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Psychosomatics 2016Withdrawal from alcohol and sedative-hypnotics can be complicated by seizures, hallucinations, or delirium. Withdrawal catatonia is another, less commonly discussed... (Review)
Review
Alcohol and Sedative-Hypnotic Withdrawal Catatonia: Two Case Reports, Systematic Literature Review, and Suggestion of a Potential Relationship With Alcohol Withdrawal Delirium.
BACKGROUND
Withdrawal from alcohol and sedative-hypnotics can be complicated by seizures, hallucinations, or delirium. Withdrawal catatonia is another, less commonly discussed complication that clinicians should appreciate.
METHODS
We present a case of alcohol withdrawal catatonia and a case of benzodiazepine withdrawal catatonia and offer a systematic review of previous cases of alcohol or sedative-hypnotic withdrawal catatonia. We outline clinical features that suggest a potential link between withdrawal catatonia and withdrawal delirium.
RESULTS
We identified 26 cases of withdrawal catatonia in the literature-all principally with catatonic stupor-with an average age of 56 years (range: 27-92) and balanced prevalence between sexes. Withdrawal catatonia tends to occur only after chronic use of alcohol or sedative-hypnotic agents with a typical onset of 3-7 days after discontinuation and duration of 3-10 days. Withdrawal catatonia is responsive to benzodiazepines or electroconvulsive therapy. Features that suggest a parallel between withdrawal catatonia and withdrawal delirium include time course, neurobiologic convergence, efficacy of benzodiazepines and electroconvulsive therapy, typical absence of abnormal electroencephalographic findings, and phenotypic classification suggested by a recent literature in sleep medicine.
CONCLUSION
Alcohol and sedative-hypnotic withdrawal may present with catatonia or catatonic features. The clinical and neurobiologic convergence between withdrawal catatonia and withdrawal delirium deserves further attention. In view of these similarities, we propose that withdrawal delirium may represent excited catatonia: these new viewpoints may serve as a substrate for a better understanding of the delirium-catatonia spectrum.
Topics: Alcohol Withdrawal Delirium; Benzodiazepines; Catatonia; Central Nervous System Depressants; Clonazepam; Electroconvulsive Therapy; Ethanol; Female; Humans; Hypnotics and Sedatives; Male; Middle Aged; Substance Withdrawal Syndrome
PubMed: 26949118
DOI: 10.1016/j.psym.2015.12.007 -
Frontiers in Genetics 2022Due to nonspecific symptoms, rare dyslipidaemias are frequently misdiagnosed, overlooked, and undertreated, leading to increased risk for severe cardiovascular disease,...
Due to nonspecific symptoms, rare dyslipidaemias are frequently misdiagnosed, overlooked, and undertreated, leading to increased risk for severe cardiovascular disease, pancreatitis and/or multiple organ failures before diagnosis. Better guidelines for the recognition and early diagnosis of rare dyslipidaemias are urgently required. Genomic DNA was isolated from blood samples of a Pakistani paediatric patient with hypertriglyceridemia, and from his parents and siblings. Next-generation sequencing (NGS) was performed, and an expanded dyslipidaemia panel was employed for genetic analysis. The NGS revealed the presence of a homozygous missense pathogenic variant c.230G>A (NM_178172.6) in exon 3 of the (glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1) gene resulting in amino acid change p.Cys77Tyr (NP_835466.2). The patient was 5.5 years old at the time of genetic diagnosis. The maximal total cholesterol and triglyceride levels were measured at the age of 10 months (850.7 mg/dl, 22.0 mmol/L and 5,137 mg/dl, 58.0 mmol/L, respectively). The patient had cholesterol deposits at the hard palate, eruptive xanthomas, lethargy, poor appetite, and mild splenomegaly. Both parents and sister were heterozygous for the familial variant in the gene. Moreover, in the systematic review, we present 62 patients with pathogenic variants in the gene and clinical findings, associated with hyperlipoproteinemia. In a child with severe hypertriglyceridemia, we identified a pathogenic variant in the gene causing hyperlipoproteinemia (type 1D). In cases of severe elevations of plasma cholesterol and/or triglycerides genetic testing for rare dyslipidaemias should be performed as soon as possible for optimal therapy and patient management.
PubMed: 36051701
DOI: 10.3389/fgene.2022.983283 -
General Hospital Psychiatry 2021Catatonia is classically associated with psychiatric conditions but may occur in medical and neurologic disorders. Status epilepticus (SE) is a seizure lasting more than... (Review)
Review
INTRODUCTION
Catatonia is classically associated with psychiatric conditions but may occur in medical and neurologic disorders. Status epilepticus (SE) is a seizure lasting more than five minutes or two or more seizures within a five-minute period without interictal recovery of consciousness. Non-convulsive status epilepticus (NCSE) is SE without prominent motor activity that may present with catatonic symptoms. The relevance of NCSE as a potential etiology for catatonia is not clear in the literature.
METHODS
A systematic review was completed to evaluate the literature on NCSE presenting with catatonia. PubMed and PsycInfo databases were searched and articles were reviewed for the presence of catatonia and NCSE.
RESULTS
15 articles describing 27 cases meeting inclusion criteria were identified. The authors add 1 case to the literature. The most common catatonic symptoms identified in NCSE were mutism and stupor. Clinical features frequent in NCSE presenting with catatonia included new catatonic symptoms, age over 50 years, comorbid neurological conditions, or a change in medications that affect seizure threshold. A documented psychiatric history was also common and may contribute to delayed diagnosis.
DISCUSSION/CONCLUSION
It is important to consider NCSE in the differential diagnosis of new catatonic symptoms. A suggested approach to diagnostic evaluation is provided.
Topics: Catatonia; Diagnosis, Differential; Electroencephalography; Humans; Middle Aged; Seizures; Status Epilepticus
PubMed: 33276270
DOI: 10.1016/j.genhosppsych.2020.11.008 -
Ophthalmic Plastic and Reconstructive...Saturday night retinopathy, the term coined by Jayam et al . in 1974, is a rare condition in which external compression of the orbit during a drug and alcohol stupor...
PURPOSE
Saturday night retinopathy, the term coined by Jayam et al . in 1974, is a rare condition in which external compression of the orbit during a drug and alcohol stupor causes a unilateral orbitopathy with ophthalmoplegia and ischemic retinopathy. This condition has been increasingly reported in the last decade, correlating with an increasing burden of substance use. This condition mirrors a similar entity typically reported in patients following spinal surgery, where a headrest supporting the patient's face compresses the orbit. The current authors combine these 2 entities, entitled external compressive ischemic orbitopathy, and present a comprehensive literature review describing this entity.
METHODS
A systematic review was carried out in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. All related publications of vision loss in the setting of orbital compression were reviewed. Data collected included patient demographics, precipitating circumstances of vision loss, presenting ocular symptoms, outcomes, and ancillary imaging.
RESULTS
In total 31 articles were selected for inclusion, yielding 46 patients. A total of 10 patients suffered orbitopathy in the setting of a drug stupor, and 36 following prone-positioned surgery. However, 79% of patients presented with visual acuity of light perception or worse. Also, 86% of patients presented with ophthalmoplegia, 92% with proptosis and orbital edema, and 86% with varying degrees of retinal ischemia. When compared with iatrogenic cases, self-induced stuporous cases demonstrated worse presenting visual acuity, ophthalmoplegia, retinal and choroidal filling, and worse final outcomes.
CONCLUSION
External compressive ischemic orbitopathy is a severe vision-threatening condition that has been increasingly reported in the last decade.
Topics: Humans; Graves Ophthalmopathy; Stupor; Decompression, Surgical; Orbit; Exophthalmos; Vision Disorders; Ophthalmoplegia; Blindness; Retinal Diseases; Ischemia
PubMed: 37486344
DOI: 10.1097/IOP.0000000000002430 -
Turkish Neurosurgery 2022To systematically evaluate the medication safety and effectiveness of Oxcarbazepine (OXC) and carbamazepine (CBZ) for the treatment of post-stroke epilepsy (PSE). (Meta-Analysis)
Meta-Analysis
AIM
To systematically evaluate the medication safety and effectiveness of Oxcarbazepine (OXC) and carbamazepine (CBZ) for the treatment of post-stroke epilepsy (PSE).
MATERIAL AND METHODS
We searched Medline and other databases to identify the randomized controlled trials (RCTs) that compare the efficacies of OXC and CBZ in treating PSE. Two authors extracted and analyzed the data independently with Revman 5.3 software. The Q-test and I2 were used to test the statistical heterogeneity. The fixed or random effect models were selected according to heterogeneity.
RESULTS
Eight RCTs that include 671 patients were involved in this study. The meta-analyses result showed that the overall efficiency of OXC was significantly better than that of CBZ (OR=4.55, 95% confidence interval (CI) (3.04?6.81)), the overall adverse events (OR=0.27, 95% CI (0.18?0.42), and the incidence of vomiting (OR=0.28, 95% CI (0.09?0.85)) of OXC was significantly less than that of CBZ. No significant differences in the incidence of rash (OR=0.45, 95% CI (0.19?1.07)), lethargy (OR=0.49, 95% CI (0.16?1.45)), and dizziness (OR=0.51, 95% CI (0.20?1.35)) were detected between OXC and CBZ.
CONCLUSION
OXC seems to be superior to CBZ in the treatment of PSE, with higher efficacy, and safety than the latter. However, more research on OXC and CBZ in the treatment of PSE is required in the later stage due to the sample size limitation of our study.
Topics: Anticonvulsants; Carbamazepine; Epilepsy; Humans; Oxcarbazepine
PubMed: 34936076
DOI: 10.5137/1019-5149.JTN.34664-21.3 -
World Journal of Pediatrics : WJP Dec 2017To review the available evidence from prospective studies on the safety and tolerability of the ketogenic diet (KD) for the treatment of refractory childhood epilepsy. (Review)
Review
BACKGROUND
To review the available evidence from prospective studies on the safety and tolerability of the ketogenic diet (KD) for the treatment of refractory childhood epilepsy.
METHODS
A comprehensive bibliographic search was performed with the aim of retrieving prospective studies that monitored adverse effects (AEs) in children after receiving the classic or medium-chain triglyceride KD therapy for refractory epilepsy.
RESULTS
A total of 45 studies were retrieved, including 7 randomized controlled trials. More than 40 categories of AEs were reported. The most common AEs included gastrointestinal disturbances (40.6%), hyperlipidemia (12.8%), hyperuricemia (4.4%), lethargy (4.1%), infectious diseases (3.8%) and hypoproteinemia (3.8%). Severe AEs, such as respiratory failure and pancreatitis, occurred in no more than 0.5% of children. Specifically, patients receiving KD therapy should be monitored for osteopenia, urological stones, right ventricular diastolic dysfunction, and growth disturbance. The total retention rates of the diet for 1 year and 2 years were 45.7% and 29.2%, respectively. Nearly half of the patients discontinued the diet because of lack of efficacy. AEs were not the main reason for the KD discontinuation. None of the 24 deaths reported after initiation of the diet was attributed to the KD.
CONCLUSIONS
KD is a relatively safe dietary therapy. However, because the KD can cause various AEs, it should be implemented under careful medical supervision. Continuous follow-up is needed to address the long-term impact of the diet on the overall health of children.
Topics: Adolescent; Child; Child, Preschool; China; Diet, Ketogenic; Drug Resistant Epilepsy; Female; Humans; Infant; Male; Patient Safety; Prognosis; Prospective Studies; Risk Assessment; Severity of Illness Index; Treatment Outcome
PubMed: 28702868
DOI: 10.1007/s12519-017-0053-2 -
The Cochrane Database of Systematic... Jun 2017Schizophrenia and related disorders such as schizophreniform and schizoaffective disorder are serious mental illnesses characterised by profound disruptions in thinking... (Review)
Review
BACKGROUND
Schizophrenia and related disorders such as schizophreniform and schizoaffective disorder are serious mental illnesses characterised by profound disruptions in thinking and speech, emotional processes, behaviour and sense of self. Clozapine is useful in the treatment of schizophrenia and related disorders, particularly when other antipsychotic medications have failed. It improves positive symptoms (such as delusions and hallucinations) and negative symptoms (such as withdrawal and poverty of speech). However, it is unclear what dose of clozapine is most effective with the least side effects.
OBJECTIVES
To compare the efficacy and tolerability of clozapine at different doses and to identify the optimal dose of clozapine in the treatment of schizophrenia, schizophreniform and schizoaffective disorders.
SEARCH METHODS
We searched the Cochrane Schizophrenia Group's Study-Based Register of Trials (August 2011 and 8 December 2016).
SELECTION CRITERIA
All relevant randomised controlled trials (RCTs), irrespective of blinding status or language, that compared the effects of clozapine at different doses in people with schizophrenia and related disorders, diagnosed by any criteria.
DATA COLLECTION AND ANALYSIS
We independently inspected citations from the searches, identified relevant abstracts, obtained full articles of relevant abstracts, and classified trials as included or excluded. We included trials that met our inclusion criteria and reported useable data. For dichotomous data, we calculated the relative risk (RR) and the 95% confidence interval (CI) on an intention-to-treat basis based on a random-effects model. For continuous data, we calculated mean differences (MD) again based on a random-effects model. We assessed risk of bias for included studies and created 'Summary of findings' tables using GRADE.
MAIN RESULTS
We identified five studies that could be included. Each compared the effects of clozapine at very low dose (up to 149 mg/day), low dose (150 mg/day to 300 mg/day) and standard dose (301 mg/day to 600 mg/day). Four of the five included studies were based on a small number of participants. We rated all the evidence reported for the main outcomes of interest as low or very low quality. No data were available for the main outcomes of global state, service use or quality of life. Very low dose compared to low doseWe found no evidence of effect on mental state between low and very low doses of clozapine in terms of average Brief Psychiatric Rating Scale-Anchored (BPRS-A) endpoint score (1 RCT, n = 31, MD 3.55, 95% CI -4.50 to 11.60, very low quality evidence). One study found no difference between groups in body mass index (BMI) in the short term (1 RCT, n = 59, MD -0.10, 95% CI -0.95 to 0.75, low-quality evidence). Very low dose compared to standard doseWe found no evidence of effect on mental state between very low doses and standard doses of clozapine in terms of average BPRS-A endpoint score (1 RCT, n = 31, MD 6.67, 95% CI -2.09 to 15.43, very low quality evidence). One study found no difference between groups in BMI in the short term (1 RCT, n = 58, MD 0.10, 95% CI -0.76 to 0.96, low-quality evidence) Low dose compared to standard doseWe found no evidence of effect on mental state between low doses and standard doses of clozapine in terms of both clinician-assessed clinical improvement (2 RCTs, n = 141, RR 0.76, 95% CI 0.36 to 1.61, medium-quality evidence) and clinically important response as more than 30% change in BPRS score (1 RCT, n = 176, RR 0.93, 95% CI 0.78 to 1.10, medium-quality evidence). One study found no difference between groups in BMI in the short term (1 RCT, n = 57, MD 0.20, 95% CI -0.84 to 1.24, low-quality evidence).We found some evidence of effect for other adverse effect outcomes; however, the data were again limited. Very low dose compared to low doseThere was limited evidence that serum triglycerides were lower at low-dose clozapine compared to very low dose in the short term (1 RCT, n = 59, MD 1.00, 95% CI 0.51 to 1.49). Low dose compared to standard doseWeight gain was lower at very low dose compared to standard dose (1 RCT, n = 27, MD -2.70, 95% CI -5.38 to -0.02). Glucose level one hour after meal was also lower at very lose dose (1 RCT, n = 58, MD -1.60, 95% CI -2.90 to -0.30). Total cholesterol levels were higher at very low compared to standard dose (1 RCT, n = 58, n = 58, MD 1.00, 95% CI 0.20 to 1.80). Low dose compared to standard doseThere was evidence of fewer adverse effects, measured as lower TESS scores, in the low-dose group in the short term (2 RCTs, n = 266, MD -3.99, 95% CI -5.75 to -2.24); and in one study there was evidence that the incidence of lethargy (RR 0.77, 95% CI 0.60 to 0.97), hypersalivation (RR 0.70, 95% CI 0.57 to 0.84), dizziness (RR 0.56, 95% CI 0.39 to 0.81) and tachycardia (RR 0.57, 95% CI 0.45 to 0.71) was less at low dose compared to standard dose.
AUTHORS' CONCLUSIONS
We found no evidence of effect on mental state between standard, low and very low dose regimes, but we did not identify any trials on high or very high doses of clozapine. BMI measurements were similar between groups in the short term, although weight gain was less at very low dose compared to standard dose in one study. There was limited evidence that the incidence of some adverse effects was greater at standard dose compared to lower dose regimes. We found very little useful data and the evidence available is generally of low or very low quality. More studies are needed to validate our findings and report on outcomes such as relapse, remission, social functioning, service utilisation, cost-effectiveness, satisfaction with care, and quality of life. There is a particular lack of medium- or long-term outcome data, and on dose regimes above the standard rate.
Topics: Agranulocytosis; Antipsychotic Agents; Clozapine; Humans; Psychotic Disorders; Schizophrenia
PubMed: 28613395
DOI: 10.1002/14651858.CD009555.pub2 -
Social Psychiatry and Psychiatric... Feb 2020Neuroleptic (antipsychotic) drugs reduce psychotic symptoms, but how they achieve these effects and how the drugs' effects are experienced by people who take them are...
PURPOSE
Neuroleptic (antipsychotic) drugs reduce psychotic symptoms, but how they achieve these effects and how the drugs' effects are experienced by people who take them are less well understood. The present study describes a synthesis of qualitative data about mental and behavioural alterations associated with taking neuroleptics and how these interact with symptoms of psychosis and people's sense of self and agency.
METHODS
Nine databases were searched to identify qualitative literature concerning experiences of taking neuroleptic medication. A thematic synthesis was conducted.
RESULTS
Neuroleptics were commonly experienced as producing a distinctive state of lethargy, cognitive slowing, emotional blunting and reduced motivation, which impaired functioning but also had beneficial effects on symptoms of psychosis and some other symptoms (e.g. insomnia). For some people, symptom reduction helped restore a sense of normality and autonomy, but others experienced a loss of important aspects of their personality. Across studies, many people adopted a passive stance towards long-term medication, expressing a sense of resignation, endurance or loss of autonomy.
CONCLUSIONS
Neuroleptic drugs modify cognition, emotions and motivation. These effects may be associated with reducing the intensity and impact of symptoms, but also affect people's sense of self and agency. Understanding how the effects of neuroleptics are experienced by those who take them is important in developing a more collaborative approach to drug treatment in psychosis and schizophrenia.
Topics: Adult; Antipsychotic Agents; Emotions; Female; Humans; Lethargy; Male; Middle Aged; Motivation; Personal Autonomy; Psychotic Disorders; Qualitative Research; Self Concept; Treatment Outcome; Young Adult
PubMed: 31875238
DOI: 10.1007/s00127-019-01819-2 -
Journal of Human Lactation : Official... Feb 2016There are increasing reports on hypernatremia, a potentially devastating condition, in exclusively breastfed newborn infants. Our purposes were to describe the clinical... (Review)
Review
There are increasing reports on hypernatremia, a potentially devastating condition, in exclusively breastfed newborn infants. Our purposes were to describe the clinical features of the condition and identify the risk factors for it. We performed a review of the existing literature in the National Library of Medicine database and in the search engine Google Scholar. A total of 115 reports were included in the final analysis. Breastfeeding-associated neonatal hypernatremia was recognized in infants who were ≤ 21 days of age and had ≥ 10% weight loss of birth weight. Cesarean delivery, primiparity, breast anomalies or breastfeeding problems, excessive prepregnancy maternal weight, delayed first breastfeeding, lack of previous breastfeeding experience, and low maternal education level were significantly associated with breastfeeding-associated hypernatremia. In addition to excessive weight loss (≥ 10%), the following clinical findings were observed: poor feeding, poor hydration state, jaundice, excessive body temperature, irritability or lethargy, decreased urine output, and epileptic seizures. In conclusion, the present survey of the literature identifies the following risk factors for breastfeeding-associated neonatal hypernatremia: cesarean delivery, primiparity, breastfeeding problems, excessive maternal body weight, delayed breastfeeding, lack of previous breastfeeding experience, and low maternal education level.
Topics: Breast Feeding; Female; Humans; Hypernatremia; Infant, Newborn; Risk Factors; Weight Loss
PubMed: 26530059
DOI: 10.1177/0890334415613079 -
Neonatology 2023Deep medullary vein (DMV) thrombosis is a rare cause of brain damage in both preterm and full-term neonates. In this study, we aimed to collect data on clinical and...
BACKGROUND
Deep medullary vein (DMV) thrombosis is a rare cause of brain damage in both preterm and full-term neonates. In this study, we aimed to collect data on clinical and radiological presentation, treatment, and outcome of neonatal DMV thrombosis.
METHODS
Systematic literature review on neonatal DMV thrombosis was carried out in PubMed, ClinicalTrial.gov, Scopus, and Web of Science up to December 2022.
RESULTS
Seventy-five published cases of DMV thrombosis were identified and analysed (preterm newborns were 46%). Neonatal distress, respiratory resuscitation, or need for inotropes were present in 34/75 (45%) of patients. Signs and symptoms at presentation included seizures (38/75, 48%), apnoea (27/75, 36%), lethargy or irritability (26/75, 35%). At magnetic resonance imaging (MRI), fan-shaped linear T2 hypointense lesions were documented in all cases. All had ischaemic injuries, most often involving the frontal (62/74, 84%) and parietal lobes (56/74, 76%). Signs of haemorrhagic infarction were present in 53/54 (98%). Antithrombotic treatment was not mentioned in any of the studies included. Although mortality was low (2/75, 2.6%), a large proportion of patients developed neurological sequelae (intellectual disability in 19/51 [37%] and epilepsy in 9/51 [18%] cases).
CONCLUSIONS
DMV thrombosis is rarely identified in the literature, even if it is possibly under-recognized or under-reported. Presentation in neonatal age is with seizures and non-specific systemic signs/symptoms that often cause diagnostic delay, despite the pathognomonic MRI picture. The high rate of morbidity, which determines significant social and health costs, requires further in-depth studies aimed at earlier diagnosis and evidence-based prevention and therapeutic strategies.
Topics: Humans; Infant, Newborn; Delayed Diagnosis; Magnetic Resonance Imaging; Brain Injuries; Thrombosis; Seizures
PubMed: 37379822
DOI: 10.1159/000530647