Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An autopsy case is reported here of a 69-year-old patient with schizophrenia, who was known retrospectively to have had a prefrontal lobotomy 32 years previously. The patient was diagnosed as schizophrenic at the age of 24 and the lobotomy was undertaken 13 years later. The patient was recently found outside in a dehydrated condition and admitted to a general hospital, where he died of respiratory failure. Bilateral cystic lesions were found in the deep white matter of the frontal lobe. The cyst walls consisted of glial fibrous tissues, and severe demyelination with axonal destruction was diffusely observed in the white matter of the frontal lobe. In the thinner frontal cortex without arcuate fibers (U fibers) close to the cavities, cytoarchitectural abnormalities were observed. In the thalamic nuclei marked retrograde degeneration and astrocytic gliosis were observed. The detailed neuropathological findings of a lobotomized schizophrenic brain are reported here. It is proposed that one should be reminded of a lobotomized brain if bilateral cysts are found.
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PMID:An autopsy case of the schizophrenic 32 years after lobotomy. 1130 43

A 21-year-old female presented excitement, auditory hallucination, monologue, and insomnia. After 1 week of risperidone administration, she showed hyperthermia, salivation, and muscle rigidity. Risperidone was discontinued, but stupor, convulsions, and respiratory distress developed. In the intensive care unit where she was transferred, catatonic symptoms such as stupor or excitement, catalepsy, and negativism were prominent. In addition, severe bronchorrhea causing respiratory failure was observed. Her catatonic symptoms, hyperthermia, and bronchorrhea resolved by ECT. After recovery, affective flattening, alogia, and avolition remained. The final diagnosis was MC associated with schizophrenia. This report suggests that MC may be complicated by severe bronchorrhea, but this condition responds to ECT.
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PMID:Malignant catatonia with severe bronchorrhea and its response to electroconvulsive therapy. 1667 86

We describe a 55-year-old man with a medical history of hypertension and schizophrenia who presented to the medical intensive care with delirium and respiratory failure requiring intubation. Chest radiography showed a complete opacification of the right hemithorax. Subsequent chest computed tomography with contrast confirmed a multiloculated right pleural effusion, compressive atelectasis, and mediastinal shift to the left. This patient required multiple tube thoracostomies and a video-assisted thoracoscopic decortication to adequately drain the multiloculated empyemas. Streptococcus acidominimus, a common bacterial pathogen in veterinary medicine, was isolated. The organism is an uncommon cause of invasive disease in humans. This is the first case report in which S. acidominimus was isolated from a multiloculated empyema in a critically ill patient causing significant morbidity and must be considered as a potential but rare pathogen.
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PMID:Streptococcus acidominimus isolated from a multiloculated empyema in a critically ill adult man with pneumonia: case report and review of literature. 1862 Jan 7

Ziprasidone is an atypical antipsychotic approved for the treatment of schizophrenia and bipolar mania in adults and is used off label in children and adolescents. Despite increasing use of ziprasidone in both adult and pediatric populations, there remains a paucity of reports describing unintentional pediatric exposures. The following report describes a patient with isolated ziprasidone ingestion who required intubation secondary to respiratory failure. A 15-month-old previously healthy boy presented to the emergency department shortly after his father found him with approximately five partially dissolved 80-mg ziprasidone tablets in his mouth. The child was flaccid and lethargic with no eye opening, withdrawing from pain only. Two hours after arrival, he developed worsening CNS depression with inability to protect his airway and underwent endotracheal intubation. A serum ziprasidone level was 330 ng/mL by LC/MS. The patient was extubated approximately 14 h later and was discharged from the hospital shortly thereafter in good health without neurological sequelae. Isolated pediatric ingestion of ziprasidone resulting in the need for significant medical intervention has not been previously reported. We report a case of respiratory failure requiring intubation following accidental ziprasidone ingestion with confirmatory serum levels.
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PMID:Respiratory failure following isolated ziprasidone ingestion in a toddler. 2068 May 40

Risperidone (RIS) is a benzisoxazole derivative, an atypical neuroleptic used in the treatment of schizophrenia and other psychoses. The therapeutic action of RIS depends not only on the parent compound but also its major active metabolite, 9-hydroxyrisperidone (9-OH-RIS), and the pharmacokinetics is modified by the genetic polymorphism of CYP2D6, the main site o RIS metabolism. Diverse symptoms of an acute RIS poisoning result from its interaction with multiple receptors, i.e. serotoninergic 5-HT2A and 5-HT7, dopaminergic D2, adrenergic alpha1 and alpha2, as well as histamine H1. The clinical picture of acute RIS poisoning consists predominantly of central nervous system and cardiovascular effects and the most severe symptoms are: hypotension, dysrrhythmias, consciousness disturbances, seizures and respiratory failure. No specific antidote for RIS poisoning is known and the treatment is only symptomatic and supportive. Quantitative determination of RIS blood concentration seems to be helpful in confirmation and monitoring of acute poisoning, nevertheless further investigations are needed to evaluate the relation between drug concentration and clinical symptoms.
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PMID:[The review of acute risperidone poisoning]. 2138 86

Historically, treatment for schizophrenia focused on sedation. The advent of the typical antipsychotics resulted in treatment aimed specifically at the underlying disease, but these agents were associated with numerous adverse effects, and were not particularly effective at treatment of the negative symptoms of schizophrenia. As a result, numerous atypical agents have been developed over the past 2 decades, including several agents within the past 5 years. Overdose of antipsychotics remains quite common in Western society. In 2010, poison control centres in the US received nearly 43,000 calls related to atypical antipsychotics alone. Due to underreporting, the true incidence of overdose with atypical antipsychotics is likely much greater. Following overdose of an atypical antipsychotic, the clinical effects observed, such as CNS depression, tachycardia and orthostasis are largely predictable based on the unique receptor binding profile of the agent. This article, which focuses on the atypical antipsychotics commonly used in the treatment of schizophrenia, discusses the features commonly encountered in overdose. Specifically, agents that result in QT prolongation and the corresponding potential for torsades de pointes, as well as unique features encountered with the various medications are discussed. The diagnosis of this overdose is largely based on history. Routine use of drug screens is unlikely to be beneficial. The primary goal of management is aggressive supportive care. Patients with significant CNS depression with associated loss of airway reflexes and respiratory failure need advanced airway management. Hypotension should be treated first with intravenous fluids, with the use of direct acting vasopressors reserved for persistent hypotension. Benzodiazepines should be used for seizures, with barbiturates used for refractory seizures. Intravenous magnesium can be administered for patients with a corrected QT interval exceeding 500 milliseconds.
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PMID:Overdose of atypical antipsychotics: clinical presentation, mechanisms of toxicity and management. 2266 23

Leigh syndrome is a mitochondrial disease characterized by subacute necrotizing encephalomyelopathy. Almost all cases of Leigh syndrome develop at infancy or early childhood and die within several years due to rapidly progressive muscle weakness and respiratory failure. Here, we present a rare case of a patient who developed Leigh syndrome associated with thiamine-responsive pyruvate dehydrogenase-complex deficiency at 2 years of age and has survived to adolescence through effective high dose thiamin therapy. At 15 years of age, the patient presented persecutory delusions and auditory hallucinations, suggesting an association between mitochondrial dysfunction and schizophrenia-like psychotic symptoms.
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PMID:Schizophrenia-like symptoms in a patient with Leigh syndrome. 3095 29

Prematurity is associated with significantly increased risk of neurobehavioral pathologies, including autism and schizophrenia. A common feature of these psychiatric disorders is prefrontal cortex (PFC) inhibitory circuit disruption due to GABAergic interneuron alteration. Cortical interneurons are generated and migrate throughout late gestation and early infancy, making them highly susceptible to perinatal insults such as preterm birth. Term and preterm PFC pathology specimens were assessed using immunohistochemical markers for interneurons. Based on the changes seen, a new preterm encephalopathy mouse model was developed to produce similar PFC interneuron loss. Maternal immune activation (MIA; modeling chorioamnionitis, associated with 85% of extremely preterm births) was combined with chronic sublethal hypoxia (CSH; modeling preterm respiratory failure), with offspring of both sexes assessed anatomically, molecularly and neurobehaviorally. In the PFC examined from the human preterm samples compared to matched term samples at corrected age, a decrease in somatostatin (SST) and calbindin (CLB) interneurons was seen in upper cortical layers. This pattern of interneuron loss in upper cortical layers was mimicked in the mouse PFC following the combination of MIA and CSH, but not after either insult alone. This persistent interneuron loss is associated with postnatal microglial activation that occurs during CSH only after MIA. The combined insults lead to long-term neurobehavioral deficits which parallel human psychopathologies that may be seen after extremely preterm birth. This new preclinical model supports a paradigm in which specific cellular alterations seen in preterm encephalopathy can be linked with a risk of neuropsychiatric sequela. Specific interneuron subtypes may provide therapeutic targets to prevent or ameliorate these neurodevelopmental risks.
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PMID:Impaired Interneuron Development in a Novel Model of Neonatal Brain Injury. 3080 88