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)

Triazolam (U-33030), an investigational hypnotic drug, was evaluated in seven insomniac subjects in the sleep laboratory. The protocol consisted of 22 consecutive nights: four placebo nights for adaptation and baseline, two weeks of drug administration (0.5 mg triazolam) for short- and intermediate-term drug effectiveness, and four placebo nights for withdrawal effects. With short-term drug use, both sleep induction and sleep maintenance improved, with total wake time decreasing markedly--a 45 per cent decrease from baseline. At the end of two weeks of drug use, none of the efficacy parameters was significantly decreased from baseline; there was only a 17 per cent decrease in total wake time. Following drug withdrawal, sleep difficulty significantly increased above baseline levels. Two of the subjects experienced episodes of amnesia during the drug administration period. The per cent of REM sleep decreased significantly during both short and intermediate drug conditions. Following drug withdrawal, the per cent of REM sleep was similar to baseline. Slow-wave (stages 3 and 4) sleep was significantly decreased for both drug conditions; and following drug withdrawal, it returned completely to the baseline leve. These data indicate that triazolam is effective for short-term use, loses most of its effectiveness with intermediate-term use, and its withdrawal is followed by a significant sorsening of sleep. These findings are discussed in relation to the potential labeling and promotion of triazolam. Finally, the findings of amnesia associated with triazolam administration need to be more thoroughly evaluated.
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PMID:Hypnotic efficacy of triazolam: sleep laboratory evaluation of intermediate-term effectiveness. 18 18

Narcolepsy is clinically associated with cataplexy, sleep paralysis and hypnagogic hallucinations. It is treated by reassurance (that there is no physical disease) and by stimulants such as ephedrine and amphetamine on an intermittent basis. The special tricyclic antidepressant clomipramine is also used, and mono-amine oxidase inhibitors (MAOIs) are useful in theory. Obstructive sleep apnoea is an important and often unrecognised cause of daytime somnolence. It is treated by weight reduction (pickwickian syndrome), hormones, or recently, with continuous positive pressure apparatus. Night terrors (pavor nocturnus) and sleepwalking typically occur during deep sleep (stage 3 and 4 throughout the episode) in children. In a night terror the child sits up with a scream, with eyes open, but inaccessible. He eventually falls asleep calmly. Sleepwalking, too, shows the features of inaccessibility and subsequent amnesia for the episode. Both conditions are normally treated with reassurance (to the parents) but may occasionally warrant benzodiazepines. Enuresis usually occurs in non-rapid eye movement (NREM) sleep, especially stages 3 and 4. The reason for the efficacy of tricyclic antidepressants is not precisely known. Delirium tremens (DT) is treated as a rebound excess of REM sleep, with benzodiazepines and other drugs. It is the withdrawal syndrome (with or without major seizures) to the barbiturate-alcohol group of drugs, which includes alcohol, chloral, paraldehyde, glutethimide, methylprylone, ethchlorvynol, meprobamate and meprobamate-diphenhydramine. Insomnia may be treated by the above drugs, by analgesics, antidepressants, major tranquillisers (neuroleptics) and miscellaneous other compounds. For the majority of patients, however, the most suitable group seems to be the benzodiazepines. The benzodiazepines are much safer than their predecessors, in both acute and chronic usage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The treatment of sleep disorders. 158 14

Within the context of the comprehensive treatment of sleep disorders, which includes medical, neurologic, psychiatric, and social interventions, use of medication is often indicated. Among the three benzodiazepine hypnotics that are available in the United States for the treatment of insomnia, flurazepam is effective for both sleep induction and maintenance, and it retains most of its efficacy over a 4-week period of nightly administration; temazepam is effective only for sleep maintenance, and triazolam improves both sleep induction and maintenance with initial but not with continued administration. Rebound phenomena are more frequent and intense with the more rapidly eliminated drug, triazolam, and to a lesser degree with temazepam. Also, with triazolam, certain behavioral side effects, such as amnesia and psychotic-like symptoms, have been reported. With flurazepam, which is a slowly eliminated benzodiazepine, daytime sedation is more frequent than with the other two drugs. When insomnia is secondary to major depression, antidepressant medication should be administered. Methylphenidate, amphetamines, or other stimulant medications are used for the symptomatic treatment of the sleepiness and sleep attacks of narcolepsy and hypersomnia. For cataplexy and the other two auxiliary symptoms of narcolepsy, imipramine or other tricyclics are the drugs of choice. Protriptyline and medroxyprogesterone have been used in treating mild cases of obstructive sleep apnea, but their efficacy is limited. Similarly, for the treatment of central sleep apnea, medroxyprogesterone and acetazolamide have shown only limited effects. Medication for patients with sleepwalking, night terrors, or nightmares should be prescribed judiciously, and primarily when treatment of an underlying psychiatric condition is desired. The neuropharmacology of sleep should also consider drugs that may cause sleep disorders. Medications with sleep disturbing effects include various antihypertensives, bronchodilators, and the energizing antidepressants. Withdrawal of REM-suppressant drugs, such as the barbiturates, may cause nightmares in association with a REM rebound. Occasionally, a drug or a combination of drugs may produce somnambulistic-like activity in some patients.
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PMID:Clinical neuropharmacology of sleep disorders. 333 64

Sleep and dreams in 15 chronic alcoholic patients with amnesia were compared with sleep and dreams of 15 age- and sex-adjusted normal subjects. The patients were subjected to psychological tests in order to determine their I.Q. and their memory disturbances. All subjects had two nights of polygraphic recordings; the first tested the natural sleep organization. During the second night, they were awakened 7 min after the onset of each REM sleep episode, and, at least once, 20 min after the onset of a stage II episode, in order to record on a tape their dream reports according to a standardized protocol. The sleep patterns of the amnesic patients did not show any significant alteration. However, after wakening during the night, patients exhibited a higher tendency to return to REMS than controls. There was still some dream activity in those patients, although noticeably less frequently, and their dream activity had a very poor verbal expression. However, there was no change with respect to the spatio-temporal organization, sensorial perceptions, motor activity and verbalizations during their dreams.
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PMID:[Sleep and dreams in Korsakoff's amnesia due to alcoholism]. 338 22

We report a case of misinterpretation of a non-REM sleep parasomnia as suicidal behavior in an early adolescent. A 12-year-old female with a history of sleepwalking but no prior psychiatric diagnosis awoke in the middle of the night with a deep laceration to her neck and complete amnesia for the event. During the initial 2-week pediatric hospitalization, it was believed that the wound was intentionally self-inflicted despite patient claims and evidence to the contrary. The patient was placed on a psychiatric hold and transferred to an appropriate facility. We review rule-out diagnoses and evidence supporting this case as an example of a violent non-REM parasomnia resulting in self-injurious behavior. Diagnostic and treatment implications are discussed.
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PMID:The misinterpretation of a non-REM sleep parasomnia as suicidal behavior in an adolescent. 1252 70

Temporal lobe epilepsy is a partial epileptic disorder in which mesial structures are responsible for the principal ictal symptoms. Its characteristic feature is the recurrence of simple and complex partial seizures, associated with postictal confusion and amnesia of the event. The facilitating effect of NREM sleep on the propagation of the seizure, as well as the sleep abnormalities provoked by epilepsy were evident in our two patients. Yawning is a physiological reflex induced by arousal and drowsiness and may appear in different neurological conditions. Its relation with epilepsy of limbic origin has been rarely reported. We describe in a 95 year old male patient, the occurrence of yawning followed by complex partial seizure during a state of drowsiness. His EEG showed independent bilateral interictal foci of temporal sharp waves and after being medicated with carbamazepine 400 mg/day, the episode did not recur. Another patient, a 17 year old female, displayed complex partial seizures and secondarily generalized seizures with yawning during the posictal period, after naps. The EEG was normal and her polysomnography showed bilateral synchronous temporal spikes and slow waves with secondarily generalization during stage 2 of NREM sleep that produce paroxysmal microarousals and increased stages 1 and 2 of NREM sleep and REM sleep diminished. After being medicated with divalproex sodium 750 mg/day, she suffered no further seizures. Temporal lobe epilepsy, sleep-wake cycles and yawning seem not only to share the same anatomic structures but also the same neurochemical mechanisms. The fact that endogenous opiods are considered as part of a protective system that stop and prevent seizures may allow us to postulate that yawning would be the expression of the endogenous opiods induced mechanisms that stop and prevent the recurrence of the temporal lobe epilepsy. Another hypothesis may be that this is only a particular form of temporal lobe epilepsy.
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PMID:[Yawning and temporal lobe epilepsy]. 1279 82

A popular view of the function of the hippocampus maintains that this structure temporarily encodes the neocortical representation of the experience of an episode. It uses the encoding to recreate repeatedly the neocortical representation. It is said that in time the episodic memory becomes consolidated in the neocortex and can be retrieved independent of the hippocampus. This paper is critical of that view and begins by raising four concerns. These include a question of how the hippocampus could encode the rich complexity of neocortical representations in sufficient detail to recreate them. And it observes that some data indicate episodic memories remain dependent on the hippocampus for life. Another view of hippocampal function is presented which addresses these concerns. Basically, this view hypothesizes that the ability to retrieve episodic memories involves the interplay between two modes of hippocampal function. Processes during the theta mode facilitate the development of context memory in the hippocampus and the registration of unique events in the neocortex, but block the influence of context memory upon the neocortex. By contrast, during the non-theta mode, context memory is projected onto the neocortex, creating a contextual framework. It is proposed that the ability to retrieve memory of episodes depends on the development, through contiguity, of associations between the representation of the episode (created during theta) and a contextual framework (evoked during non-theta). From this perspective, the episode does not need to be encoded in the hippocampus, but remains dependent indefinitely on associations formed between the episodic memory in the neocortex and a context memory maintained in hippocampal structures. However, for the associations that enable retrieval to form, the creation of the representation of an episode during theta must be followed quickly by the evocation of a contextual framework. During an extended period of the theta mode as occurs during REM sleep dreaming, these associations cannot usually be formed, resulting in amnesia for most dreams.
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PMID:Episodic memory and the hippocampus: another view. 1550 62

Bipedal locomotion and fine motility of hand and larynx of humans introduced musculoskeletal adaptations, new pyramidal, corticostriatal, corticobulbar, nigrostriatal, and cerebellar pathways and expansions of prefrontal, cingular, parieto-temporal and occipital cortices with derived new brain capabilities. All selectively degenerate in aged homo sapiens following 16 syndromic presentations: (1) Parkinsonism: nigrostriatal control for fast automatic movements of hand, larynx, bipedal posture and gait ("simian gait and hand"). (2) Frontal (highest level) gait disorders (lower body parkinsonism, gait apraxia, retropulsion): prefrontostriatal executive control of bipedal locomotion. (3) ataxia: new synergistic coordination of bipedal gait and fine motility. (4) Dyskinesias (chorea, dystonia, tremor...): intrusions of simian basal ganglia motor subroutines. (5) motoneuron diseases: new proximo-distal and bulbar motoneurones, preserving older ones (oculomotor, abdominal...). (6) Archaic reflexes: prefrontal disinhibition of old mother/tree-climbing-oriented reflexes (sucking, grasping, Babinski/triple retraction, gegenhalten), group alarms (laughter, crying, yawning, grunting...) or grooming (tremor=scratching). (7) Dysautonomia: contextual regulation (orthostatism...). (8) REM sleep disorders of new cortical functions. (9) Corticobasal syndrome: melokinetic control of hand prehension-manipulation and language (retrocession to simian patterns). (10) Frontal/temporal lobe degeneration: medial-orbitofrontal behavioural variant: self monitoring of internal needs and social context: apathy, loss of personal hygiene, stereotypia, disinhibition, loss of concern for consequences of acts, social rules, danger and empathy; dorsolateral executive variant: inadequacy to the context of action (goal, environmental changes...); progressive non-fluent aphasia: executive and praxic processing of speech; temporal variant: abstract concepts for speech, gestures and vision (semantic dementia, progressive nonfluent aphasia) (11) Temporomesial-limbic-paralimbic-associative cortical dementias (Alzheimer's disease, Lewy body, progressive amnesia): processing of explicit cognition: amnesic syndrome, processing of hand, larynx and eye: disorientation, ideomotor apraxia, agnosia, visuospatial processing, transcortical aphasia. (12) Focal posterior atrophy (Benson, progressive apraxia): visuomotor processing of what and where. (13) Macular degeneration: retinal "spot" for explicit symbols. (14) "Psychiatric syndromes": metacognition, self monitoring and regulation of hierarchical processing of metacognition: hallucinations, delusions, magic and mystic logic, delusions, confabulations; drive: impulsivity, obsessive-compulsive disorders, mental automatisms; social interactions: theory of mind, autism, Asperger. (15) Mood disorders: control on emotions: anxio-depressive and bipolar disorders, moria, emotional lability. (16) Musculoskeletal: inclusion body myositis: muscles for bipedal gait and fine motility. Paget's disease: bones for bipedal gait and cranium. Understanding of the genetic mechanisms underlying the evolution of these recent human brain regions and paleoneurology my be the key to the focal, asymmetrical or systemic character of neurodegeneration, the pathologic heterogeneity/overlap of syndromic presentations associating gait, hand, language, cognition, mood and behaviour disorders.
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PMID:Paleoneurology: neurodegenerative diseases are age-related diseases of specific brain regions recently developed by Homo sapiens. 1870 90

Parasomnias are sleep-related abnormal behaviors. They are frequent and overlooked causes of nocturnal disruptive behavior in the elderly, especially when patients are cognitively impaired. Confusion and violence can result in sleep disruption, injuries for the patients or their bed partners, caregivers distress, and they can be a motive for institutionalization. Parasomnias include the NonREM sleep disorders of arousal (sleepwalking, sleep terrors, confusional arousals and sleep-related eating disorder), the REM sleep behavior disorder (RBD) and more rarely the parasomnia overlap syndrome, which associates both NREM and REM parasomnias. Patients with NREM sleep parasomnias are confused, eyes open, with a glazed look during their nocturnal behaviors, and they have a post-episode amnesia. They shout and bolt from the bed (night terrors), look about in a confused manner, walk and speak (sleepwalking), and eat peculiar or inedible food (sleep-related eating disorders). These behaviors, which are frequent in young adults, may be triggered by short-half live hypnotics in elderly. During the parasomnia, the brain is partially awake (enough to perform complex motor and verbal action), and partially asleep (without conscious awareness or responsibility). RBD is characterized by a loss of the normal muscle atonia that accompanies REM sleep. Patients have excessive motor activity such as punching, kicking, or crying out in association with dream content. RBD are frequent in Parkinson's disease and dementia with Lewy bodies and may precede the cognitive or motor symptoms of these diseases by 5 to 10 years. RBD can also be promoted by antidepressants. When combined with thorough clinical interviews, the video-polysomnography is a powerful tool, especially for discriminating the parasomnia from nocturnal frontal lobe epilepsy, sleep apneas and periodic leg movements. Ensuring safety and withdrawing deleterious treatments are useful in patients with violent activities, potential injurious or bothersome to other household members. Clonazepam and melatonin (3-12 mg) are highly effective for treating RBD.
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PMID:[Disruptive nocturnal behavior in elderly subjects: could it be a parasomnia?]. 2052 41

We report the case of a 43-year-old woman presenting with nocturnal episodes of pain and screaming during sleep starting at age 30. There was no childhood or family history of parasomnia. The events had gradually become more frequent over the years, occurring in the first half of the night within 2 h of sleep onset. There were no triggers, and she had partial amnesia for the events. A diagnosis of adult-onset sleep terrors was made on clinical grounds and supported polysomnographically. Seizures and periodic limb movements were excluded as triggering factors. There was some mild sleep disordered breathing (predominantly non-desaturating hypopnea with a propensity for REM sleep of debatable significance). Imaging of the brain and spine and neurophysiological investigations ruled out lesions, entrapments, or neuropathies as possible causes of pain. Treatment (clonazepam, paroxetine, or gabapentin) was poorly tolerated and made no difference to the nocturnal episodes, while trazodone worsened them. This is the first report of hypnopompic psychic pain in association with a NREM parasomnia. We hypothesize that the pain may represent a sensory hallucination analogous to the more commonly recognized visual NREM parasomnia-associated hypnopompic visual hallucinations and that, as such, it may arise during arousal of the sensory neocortex as confabulatory response.
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PMID:Adult-onset NREM parasomnia with hypnopompic hallucinatory pain: a case report. 2337 77


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