Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depersonalization/derealization disorder is characterized by depersonalization often co-occurring with derealization in the absence of significant psychosis, memory, or identity disturbance. Depersonalization/derealization is categorized as one of the dissociative disorders, which also includes dissociative amnesia, dissociative fugue, dissociative identity disorder, and forms of dissociative disorder not otherwise specified. Although these disorders may be under-diagnosed or misdiagnosed, many persons with psychiatric illness who have experienced trauma report symptoms consistent with dissociative disorders. There are limited scientific data on prevalence of depersonalization/derealization disorder specifically. This paper reviews clinical, phenomenological and epidemiological information regarding diagnosis and treatment of dissociative disorders in general, and illustrates common presenting histories of persons with derealization/depersonalization disorder utilizing composite cases. The clinical vignettes focus on recommended psychotherapy and pharmacotherapy interventions as part of a comprehensive multidisciplinary treatment plan for these individuals.
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PMID:STRESS AND TRAUMA: Psychotherapy and Pharmacotherapy for Depersonalization/Derealization Disorder. 2533 44

Kleine-Levin syndrome is a rare recurrent encephalopathy primarily affecting teenagers, characterized by relapsing-remitting episodes of hypersomnia along with cognitive, psychiatric and behavioral disturbances. During episodes, patients suddenly present hypersomnia (with sleep lasting 15-21 h/d), cognitive impairment (major apathy, confusion, slowness, amnesia), and a specific feeling of derealization (dreamy state, altered perception). Less frequently, they may also experience hyperphagia (66%), hypersexuality (53%, principally men), depressed mood (53%, principally women), anxiety, hallucinations, and acute brief psychosis (33%). Brain functional imaging is often abnormal. Stimulants are poorly beneficial during episodes, whereas lithium and valproate help reducing the episodes frequency and duration.
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PMID:Kleine-Levin Syndrome. 2605 63

We report on a female patient presenting with primary progressive aphasia (PPA) and her brother presenting with psychosis. Both siblings had an R5H-mutation in exon 1 of the MAPT-gene. The PPA patient presented for the first time at the age of 72 years with a 4-year-history of language impairment. After a progressive course the patient died at the age of 76 years. The R5H-MAPT-gene mutation detected in the siblings has been described only once in 2002 by Hayashi et al. [1]. In this previous case from Japan, a 75-year-old patient initially displayed amnesia and disorientation. He became bedridden, with progressive mutism and rigidity of the upper extremities. Noteworthy are the manifold signs and symptoms in R5H-mutations and the late age of onset. For future trials, the detection of biomarkers for frontotemporal lobar degeneration in presymptomatic cohorts like the genetic frontotemporal dementia initiative (GENFI) is of help for stratifying subjects at risk.
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PMID:[A Pair of Siblings with a rare R5H-Mutation in Exon 1 of the MAPT-Gene]. 2620 45

Sub-anaesthetic ketamine is of special interest for depression research due to its rapid and potent but short-lived antidepressant response (after-effect). The presented case is the first one in the literature which deals in detail with the transfer from ketamine's antidepressant action to ketamine addiction. A 50-year-old anaesthetic nurse, who had never been treated with antidepressants before, started with self-injecting ketamine racemate 50 mg IM once a week to cope with her major depression. She continuously stole ketamine from hospital stocks. Due to a gradually developing tolerance to ketamine's antidepressant action, she stepwise increased dose and frequency of ketamine self-injections up to daily 2 g IM (three-fold her anaesthetic dose) over six months. This was accompanied by the development of ketamine addiction, loss of consciousness, dissociative immobility, and amnesia. Inpatient detoxification treatment was characterized by a strong craving for ketamine and, later on, by the occurrence of a severe depressive episode remitting on venlafaxine. A 14-week follow-up documented a normal condition without any ketamine sequelae, such as craving, psychosis, depression, or cognitive abnormalities. Thus, awareness of ketamine addiction potential, even in patients who received ketamine for antidepressant purposes, is important.
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PMID:Long-Term Ketamine Self-Injections in Major Depressive Disorder: Focus on Tolerance in Ketamine's Antidepressant Response and the Development of Ketamine Addiction. 2631 49

Traumatic brain injury (TBI) is a complex neurologic and neuropathologic process that may affect the patient's behavior permanently. Clinically, TBI is associated with a wide gamut of neurologic and psychiatric disorders, such as amnesia, cognitive decline, seizures, attention and concentration deficits, depression, manic behavior, psychosis, hostile and violent behavior, and personality alterations. Therapy and rehabilitative efforts should be designed based on the type of injury and the patient's specific needs. Gaining familiarity with the behavioral disorders outlined in this article and understanding how to identify and treat them plays a significant role in the management of patients with TBI.
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PMID:Traumatic Brain Injury and Behavior: A Practical Approach. 2661 95

Encephalitis is a brain inflammation, which could involve also the meninges. The etiology of encephalitis could be: viral, bacterial, fungal or autoimmune. Anti-NMDAR encephalitis is an immune disorder, easy to diagnose and is a treatable condition. Most patients with anti-NMDAR encephalitis develop a multistage illness that progresses from psychosis, memory deficits, seizures, to catatonic state and breathing instability. We present a case report of a 20-year old woman, who presented: amnesia, visual hallucination, illusions, seizures after that occurred following autoimmune encephalitis. The exact incidence of anti-NMDAR encephalitis is unknown, but it seems to be more frequent than any other known paraneoplastic encephalitis. The present case is important considering that autoimmune encephalitis is a rare frequency disorder in Romania, with patients presenting resounding psychiatric and neurological manifestations.
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PMID:PSYCHOTIC DISORDERS GENERATED BY AUTOIMMUNE ENCEPHALITIS (CLINICAL CASE). 2679 48

More than a third of the population report childhood adversity, and these experiences are associated with an increased risk of clinical and subclinical psychosis. The reason why some people go on to develop mental health problems and others do not is a key question for study. It has been hypothesized that dissociative processes mediate the relationship between early adversity and psychosis. The current study assessed whether dissociation, and specifically depersonalization (one component of dissociation), plays a mediating role in the relationship between childhood maltreatment and both hallucination proneness and delusional ideation. The study used a cross-sectional design and recruited a student sample to assess these relationships in a nonclinical group. Dissociation mediated the relationship between early maltreatment and both hallucination proneness and delusional ideation. In terms of specific dissociative processes, depersonalization did not mediate hallucination proneness or delusional ideation. Absorption mediated hallucination proneness; dissociative amnesia (negatively) and absorption mediated delusional ideation. It is likely that dissociation interferes with the encoding of traumatic information in nonclinical as well as clinical groups and in certain ways. Absorption may be particularly relevant. For some people, traumatic memories may intrude into conscious awareness in adulthood as psychotic-type experience.
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PMID:Dissociation mediates the relationship between childhood maltreatment and subclinical psychosis. 2704 64

Voltage-gated potassium channel (VGKC)-complex antibodies are defined by the radioimmunoprecipitation of Kv1 potassium channel subunits from brain tissue extracts and were initially discovered in patients with peripheral nerve hyperexcitability (PNH). Subsequently, they were found in patients with PNH plus psychosis, insomnia, and dysautonomia, collectively termed Morvan's syndrome (MoS), and in a limbic encephalopathy (LE) with prominent amnesia and frequent seizures. Most recently, they have been described in patients with pure epilepsies, especially in patients with the novel and distinctive semiology termed faciobrachial dystonic seizures (FBDS). In each of these conditions, there is a close correlation between clinical measures and antibody levels. The VGKC-complex is a group of proteins that are strongly associated in situ and after extraction in mild detergent. Two major targets of the autoantibodies are leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein 2 (CASPR2). The patients with PNH or MoS are most likely to have CASPR2 antibodies, whereas LGI1 antibodies are found characteristically in patients with FBDS and LE. Crucially, each of these conditions has a good response to immunotherapies, often corticosteroids and plasma exchange, although optimal regimes require further study. VGKC-complex antibodies have also been described in neuropathic pain syndromes, chronic epilepsies, a polyradiculopathy in porcine abattoir workers, and some children with status epilepticus. Increasingly, however, the antigenic targets in these patients are not defined and in some cases the antibodies may be secondary rather than the primary cause. Future serologic studies should define all the antigenic components of the VGKC-complex, and further inform mechanisms of antibody pathogenicity and related inflammation.
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PMID:Voltage-gated potassium channel-complex autoimmunity and associated clinical syndromes. 2711 78

Voltage-gated potassium channel (VGKC) complex antibodies are auto-antibodies, initially identified in acquired neuromyotonia (aNMT; Isaacs' syndrome), which cause muscle cramps and difficulty in opening the palm of the hands. Subsequently, these antibodies were found in patients presenting with aNMT along with psychosis, insomnia, and dysautonomia, collectively termed Morvan's syndrome (MoS), and in a limbic encephalopathy (LE) patient with prominent amnesia and frequent seizures. Typical LE cases have a distinctive adult-onset, frequent, brief dystonic seizure semiology that predominantly affects the arms and ipsilateral face. It has now been termed faciobrachial dystonic seizures (FBDS). The VGKC complex is a group of proteins that are strongly associated in situ and after extraction in the mild detergent digitonin. Recent studies indicated that the VGKC complex antibodies are mainly directed toward associated proteins (for example LGI1, Caspr2) that complex with VGKCs themselves. Patients with aNMT or MoS are most likely to have Caspr2 antibodies, whereas LGI1 antibodies are found characteristically in patients with FBDS and LE. We systematically identified and quantified autoantibodies in patient sera with VGKC-complex antibody associated encephalopathy and showed the relationship between individual antibodies and patient's symptoms. Furthermore, we revealed how autoantibodies disrupt the physiological functions of target proteins. LGI1 antibodies neutralize the interaction between LGI1 and ADAM22, reducing the synaptic AMPA receptors.
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PMID:[Voltage-Gated Potassium Channel-Complex Antibodies Associated Encephalopathy and Related Diseases]. 2766 87

Behaviourally spontaneous confabulation denotes a distinct syndrome consisting of confabulations that patients act upon, disorientation, and amnesia. It corresponds to the stable form of the original Korsakoff syndrome. While the syndrome may also occur in confusional states and degenerative dementia, this article is about the syndrome as it occurs after acute and focal brain damage. The patients act according to ideas and obligations that can mostly be traced back to real experiences in their past, but which are not currently valid guides of thinking and behaviour. This inability to abandon behavioural guides (anticipations) that are currently not valid corresponds to a failure of behavioural extinction and to the inability to abandon a previously rewarded choice in reversal learning when the expected reward (outcome) fails to occur, that is, following extinction trials. This article describes evidence from human and animal experiments showing that the posterior medial orbitofrontal cortex (OFC), which is typically damaged in these patients, and connected structures of the reward system contain the neural apparatus to signal the non-occurrence of anticipated outcomes, thereby presumably synchronizing thought and behaviour with current reality. Failure of this function, which we call orbitofrontal reality filtering, is associated with behaviourally spontaneous confabulation and disorientation after acute and focal brain damage, but not with other forms of confabulation, and not with reality confusion in degenerative dementia. Potential links with psychosis and decision making will be discussed.
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PMID:What does extinction have to do with confabulation? 2785 71


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