forum that he had found on a dark web marketplace. In this report, we highlight the process by which we facilitated pentobarbitone analysis with a rapid turnaround time, which helped to inform clinical management and raise awareness among clinicians. The access was made through the Prescription, Recreational and Illicit Substance Evaluation (PRISE) programme, which is a collaborative network among the New South Wales (NSW) Ministry of Health, NSW Poisons Information Centre (PIC), and NSW Health Pathology Forensic & Analytical Science Service (FASS). Key points • We report a patient with confirmed severe pentobarbitone toxicity who developed coma, respiratory failure, barbiturate related skin and vascular manifestations who required intensive care for 6 days. • The diagnosis of pentobarbitone poisoning can be missed as it is not routinely included in Australian standard hospital urine drug screens, and it may not cross-react with phenobarbitone testing which may be more readily available. • Timely access to comprehensive toxicology testing with rapid turnaround time assists diagnosis for unknown toxicity, and enhances case management and public health interventions. • The PRISE programme in Australia is a collaboration between multiple health functional units in NSW, Australia that provides timely access to extensive toxicology testing for severe and unusual toxicity from drugs or substance-related toxicities. [ABSTRACT FROM AUTHOR]

There are many nonopioid central nervous system depressant substances that share a gamma‐aminobutyric acid (GABA) receptor–related mechanism of action. These sedatives‐hypnotics can be indicated to treat anxiety, seizures, depression, and insomnia but are also used as substances of abuse and used to facilitate sexual assault. Barbiturates, methaqualone, and glutethimide were among the first type A GABA receptor–mediated sedative‐hypnotics. Their clinical use was limited for most indications by serious adverse events and strong abuse potential but continue to be used illicitly around the world. The benzodiazepines supplanted barbiturates for most indications because they were less likely to cause severe adverse events in monotherapy. Flunitrazepam is a newer benzodiazepine that is preferentially used recreationally and to facilitate sexual assault. Flunitrazepam has greater potency and higher affinity for the type A GABA receptor than most benzodiazepines. Gamma‐hydroxybutyric acid is sought illicitly for its hypnotic, euphoric and anabolic effects as well as to facilitate sexual assault. When any of these GABAergic drugs are used in high doses or with other sedative hypnotic agents, respiratory depression, coma, and death have occurred. Chronic use of these GABAergic drugs can lead to significant withdrawal syndromes. Phenibut and selank are poorly studied Russian drugs with GABAergic mechanisms that are inexplicably sold to US consumers as dietary supplements. Poison control center calls regarding phenibut have increased substantially over the past 5 years. Desired euphoriant effects account for the recreational and illicit use of many GABA‐modulating agents. However, illicit use can lead to significant toxicities related to abuse, dependence, and subsequent withdrawal syndromes. Significant evaluation of developing agents with GABA properties should be conducted to determine abuse potential before public access ensues. [ABSTRACT FROM AUTHOR]

• The barbituric acid-based 1,3-dimethyl-2,4,6-trioxo-hexahydro-pyrimidine-5-(2,6-dimethylphenylamino)methylene, 1,3-dimethyl-2,4,6-trioxo-hexahydro-pyrimidine-5-(8-quinolylamino)methylene as ligands and six novel copper(II) and nickel(II) complexes were synthesized and characterized by elemental analysis, FT-IR spectroscopy. • Single crystal X-ray crystallography was performed to determine all molecules' crystal structures. • All molecules demonstrate essential molecular arrangements. • The Hirshfeld surface analysis method was used to explore the intermolecular interactions. It is well known that solvent molecules and additional agents significantly impact crystal structures. In relation to this, the barbituric acid-based 1,3-dimethyl-2,4,6-trioxo-hexahydro-pyrimidine-5-(2,6-dimethylphenylamino)methylene (HL1) as ligand and three novel copper(II) complexes, 2[Cu(L1) 2 ] (1), 2[Cu(L1) 2 (4,4′bpy)] (2), Cu(L1) 2 (CH 3) 2 SO (3), (where H is the deprotonatable hydrogen) were synthesized and characterized by elemental analysis, FT-IR spectroscopy. As a comparison, a potentially tridentate barbituric acid-based ligand, 1,3-dimethyl-2,4,6-trioxo-hexahydro-pyrimidine-5-(8-quinolylamino)methylene (HL2), and its three new copper(II) and nickel(II) complexes, Cu(L2) 2 (4), Cu(L2) 2 (5) and Ni(L2) 2 (6), were also synthesized and characterized by elemental analysis, FT-IR spectroscopy. The crystal structures of the ligands and their complexes were determined based on an X-ray diffraction study. X-ray diffraction studies have shown that the ligands HL1 and HL2 exist in keto-enamine form. The crystal structure of complexes of HL1 revealed that Cu center is distorted square-planar in 2[Cu(L1) 2 ] (1), while it is found in distorted square-pyramidal in relation to additional agent (4,4′ bpyridine) and solvent (DMSO) conditions in 2[Cu(L1) 2 (4,4′bpy)] (2) and Cu(L1) 2 (CH 3) 2 SO (3), respectively. In the crystal structure, [M(L2) 2 ] (M = Cu (4 and 5), Ni (6)), metal ions possess a distorted octahedral environment, and the HL2 ligands coordinate with a meridional geometry. Structures of all complexes reveal a tendency to form C–H···O, C–H···π and π···π interactions, except for molecule Cu(L1) 2 (CH 3) 2 SO (3) in terms of C–H···O bonds which was not observed. Exploring noncovalent interactions indicates similar molecular structures in [M(L2) 2 ] (M = Cu (4 and 5), Ni (6)) suggesting the difference in packing due to the solvent of crystallization (CH 2 Cl 2) in the lattice of Cu(L2) 2 (5) and the different metal ion in the molecular structure of Ni(L2) 2 (6). The packing in the structures of HL1 complexes is found to be strongly dependent on the additional agent (4,4′ bpyridine) and solvent (DMSO) fused in molecular structure with different supramolecular assemblies such as 1D chains, π···π dimers, 2D sheets, etc. In addition, Hirshfeld surface analysis and 2D fingerprint plots were employed to verify intermolecular interactions in both ligands and their complexes. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract Intracranial pressure (ICP) has to be maintained quite constant, because increased ICP caused by cerebrovascular disease and head trauma is fatal. Although controlling ICP is clinically critical, only few therapeutic methods are currently available. Barbiturates, a group of sedative‐hypnotic drugs, are recognized as secondary treatment for controlling ICP. We proposed a novel “step‐down infusion” method, administrating barbiturate (thiamylal) after different time point from the start of treatment under normothermia, at doses of 3.0 (0–24 h), 2.0 (24–48 h), 1.5 (48–72 h), and 1.0 mg/kg/h (72–96 h), and evaluated its safety and effectiveness in clinical. In 22 patients with severe traumatic brain injury or severe cerebrovascular disease (Glasgow coma scale ≤8), thiamylal concentrations and ICP were monitored. The step‐down infusion method under normothermia maintained stable thiamylal concentrations (65 mmHg), and no threatening changes in serum potassium or any hemodynamic instability were observed. Our novel “step‐down infusion” method under normothermia enabled to maintain stable, safe thiamylal concentrations to ensure both ICP reduction and CPP maintenance without any serious side effects, may provide a novel and clinically effective treatment option for patients with increased ICP.

Introduction: Seizures are seen in 13% of cases in palliative care. Phenobarbital is a drug from the barbiturates' family most used for its anticonvulsant and sedative properties, and therefore the drug of choice in palliative care suitable for the management of seizures and agitation. The study aimed to evaluate the role of phenobarbital in palliative care settings. Methods: A systematic literature review was conducted using predetermined keywords. Data was compiled and inclusion and exclusion criteria were established concerning the role of phenobarbital in palliative care. Five case studies met these criteria and were evaluated. Retrospective analysis of the data in the studies, along with randomized clinical trial about the use of at the end of life were reviewed by two independent reviewers. Results: Results of this review showed that phenobarbital is efficacious in the management of seizures and agitation, can be easily administered via different routes and utilized in various palliative care settings. No serious adverse skin reactions were noted with the use of phenobarbital and it did not abruptly end a patient's life when used at appropriate doses. Conclusions: Although phenobarbital is an old drug and is an approved anticonvulsant, its sedating properties make it to be useful not only for seizure management, but also in patients experiencing agitation, physical and psychological distress, and restlessness. More studies are warranted in the sole practice of using phenobarbital and further explore its role in palliative care. [ABSTRACT FROM AUTHOR]

Intracranial pressure (ICP) has to be maintained quite constant, because increased ICP caused by cerebrovascular disease and head trauma is fatal. Although controlling ICP is clinically critical, only few therapeutic methods are currently available. Barbiturates, a group of sedative-hypnotic drugs, are recognized as secondary treatment for controlling ICP. We proposed a novel "step-down infusion" method, administrating barbiturate (thiamylal) after different time point from the start of treatment under normothermia, at doses of 3.0 (0-24 h), 2.0 (24-48 h), 1.5 (48-72 h), and 1.0 mg/ kg/h (72-96 h), and evaluated its safety and effectiveness in clinical. In 22 patients with severe traumatic brain injury or severe cerebrovascular disease (Glasgow coma scale ≤8), thiamylal concentrations and ICP were monitored. The step-down infusion method under normothermia maintained stable thiamylal concentrations (<26.1 µg/ ml) without any abnormal accumulation/elevation, and could successfully keep ICP <20 mmHg (targeted management value: ICP <20 mmHg) in all patients. Moreover the mean value of cerebral perfusion pressure (CPP) was also maintained over 65 mmHg during all time course (targeted management value: CPP >65 mmHg), and no threatening changes in serum potassium or any hemodynamic instability were observed. Our novel "step-down infusion" method under normothermia enabled to maintain stable, safe thiamylal concentrations to ensure both ICP reduction and CPP maintenance without any serious side effects, may provide a novel and clinically effective treatment option for patients with increased ICP. [ABSTRACT FROM AUTHOR]

Introduction: Valerian, scientifically known as Valeriana officinalis, is a herbaceous plant with numerous medicinal properties. Its root serves as a painkiller and antispasmodic, containing valeric acid that has anti-musclecontraction properties. Valerian has various medical uses, such as sedative, hypnotic, anti-anxiety, anti-spasmodic, antidepressant, anti-hysteric, anti-hypertensive, and diuretic effects. For this reason, valerian has been introduced by the Food and Drug Administration (FDA) as a food supplement to reduce anxiety. The purpose of this study is to investigate the sedative effect of the valerian plant. Methods and Materials: This review was conducted by searching the keywords valerian, catnip, and sedation through journal database platforms such as Google Scholar, Pubmed, and ScienceDirect as search engines for journals related to this article between 2001 and 2023. 37 articles were studied, and after removing articles that did not match the purpose of this research and duplicates, a total of 21 articles were used in this research. Result: The research showed that this plant is known as an agonist of gamma-aminobutyric GABA receptors. Studies also show that this plant inhibits valeric acid, the enzyme responsible for GABA catabolism, and increases the concentration of GABA in the brain, reduces the activity of different brain nuclei, and causes sedative effects. Also, the property of this plant is similar to benzodiazepines and barbiturates. Conclusion: According to the attained results, natural materials are superior to synthetic drugs due to fewer side effects and no alterations in the physiological and biochemical pathways, so it is suggested to conduct more comprehensive research in this area. [ABSTRACT FROM AUTHOR]

Barbiturate-related deaths have increased in Australia in two major demographic groups: older people with physical health problems and younger people with mental health problems. The former are the intended beneficiaries of laws that allow euthanasia. The latter have been described as collateral damage from increased access to barbiturates, a class of drug often used for euthanasia, regardless of its legality or illegality. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate barbiturate anaesthetic therapy using thiamylal for febrile refractory status epilepticus (fRSE) in children.Methods: This was a review of a prospectively-collected database between April 2012-March 2016 for fRSE cases treated with thiamylal anaesthetic therapy in a single paediatric hospital in Japan. The sample comprised 23 children (median age, 23 months) with fRSE that underwent thiamylal anaesthetic therapy for convulsive seizures lasting longer than 60 min, sustained after intravenous administration of benzodiazepine and non-benzodiazepine anticonvulsants. The intervention comprised protocol-based thiamylal anaesthetic therapy with bolus administration. We measured the dose and time required to achieve the burst suppression pattern (BSP) on electroencephalography, seizure recurrence, death, neurological sequelae, and complications.Results: All patients except one reached the BSP. The thiamylal median dose until reaching the BSP was 27.5 mg/kg, and the median time from thiamylal administration to reaching the BSP was 109.5 min. There was one case of immediate treatment failure and one of withdrawal seizure, but no breakthrough seizure. No deaths occurred during treatment, and neurological sequelae occurred in four cases (17%). Vasopressors were administered in all cases. Other complications included 11 cases of pneumonia and one of enterocolitis.Conclusion: We revealed the time and dose required to reach the BSP with thiamylal anaesthetic therapy using bolus administration in children. Our results suggested that reaching the BSP with bolus administration requires markedly less time than without bolus administration, rarely causes seizure recurrence in paediatric fRSE, and causes haemodynamic dysfunction and infections as often as observed without bolus administration. [ABSTRACT FROM AUTHOR]

Parkinson’s disease (PD) is one of the most common neurodegenerative disorders, and is caused by the death of dopamine neurons and neuroinflammation in the striatum and substantia nigra. Furthermore, the inflammatory response in PD is closely related to glial cell activation. This study examined the neuroprotective effects of the barbiturate derivative, MHY2699 [5-(4-hydroxy 3,5-dimethoxybenzyl)-2 thioxodihydropyrimidine-4,6(1H,5H)-dione] in a mouse model of PD. MHY2699 ameliorated MPP⁺-induced astrocyte activation and ROS production in primary astrocytes and inhibited the MPP⁺-induced phosphorylation of MAPK and NF-κB. The anti-inflammatory effects of MHY2699 in protecting neurons were examined in an MPTP-induced mouse model of PD. MHY2699 inhibited MPTP-induced motor dysfunction and prevented dopaminergic neuronal death, suggesting that it attenuated neuroinflammation. Overall, MHY2699 has potential as a neuroprotective treatment for PD.

Abstract Background Seizure duration in electroconvulsive therapy (ECT) is positively related with patients’ outcome. This study sought to investigate the impact of anesthetic management on seizure duration, and the impact of selected drugs (theophylline, remifentanil, S-ketamine) on seizure duration. Methods Retrospective analysis of all patients undergoing ECT at our institution from January 2011 to April 2012 was performed based on electronic medical chart and review of existing quality improvement data. Patient data (N = 78), including gender, age, height, weight, and administered drugs, energy levels, and electroencephalic seizure duration were analyzed. Statistical analysis was performed using a generalized linear model. Results A total of 78 patients (male = 39, female = 39, age 51 ± 12 years) were included. Average number of session was 10 ± 6 (1–30). In our patient population, theophylline administration was the only parameter, which significantly prolonged seizure duration, whereas S-ketamine, remifentanil, thiopental, age, sex, session or energy level had no significant effect. Conclusion Theophylline can be a useful adjunct for patients with inadequate seizure duration. If there is a concomitant beneficial effect on patients’ outcome needs to be investigated in further studies.

The gastric stability of eight barbiturates (BARs) (barbital, primidone, allobarbital, phenobarbital, cyclobarbital, pentobarbital, secobarbital, and thiobutabarbital (TBB)) was examined in artificial gastric juice using LC/UV detection. Among the eight BARs, only TBB was degraded at higher temperatures. Furthermore, the degradation product of TBB was isolated, structurally analyzed, and finally identified as 5-butan-2-yl-5-ethyl-1,3-diazinane-2,4,6-trione, also known as butabarbital. The study elucidated that butabarbital was formed by substituting the sulfur atom of the carbonyl group at the 2-position of TBB with an oxygen atom under acidic condition.

Background: Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy., Methods: The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted., Results: The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3±10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative., Conclusions: The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3±10.1 mg/kg/hr., Competing Interests: No competing interests were disclosed., (Copyright: © 2023 Sookplung P et al.)

Human prolyl hydroxylases are involved in the modification of transcription factors, procollagen, and ribosomal proteins, and are current medicinal chemistry targets. To date, there are few reports on inhibitors selective for the different types of prolyl hydroxylases. We report a structurally informed template‐based strategy for the development of inhibitors selective for the human ribosomal prolyl hydroxylase OGFOD1. These inhibitors did not target the other human oxygenases tested, including the structurally similar hypoxia‐inducible transcription factor prolyl hydroxylase, PHD2. Humans have 60–70 2OG‐dependent oxygenases, of which some are important therapeutic targets. A priority in the development of oxygenase inhibitors is to identify scaffolds selective for a particular enzyme, made challenging by the highly conserved oxygenase active sites. This work reports the development of potent inhibitors for the oxygenase OGFOD1, which do not inhibit related enzymes, such as the physiologically important oxygenase PHD2. [ABSTRACT FROM AUTHOR]

A fatal concentration of pentobarbital found in a coroner's case where the history had not indicated use of this drug prompted a review of fatalities in Ontario from 2012 to 2015. Coroner's case files, including police and toxicology reports, were reviewed in twenty deaths, in which pentobarbital was identified as the primary cause of death. In all of the deaths (11 females, 9 males), the blood concentration of pentobarbital was greater than 10 mg/L. There were three to eight deaths per year and each was classified as suicide. In 11 cases, there was clear evidence that the drug was purchased over the internet from Mexico or China and imported into Canada. In four cases, it appears that the pentobarbital was labeled as a different, innocuous chemical to facilitate crossing the border without scrutiny. The findings underscore the value of a thorough scene investigation, including details of evidence that may be considered unrelated. [ABSTRACT FROM AUTHOR]

The developing brain is uniquely susceptible to drug-induced increases in programmed cell death or apoptosis. Many compounds, including anticonvulsant drugs, anesthetic agents, and ethanol, when administered in a narrow postnatal window in rodents, result in increased pruning of neurons. Here, we report that dimethyl sulfoxide (DMSO) triggers widespread neurodegeneration in the immature (postnatal day, P7) rat brain, an effect consistent with a prior report in neonatal mice. We found that the synthetic cannabinoid receptor agonist WIN 55,212-2 (WIN) exerts a neuroprotective effect against DMSO-induced cell death. We extended these findings to determine if WIN is neuroprotective against another drug class known to increase developmental cell death, namely antiseizure drugs. The antiseizure drug phenobarbital (PB) remains the primary treatment for neonatal seizures, despite significantly increasing cell death in the developing rodent brain. WIN exerts antiseizure effects in immature rodent seizure models, but increases the toxicity associated with neonatal ethanol exposure. We thus sought to determine if WIN would protect against or exacerbate PB-induced cell death. Unlike either the prior report with ethanol or our present findings with DMSO, WIN was largely without effect on PB-induced cell death. WIN alone did not increase cell death over levels observed in vehicle-treated rats. These data suggest that WIN has a favorable safety profile in the developing brain and could potentially serve as an adjunct therapy with phenobarbital (albeit one that does not attenuate PB-induced toxicity). [ABSTRACT FROM AUTHOR]

Graphical abstract Highlights • Multicomponent reaction (MCR) access to perfluoroalkylated cis -spiropyrido[2,1- a ]isoquinoline-1,5'-pyrimidine derivatives. • The proton-promoted transformation of trans -isomer to cis -isomer. • Regioselectivity of the 1,4-dipolar cycloaddition. Abstract The 1,4-dipoles derived from isoquinolines and methyl perfluoroalk-2-ynoates reacted readily with arylidene-substituted N , N -dimethylbarbituric acids resulting in the first diastereoselective synthesis of perfluoroalkylated cis -spiropyrido[2,1- a ]isoquinoline-1,5'-pyrimidine derivatives in good to excellent yields under mild conditions. The reaction mechanism was proposed to illustrate the formation of the diastereoisomers and proton-promoted transformation of trans -spiropyrido[2,1- a ]isoquinoline-1,5'-pyrimidines to the more thermodynamically stable cis -isomers. The DFT calculation demonstrated the diastereoselectivity of the reaction. [ABSTRACT FROM AUTHOR]

In the past two decades, the solvomorphism phenomenon in organic materials has attracted much attention, especially in the pharmaceutical and materials industries. Cocrystallization with solvent molecules can lead to modified physical and chemical properties of materials. We present here two new solvomorphs (pseudopolymorphs) of tyraminium 5,5‐diethylbarbiturate [2‐(4‐hydroxyphenyl)ethanaminium 5,5‐diethyl‐2,4,6‐trioxotetrahydro‐2H‐pyrimidin‐1‐ide, C8H12NO+·C8H11N2O3−] with unusual structural features. Pseudopolymorph (I) follows the symmetry of the P21/n space group and has four tyraminium cations, four barbitalate anions and four molecules of chloroform in the asymmetric unit. Pseudopolymorph (II) crystallizes in the space group Rc with one tyraminium cation, one barbitalate anion and a small amount of disordered solvent (ethanol and water) located in the cavities. Hirshfeld surface analysis and the Non‐Covalent Interaction (NCI) index were used to examine and compare the crystal packing features and intermolecular interactions in (I) and (II). Both materials crystallize with large unit cells and contain nontypical barbitalate ions formed through deprotonation of the barbital N3 position. Pseudopolymorph (I) is an example of a crystal structure with a rarely observed value of Z′ = 4. Analysis of the hydrogen‐bond patterns in (II) showed an unusual arrangement of three barbitalate anions in R33(12) rings, which is the first example of such a hydrogen‐bond motif in barbital structures. The mutual arrangement of the ions in the crystal structure of (II) leads to the formation of specific cavities along the c direction. A tyraminium barbitalate solvomorph (pseudopolymorph) contains disordered chloroform molecules and its Z′ value is 4. A second solvomorph, a rare example of a crystal structure with a hydrogen‐bonded (12) ring motif, exhibits a layered structure, with cavities containing disordered water and ethanol molecules. [ABSTRACT FROM AUTHOR]