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Current Pediatric Reviews 2020Sleep terrors are common, frightening, but fortunately benign events. Familiarity with this condition is important so that an accurate diagnosis can be made. (Review)
Review
BACKGROUND
Sleep terrors are common, frightening, but fortunately benign events. Familiarity with this condition is important so that an accurate diagnosis can be made.
OBJECTIVE
To familiarize physicians with the clinical manifestations, diagnosis, and management of children with sleep terrors.
METHODS
A PubMed search was completed in Clinical Queries using the key terms "sleep terrors" OR "night terrors". The search strategy included meta-analyses, randomized controlled trials, clinical trials, observational studies, and reviews. Only papers published in the English literature were included in this review. The information retrieved from the above search was used in the compilation of the present article.
RESULTS
It is estimated that sleep terrors occur in 1 to 6.5% of children 1 to 12 years of age. Sleep terrors typically occur in children between 4 and 12 years of age, with a peak between 5 and 7 years of age. The exact etiology is not known. Developmental, environmental, organic, psychological, and genetic factors have been identified as a potential cause of sleep terrors. Sleep terrors tend to occur within the first three hours of the major sleep episode, during arousal from stage three or four non-rapid eye movement (NREM) sleep. In a typical attack, the child awakens abruptly from sleep, sits upright in bed or jumps out of bed, screams in terror and intense fear, is panicky, and has a frightened expression. The child is confused and incoherent: verbalization is generally present but disorganized. Autonomic hyperactivity is manifested by tachycardia, tachypnea, diaphoresis, flushed face, dilated pupils, agitation, tremulousness, and increased muscle tone. The child is difficult to arouse and console and may express feelings of anxiety or doom. In the majority of cases, the patient does not awaken fully and settles back to quiet and deep sleep. There is retrograde amnesia for the attack the following morning. Attempts to interrupt a sleep terror episode should be avoided. As sleep deprivation can predispose to sleep terrors, it is important that the child has good sleep hygiene and an appropriate sleeping environment. Medical intervention is usually not necessary, but clonazepam may be considered on a short-term basis at bedtime if sleep terrors are frequent and severe or are associated with functional impairment, such as fatigue, daytime sleepiness, and distress. Anticipatory awakening, performed approximately half an hour before the child is most likely to experience a sleep terror episode, is often effective for the treatment of frequently occurring sleep terrors.
CONCLUSION
Most children outgrow the disorder by late adolescence. In the majority of cases, there is no specific treatment other than reassurance and parental education. Underlying conditions, however, should be treated if possible and precipitating factors should be avoided.
Topics: Child; Child, Preschool; Diagnosis, Differential; Humans; Infant; Night Terrors; Prognosis; Sleep
PubMed: 31612833
DOI: 10.2174/1573396315666191014152136 -
Neuropsychiatric Disease and Treatment 2017In this review, we present a survey on Korsakoff's syndrome (KS), a residual syndrome in patients who suffered from a Wernicke encephalopathy (WE) that is predominantly... (Review)
Review
In this review, we present a survey on Korsakoff's syndrome (KS), a residual syndrome in patients who suffered from a Wernicke encephalopathy (WE) that is predominantly characterized by global amnesia, and in more severe cases also by cognitive and behavioral dysfunction. We describe the history of KS and its definition, its epidemiology, and the lack of consensus criteria for its diagnosis. The cognitive and behavioral symptoms of KS, which include anterograde and retrograde amnesia, executive dysfunction, confabulation, apathy, as well as affective and social-cognitive impairments, are discussed. Moreover, recent insights into the underlying neurocognitive mechanisms of these symptoms are presented. In addition, the evidence so far on the etiology of KS is examined, highlighting the role of thiamine and alcohol and discussing the continuity hypothesis. Furthermore, the neuropathology of KS is reviewed, focusing on abnormalities in the diencephalon, including the mammillary bodies and thalamic nuclei. Pharmacological treatment options and nonpharmacological interventions, such as those based on cognitive rehabilitation, are discussed. Our review shows that thiamine deficiency (TD) is a crucial factor in the etiology of KS. Although alcohol abuse is by far the most important context in which TD occurs, there is no convincing evidence for an essential contribution of ethanol neurotoxicity (EN) to the development of WE or to the progression of WE to KS. Future research on the postmortem histopathological analysis of brain tissues of KS patients is crucial for the advancement of our knowledge of KS, especially for associating its symptoms with lesions in various thalamic nuclei. A necessary requirement for the advancement of studies on KS is the broad acceptance of a comprehensive definition and definite diagnostic criteria. Therefore, in this review, we propose such a definition of KS and draft outlines for prospective diagnostic criteria.
PubMed: 29225466
DOI: 10.2147/NDT.S130078 -
Journal of Integrative Neuroscience Jan 2022Converging evidence from biopsychosocial research in humans and animals demonstrates that chronic sensory stimulation (via excessive screen exposure) affects brain... (Review)
Review
Digital dementia in the internet generation: excessive screen time during brain development will increase the risk of Alzheimer's disease and related dementias in adulthood.
Converging evidence from biopsychosocial research in humans and animals demonstrates that chronic sensory stimulation (via excessive screen exposure) affects brain development increasing the risk of cognitive, emotional, and behavioural disorders in adolescents and young adults. Emerging evidence suggests that some of these effects are similar to those seen in adults with symptoms of mild cognitive impairment (MCI) in the early stages of dementia, including impaired concentration, orientation, acquisition of recent memories (anterograde amnesia), recall of past memories (retrograde amnesia), social functioning, and self-care. Excessive screen time is known to alter gray matter and white volumes in the brain, increase the risk of mental disorders, and impair acquisition of memories and learning which are known risk factors for dementia. Chronic sensory overstimulation (i.e., excessive screen time) during brain development increases the risk of accelerated neurodegeneration in adulthood (i.e., amnesia, early onset dementia). This relationship is affected by several mediating/moderating factors (e.g., IQ decline, learning impairments and mental illness). We hypothesize that excessive screen exposure during critical periods of development in Generation Z will lead to mild cognitive impairments in early to middle adulthood resulting in substantially increased rates of early onset dementia in later adulthood. We predict that from 2060 to 2100, the rates of Alzheimer's disease and related dementias (ADRD) will increase significantly, far above the Centres for Disease Control (CDC) projected estimates of a two-fold increase, to upwards of a four-to-six-fold increase. The CDC estimates are based entirely on factors related to the age, sex, race and ethnicity of individuals born before 1950 who did not have access to mobile digital technology during critical periods of brain development. Compared to previous generations, the average 17-19-year-old spends approximately 6 hours a day on mobile digital devices (MDD) (smartphones, tablets, and laptop computers) whereas individuals born before 1950 at the same age spent zero. Our estimates include the documented effects of excessive screen time on individuals born after 1980, Millennials and Generation Z, who will be the majority of individuals ≥65 years old. An estimated 4-to-6-fold increase in rates of ADRD post-2060 will result in widespread societal and economic distress and the complete collapse of already overburdened healthcare systems in developed countries. Preventative measures must be set in place immediately including investments and interventions in public education, social policy, laws, and healthcare.
Topics: Adolescent; Adult; Aged; Alzheimer Disease; Amnesia; Brain; Child; Cognitive Dysfunction; Human Development; Humans; Middle Aged; Screen Time; Young Adult
PubMed: 35164464
DOI: 10.31083/j.jin2101028 -
Science (New York, N.Y.) May 2015Memory consolidation is the process by which a newly formed and unstable memory transforms into a stable long-term memory. It is unknown whether the process of memory...
Memory consolidation is the process by which a newly formed and unstable memory transforms into a stable long-term memory. It is unknown whether the process of memory consolidation occurs exclusively through the stabilization of memory engrams. By using learning-dependent cell labeling, we identified an increase of synaptic strength and dendritic spine density specifically in consolidated memory engram cells. Although these properties are lacking in engram cells under protein synthesis inhibitor-induced amnesia, direct optogenetic activation of these cells results in memory retrieval, and this correlates with retained engram cell-specific connectivity. We propose that a specific pattern of connectivity of engram cells may be crucial for memory information storage and that strengthened synapses in these cells critically contribute to the memory retrieval process.
Topics: Amnesia, Retrograde; Amygdala; Animals; Conditioning, Classical; Dendrites; Dentate Gyrus; Fluorescent Dyes; Luminescent Proteins; Memory, Long-Term; Mice; Neuronal Plasticity; Protein Synthesis Inhibitors; Staining and Labeling; Synapses; Red Fluorescent Protein
PubMed: 26023136
DOI: 10.1126/science.aaa5542 -
Cold Spring Harbor Perspectives in... Aug 2015Conscious memory for a new experience is initially dependent on information stored in both the hippocampus and neocortex. Systems consolidation is the process by which... (Review)
Review
Conscious memory for a new experience is initially dependent on information stored in both the hippocampus and neocortex. Systems consolidation is the process by which the hippocampus guides the reorganization of the information stored in the neocortex such that it eventually becomes independent of the hippocampus. Early evidence for systems consolidation was provided by studies of retrograde amnesia, which found that damage to the hippocampus-impaired memories formed in the recent past, but typically spared memories formed in the more remote past. Systems consolidation has been found to occur for both episodic and semantic memories and for both spatial and nonspatial memories, although empirical inconsistencies and theoretical disagreements remain about these issues. Recent work has begun to characterize the neural mechanisms that underlie the dialogue between the hippocampus and neocortex (e.g., "neural replay," which occurs during sharp wave ripple activity). New work has also identified variables, such as the amount of preexisting knowledge, that affect the rate of consolidation. The increasing use of molecular genetic tools (e.g., optogenetics) can be expected to further improve understanding of the neural mechanisms underlying consolidation.
Topics: Animals; Hippocampus; Humans; Memory; Neocortex
PubMed: 26238360
DOI: 10.1101/cshperspect.a021766 -
American Family Physician Jan 2022Transient global amnesia (TGA) is a clinical syndrome characterized by anterograde amnesia, mild retrograde amnesia, and confusion up to 24 hours. Most commonly seen in...
Transient global amnesia (TGA) is a clinical syndrome characterized by anterograde amnesia, mild retrograde amnesia, and confusion up to 24 hours. Most commonly seen in patients older than 50 years, TGA results from the temporary impairment of short-term memory formation. Clinically, patients have time disorientation and often ask repeated questions regarding the day's events. Vomiting, headache, blurry vision, dizziness, and nausea may be present. A physically or psychologically stressful precipitating event, such as emotional stress, significant physical exertion, exposure to extreme temperatures, high-altitude conditions, Valsalva maneuver, acute illness, or sexual intercourse, is often the cause. The pathophysiology of TGA is not well understood but may be related to impaired venous drainage of the hippocampus. The diagnosis is primarily clinical, but recent studies suggest that magnetic resonance imaging may be helpful. TGA is self-limited and resolves within 24 hours. There is no established treatment for episodes. The lifetime recurrence rate is 2.9% to 23.8%. Recent evidence suggests an association between TGA and migraine headaches as well as takotsubo cardiomyopathy. No apparent increased risk of cerebrovascular events occurs in patients who have had an episode of TGA. There is conflicting evidence as to whether an episode of TGA predisposes to future seizures or dementia.
Topics: Adult; Amnesia, Transient Global; Coitus; Confusion; Female; Hippocampus; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Migraine Disorders; Physical Exertion; Risk Factors; Stress, Psychological; Takotsubo Cardiomyopathy; Time Factors
PubMed: 35029951
DOI: No ID Found -
Archives of Women's Mental Health Feb 2017Donkin psychoses are eclamptic psychoses without seizures. As symptomatic psychoses resulting from cerebral endothelial damage, they may explain the lucid intervals that...
Donkin psychoses are eclamptic psychoses without seizures. As symptomatic psychoses resulting from cerebral endothelial damage, they may explain the lucid intervals that sometimes occur between eclampsia and the eruption of psychosis. They have the same features as eclamptic psychoses, with onset during pregnancy or the early puerperium, especially in first-time mothers, a short duration and full recovery in most. The clinical picture is usually delirium, but mania is also seen, and some patients have retrograde amnesia or other cognitive defects. Donkin psychosis should be considered in the differential diagnosis of childbearing psychoses, and collaborative research is needed to clarify their differences.
Topics: Adult; Bipolar Disorder; Brain Edema; Eclampsia; Female; Humans; Pregnancy; Psychotic Disorders
PubMed: 27718021
DOI: 10.1007/s00737-016-0677-6 -
Progress in Neurobiology May 2021Seizures cause retrograde amnesia, but underlying mechanisms are poorly understood. We tested whether seizure activated neuronal circuits overlap with spatial memory...
Seizures cause retrograde amnesia, but underlying mechanisms are poorly understood. We tested whether seizure activated neuronal circuits overlap with spatial memory engram and whether seizures saturate LTP in engram cells. A seizure caused retrograde amnesia for spatial memory task. Spatial learning and a seizure caused cFos expression and synaptic plasticity overlapping set of neurons in the CA1 of the hippocampus. Recordings from learning-labeled CA1 pyramidal neurons showed potentiated synapses. Seizure-tagged neurons were also more excitable with larger rectifying excitatory postsynaptic currents than surrounding unlabeled neurons. These neurons had enlarged dendritic spines and saturated LTP. A seizure immediately after learning, reset the memory engram. Seizures cause retrograde amnesia through shared ensembles and mechanisms.
Topics: Amnesia, Retrograde; CA1 Region, Hippocampal; Excitatory Postsynaptic Potentials; Hippocampus; Humans; Neuronal Plasticity; Pyramidal Cells; Seizures; Synapses
PubMed: 33388373
DOI: 10.1016/j.pneurobio.2020.101984 -
Frontiers in Cellular Neuroscience 2021Retrograde amnesia is the inability to remember events or information. The successful acquisition and memory of information is required before retrograde amnesia may... (Review)
Review
Retrograde amnesia is the inability to remember events or information. The successful acquisition and memory of information is required before retrograde amnesia may occur. Often, the trigger for retrograde amnesia is a traumatic event. Loss of memories may be caused in two ways: either by loss/erasure of the memory itself or by the inability to access the memory, which is still present. In general, memories and learning are associated with a positive connotation although the extinction of unpleasant experiences and memories of traumatic events may be highly welcome. In contrast to the many experimental models addressing learning deficits caused by anterograde amnesia, the incapability to acquire new information, retrograde amnesia could so far only be investigated sporadically in human patients and in a limited number of model systems. Apart from models and diseases in which neurodegeneration or dementia like Alzheimer's disease result in loss of memory, retrograde amnesia can be elicited by various drugs of which alcohol is the most prominent one and exemplifies the non-specific effects and the variable duration. External or internal impacts like traumatic brain injury, stroke, or electroconvulsive treatments may similarly result in variable degrees of retrograde amnesia. In this review, I will discuss a new genetic approach to induce retrograde amnesia in a mouse model and raise the hypothesis that retrograde amnesia is caused by altered intracellular calcium homeostasis. Recently, we observed that neuronal loss of neuroplastin resulted in retrograde amnesia specifically for associative memories. Neuroplastin is tightly linked to the expression of the main Ca extruding pumps, the plasma membrane calcium ATPases (PMCAs). Therefore, neuronal loss of neuroplastin may block the retrieval and storage of associative memories by interference with Ca signaling cascades. The possibility to elicit retrograde amnesia in a controlled manner allows to investigate the underlying mechanisms and may provide a deeper understanding of the molecular and circuit processes of memory.
PubMed: 34975406
DOI: 10.3389/fncel.2021.746198