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

We reported a case of acute water intoxication from compulsive water-drinking, who showed triphasic waves on EEG. The patient was a 50-year-old man who had been undergoing medical treatment in a mental hospital since he was suffering from schizophrenia diagnosed at the age of 35. He had sometimes had a tendency to drink a large amount of water since 45 years old. He began to drink water compulsively since three days ago. He vomited just after he drank excessive water with his mouth directly to the tap for several minutes, and soon fell into loss of consciousness. He was transmitted to our hospital because of acute consciousness disturbance on the next day. On neurological examination, he was profoundly comatose with miosis and conjugate deviation to the right side. His extremities showed decorticate posturing. On admission, serum sodium level was 101 mEq/l, and plasma osmolality was 208 mOsm/l. Serum enzymes derived from muscle and myoglobin were markedly elevated. But there was no laboratory evidence of the other metabolic disorders such as hepatic or renal disease. Computed tomography of the brain disclosed severely diffuse swelling with largely obliterated sulci and narrowed ventricles. EEG showed triphasic waves predominantly over centro-parieto-occipital portion, behind which there was slow wave activity with a loss of normal alpha wave activity. Immediately, treatment began by a combination of saline and glyceol infusion for the purpose of correcting severe hyponatremia, subsequently removing brain edema. As serum sodium level gradually returned to normal, the brain CT findings were getting better.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of acute water intoxication showing triphasic waves on EEG]. 193 65

Ganser, in 1897, described a syndrome that the main symptoms were: Impaired consciousness, distorted communication (Maladjusted answers, looking like dementia nonsense). This syndrome was first included to hysteria. Gradually, the most striking aspect, approximate answers, has been stretch as regards to his pathogeny, to other concepts like post-traumatic disease, depression and especially schizophrenia. In this way, the Ganser's syndrome now cover a large scale of troubles related to perturbation of communication and with non psychopathologic relation to the primitive syndrome.
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PMID:[The Ganser syndrome and its ups and downs]. 267 90

Thirty patients (24 inpatients and 6 outpatients) with a clinical diagnosis of SLE were examined between September 1, 1998 and August 1, 1999 in the rheumatology clinic of Jichi Medical School Hospital. All of these patients fulfilled the 1982 revised criteria of the American Rheumatism Association for the classification of SLE and had some psychiatric manifestations (psychiatric SLE; P-SLE group). Mean patient age was 38.6 +/- 13.0, and there were 5 males and 25 females. When classified into 5 subgroups according to the most prominent symptoms, the distribution was as follows: consciousness disturbance group: 6 (20%), schizophrenia-like group: 5 (16.7%), mood disorder group: 7 (23.3%), neurosis-like group: 10 (33.3%), and convulsive disorder group: 2 (6.7%). Among all 37 psychiatric episodes, symptoms appeared in 37.8% of cases during the acute phase of SLE (during onset or recurrence) and in 62.9% during the chronic phase (during remission). The profile of the P-SLE group showed that the psychiatric symptoms of the SLE patients were milder and more chronic than those described in previous reports. To begin to comprehend the psychopathology of SLE, we put forward the concept of "Psychiatric basal state" and "psychiatric conjugated state". The former is considered a direct reflection of the acute-phase SLE process on mental condition. It is defined clinically as psychiatric symptoms that parallel the activity of SLE and respond well to steroid therapy. The latter include all other psychiatric problems in which one cannot rule out the effects of pharmacological, somatic, personality, and environmental effects on psychiatric symptoms. Only 3 patients in the P-SLE group fulfilled the criteria for the "psychiatric basal state". All three patients belonged to the consciousness disturbance group, whose clinical features were defined as slight clouding of consciousness, so-called "Amentia" in the sense of the German terminology. The clinical profile of this state is: 1. the patients are young (about 16 years old), 2. the onset of psychiatric symptoms is within 5 years after the onset of SLE, 3. confusion and disorientation are the most characteristic features, and 4. the clinical course of this state is almost 2 months. The experience structure of the "psychiatric basal state" consists of: 1. difficulty in selecting and holding a topic in cognition, 2. confusion and emotional instability as the basal mood, and 3. primitive and floating forms of delusions and hallucinations. Using this concept of the "psychiatric basal state" as a clue, we can hypothesize the continuity of diverse psychiatric symptoms in SLE. The "proper process of SLE (Harada)" has a disintegrating effect on the "ego" and it allows various psychopathological phenomena to emerge in the experience field. Against this background, additional factors, such as secondary organ damage, personality structure, and social environment, induce organization of the "psychiatric conjugated state".
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PMID:[A clinical study of psychopathology in systemic lupus erythematosus]. 1102 78

We report three patients with a history of neuroleptic malignant syndrome for whom modified electroconvulsive therapy (m-ECT) was scheduled. Two patients suffered from schizophrenia, and one suffered from depression. Their symptoms, such as hyperthermia, consciousness disturbance, myotonus, tremor, sweating, and tachycardia, improved gradually with administration of dantrolene and fluid infusion. However, their psychotic state was exacerbated. Therefore, m-ECT was scheduled. When patients were restless at the hospital ward, they were sedated with propofol and transferred to the operating room. General anesthesia was induced with thiopental 2.5-5 mg x kg(-1). After loss of consciousness, vecuronium bromide 0.01 mg x kg(-1) followed by a dose of 0.1 mg x kg(-1) was administered and ventilation was assisted using a face mask and 100% oxygen. After the ECT stimulus, the patients were sedated with propofol until full recovery from muscle relaxation. Although anesthesia time (mean 38 min) was slightly longer (19 min) than in those anesthetized with thiopental and suxamethonium chloride, m-ECT was performed safely and effectively.
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PMID:[Anesthetic management for electroconvulsive therapy in the patients with a history of neuroleptic malignant syndrome]. 1946 6

A 19-year-old female in her 2nd trimester (17 weeks) of pregnancy became irritable a few days before admission. She became unable to open her mouth and could not talk. She was admitted to the psychiatric hospital due to a rapid change in behavior and a consciousness disturbance. She was diagnosed as having schizophrenia by a psychiatrist. Her EEG showed diffuse high voltage and slow waves. Acute encephalitis was then suspected. Her past and family histories were not suggestive of viral infection. On physical examination, she had a low grade fever. She had hyperhidrosis, autophagia, and repeated oral dyskinesia. Her consciousness level fluctuated from somnolence to stupor. Although her blood CRP level was mildly elevated and she had mild pleocytosis, HSV-PCR was negative in the cerebrospinal fluid (CSF). Abdominal ultrasound examination and MRI showed no ovarian teratoma. Computed tomography (CT) and magnetic resonance imaging (MRI) showed no brain abnormalities. Before analysis for specific nervous system antibodies, the initial diagnosis was non-herpetic limbic encephalitis. She was twice treated with a 6-day course of methylprednisolone (500 mg/day) infusion. She was also given phenobarbital since she had a tonic-clonic seizure about 1 month after admission. Finally, she had a normal delivery at 37 weeks. The baby was healthy, and the patient was discharged without sequelae. We concluded that her diagnosis was anti-N-methyl-D-aspartate (NMDA) receptor (anti-NMDAR) encephalitis based on the presence of anti-NMDAR antibody in the CSF. This report is the first description of a patient with anti-NMDAR antibody encephalitis. The precise mechanism of this encephalitis is not clear, although there have been several reports of autoimmune encephalitis during pregnancy. The patient's CSF anti-NMDAR antibody titer during treatment was measured. Before treatment, the CSF anti-NMDAR antibody titer was strongly positive, but it decreased during treatment and then disappeared after delivery. We hypothesized that the presence of the embryo or placenta may have triggered an antigenic signal and/or antibody through inappropriate immunological modulation.
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PMID:[Anti-NMDA receptor encephalitis during pregnancy]. 2019 92

Anti-NMDA receptor encephalitis, reported by Dalmau et al., is a paraneoplastic encephalitis frequently associated with ovarian teratoma. After the manifestation of schizophrenia-like psychotic symptoms in the initial stage, serious neurological symptoms such as convulsions and central hypoventilation develop. We report two cases of 17-year-old girls with anti-NMDA receptor encephalitis who exhibited different clinical courses. Case 1 showed a typical course of anti-NMDA receptor encephalitis associated with sustained consciousness disturbance requiring long-term artificial respiration. Case 2 underwent surgery for an ovarian teratoma in the early stages of the disorder, did not show convulsions or central hypoventilation, and recovered without any sequelae. Early resection of the ovarian teratoma and the immune suppression therapy may have contributed to the rapid recovery and favorable outcome in case 2. Psychiatrists are the first to see a majority of patients with anti-NMDA receptor encephalitis because of psychiatric symptoms and behavioral changes observed in the initial stage. For successful treatment, psychiatrists need to cooperate with neurologists and gynecologists early in the course of this disorder. Psychiatrists' knowledge of the symptoms and clinical course of this form of encephalitis is essential for early detection and adequate treatment, which may be life-saving and contribute to good functional outcomes.
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PMID:[Two cases of anti-NMDA receptor encephalitis]. 2170 52

Paraneoplastic neurological syndrome (PNS) is a rare disorder caused by the remote effects of cancer and is considered as immune-responses to the molecules on cancer which cross-react with self-antigens in the nervous system. Since the 1980s, several specific anti onconeural antibodies have been reported, which are useful diagnostic markers of PNS and occult cancer. Only a few onconeural antibodies have been identified as primary effectors of neurological damage. Recently sophisticated methods for the detection of new or low titer antibodies have been developed. Several new auto-antibodies against receptors or ion channels on the surface of neuronal membrane, such as NMDA receptors, AMPA receptors, GABA(B) receptors and VGKC complexes, have been reported in the patients with encephalopathy including limbic encephalitis. These diseases can be associated with tumor, but they are more often non-paraneoplastic. These antibodies are generally good biomarkers for effective immunomodulatory treatment for immune-mediated encephalitis with not only consciousness disturbance but also dementia, seizures and psychiatric symptoms which sometimes mimic schizophrenia. Further studies are required to clarify the exact mechanisms underlying neuronal damage in immune-mediated neurological diseases including PNS, which may lead to the development of more rational therapies and greater understanding of immunology in the nervous system.
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PMID:[Pareneoplastic neurological syndrome --update]. 2227 85

The prevalence of polydipsia among patients with schizophrenia is 6%-20%. Around 10%-20% of patients with polydipsia may develop hyponatremia and even complicated with rhabdomyolysis. Here we presented a 40-year-old man with schizophrenia, who had received paliperidone 15 mg/d for more than one year, and polydipsia was noted. In Jan, 2014, he developed hyponatremia (Na 113 mEq/L) with consciousness disturbance. After 3% NaCl (500 cc/d) intravenous supplement for three days, the hyponatremia was corrected, but rhabdomyolysis developed with a substantial elevation in the level of creatine kinase (CK) to 30505 U/L. After hydration, the CK level gradually decreased to 212 U/L. Both the hyponatremia itself and quick supplementation of NaCl can cause rhabdomyolysis. If rhabdomyolysis is not recognized, insufficient hydration or water restriction for polydipsia may further exacerbate the rhabdomyolysis with a lethal risk. In this case, we highlight the possible complication of rhabdomyolysis with polydipsia-induced hyponatremia. In addition to monitoring the serum sodium level, the monitoring of CK is also important; and switching of antipsychotic may improve the polydipsia.
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PMID:Polydipsia, hyponatremia and rhabdomyolysis in schizophrenia: A case report. 2554 Jul 30

Objectives: Despite intensive research, schizophrenia and schizoaffective disorders continue to be theoretical constructs that describe clinical syndromes and no pathophysiologically defined diseases. Moreover, there are no clear biomarkers at hand. Therefore, these diagnoses are still set up based on clinical ICD-10/DSM-5 criteria and the exclusion of alcohol-/drug-associated, systemic or other brain organic causes.Methods: Recently, autoimmune encephalitis with psychotic symptoms caused by specific antineuronal antibodies has been identified as a rare, but potentially treatable differential diagnosis. However, these inflammatory brain diseases are not reliably detected by our current routine diagnostic workup in psychiatry. This qualitative review provides structured diagnostic and therapeutic support for clinical practice.Results: Disturbances of consciousness and orientation, catatonia, speech dysfunction, focal neurological signs, epileptic seizures/EEG abnormalities or autonomic dysfunction are warning signs in psychiatric patients which should always induce cerebrospinal fluid analysis with determination of antineuronal autoantibodies. Currently established immunotherapy strategies are summarised, taking into account international expert advice.Conclusions: Guided by clinical warning signs, our qualitative review enables rapid and reliable diagnosis of definite autoimmune encephalitis. This is of high relevance for the affected individuals, since early and sufficiently intense immunotherapy often leads to a good prognosis despite severe illness.
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PMID:Autoimmune encephalitis with psychosis: Warning signs, step-by-step diagnostics and treatment. 3051 53