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MeSH Review

Amnesia

 
 
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Disease relevance of Amnesia

  • Ataxia, sedation, amnesia, ethanol and barbiturate potentiation, tolerance, dependence, and the potential for drug abuse plague the clinical use of anxiolytic benzodiazepines [1].
  • MHI was defined as either a documented loss of consciousness or evidence of posttraumatic amnesia and an emergency department Glasgow Coma Scale score of 14 or 15 [2].
  • Three patients with bitemporal epilepsy made up a considerable proportion of those who never remembered their aura before secondary generalized tonic-clonic seizures (2 of 3) and of those who had a transient postictal amnesia of their aura (2 of 3) [3].
  • RESULTS: Posttraumatic amnesia had a clear, predictable relationship to length of coma in patients with diffuse axonal injury (R2 = .58, P < .0001) [4].
  • Severity of brain injury, as measured by a low GCS score, prolonged unconsciousness, and posttraumatic amnesia (PTA) without local brain lesion, should not be considered risk factor for LPTSs [5].
 

Psychiatry related information on Amnesia

  • Age regression measures of memory in patients with epilepsy show that increased incidence of amnesia/dementia is not the consequence of progressive epilepsy [6].
  • Bitemporal injections of puromycin that primarily affect the hippocampal-entorhinal area induce amnesia of aversive maze-learning in mice for 3 days after training but are ineffective 6 or more days after training [7].
  • Thus, A beta-induced actin-dependent GLAST redistribution and relevant synaptic malfunction may be a cellular basis for the amnesia of Alzheimer's disease [8].
  • Analysis of individual case reports from marketing through 1985 for triazolam vs temazepam showed 133 vs two for confusion, 109 vs three for amnesia, 59 vs two for bizarre behavior, 58 vs four for agitation, and 40 vs one for hallucinations [9].
  • Discontinuation of carbamazepine and clonazepam was followed by episodic amnesia, purposeless behavior, déjà vu, and confusion [10].
 

High impact information on Amnesia

  • Social amnesia in mice lacking the oxytocin gene [11].
  • Here we show that consolidated fear memories, when reactivated during retrieval, return to a labile state in which infusion of anisomycin shortly after memory reactivation produces amnesia on later tests, regardless of whether reactivation was performed 1 or 14 days after conditioning [12].
  • However, PBZ-treated animals did not develop amnesia [13].
  • When administered after training, the stimulants caffeine or nicotine blocked amnesia for the task that had been produced by injections of the protein synthesis inhibitor anisomycin given prior to training [14].
  • The pentapeptides methionine-enkephalin and leucine-enkephalin are both able to reduce experimentally induced amnesia in rats [15].
 

Chemical compound and disease context of Amnesia

 

Biological context of Amnesia

 

Anatomical context of Amnesia

  • At these later times, additional puromycin sites covering widespread forebrain areas are necessary to induce amnesia, a result that we attribute to the cerebral spread of the engram during the 6-day period [7].
  • Human amnesia and the medial temporal region: enduring memory impairment following a bilateral lesion limited to field CA1 of the hippocampus [25].
  • Compared with the normal control group, the patient groups displayed different patterns of sparing and loss of the two components of memory: in PD, only STM was impaired; in medial temporal lobe amnesia, only LTM was impaired; and in AD, STM and LTM were both impaired [26].
  • The latter consisted of sudden onset of coma or confusion followed by a persistent amnesia of varying severity, with or without language impairment and frontal lobe signs [27].
  • The severe amnesia associated with damage to the mammillary bodies, midline nuclei, mammillothalamic tract, and/or dorsomedial nucleus of the thalamus (eg, Korsakoff and NA) is characterized by encoding deficits that never approximate normal performance [28].
 

Gene context of Amnesia

  • Cholecystokinin-related peptides, after systemic or central administration, prevent carbon monoxide-induced amnesia in mice [29].
  • In coincidence with this time course of activity, an ERK1/2 pathway inhibitor, PD098059, induced amnesia only when administered 45 min after training but not when administered immediately pre- or post-training [30].
  • Intracerebral administration of antisense ODNs to BDNF 6-12 h prior to training induced amnesia for the avoidance response by 3 h after training [31].
  • The effects of intracerebroventricular injections of the neurokinin-2 (NK-2) receptor agonist neurokinin A and the neurokinin-3 (NK-3) receptor agonist senktide on scopolamine (sc)-induced amnesia were investigated based on spontaneous alternation performance in mice [32].
  • The LRP antagonist receptor-associated protein prevented the APP-KPI internalization and LRP-apolipoprotein E association and this resulted in amnesia [33].
 

Analytical, diagnostic and therapeutic context of Amnesia

References

  1. Benzodiazepines on trial: a research strategy for their rehabilitation. Costa, E., Guidotti, A. Trends Pharmacol. Sci. (1996) [Pubmed]
  2. Emergency department discharge of patients with a negative cranial computed tomography scan after minimal head injury. Livingston, D.H., Lavery, R.F., Passannante, M.R., Skurnick, J.H., Baker, S., Fabian, T.C., Fry, D.E., Malangoni, M.A. Ann. Surg. (2000) [Pubmed]
  3. Amnesia of the epileptic aura. Schulz, R., Lüders, H.O., Noachtar, S., May, T., Sakamoto, A., Holthausen, H., Wolf, P. Neurology (1995) [Pubmed]
  4. Traumatic brain injury. Predicting course of recovery and outcome for patients admitted to rehabilitation. Katz, D.I., Alexander, M.P. Arch. Neurol. (1994) [Pubmed]
  5. Early and late posttraumatic seizures in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on long-term outcome. Asikainen, I., Kaste, M., Sarna, S. Epilepsia (1999) [Pubmed]
  6. The phantom of progressive dementia in epilepsy. Helmstaedter, C., Elger, C.E. Lancet (1999) [Pubmed]
  7. Blockade of beta 1- but not of beta 2-adrenergic receptors replicates propranolol's suppression of the cerebral spread of an engram in mice. Flexner, J.B., Flexner, L.B., Church, A.C., Rainbow, T.C., Brunswick, D.J. Proc. Natl. Acad. Sci. U.S.A. (1985) [Pubmed]
  8. Beta-amyloid enhances glial glutamate uptake activity and attenuates synaptic efficacy. Ikegaya, Y., Matsuura, S., Ueno, S., Baba, A., Yamada, M.K., Nishiyama, N., Matsuki, N. J. Biol. Chem. (2002) [Pubmed]
  9. Adverse behavioral reactions attributed to triazolam in the Food and Drug Administration's Spontaneous Reporting System. Wysowski, D.K., Barash, D. Arch. Intern. Med. (1991) [Pubmed]
  10. Apparent complex partial seizures in a bipolar patient after withdrawal of carbamazepine. Garbutt, J.C., Gillette, G.M. The Journal of clinical psychiatry. (1988) [Pubmed]
  11. Social amnesia in mice lacking the oxytocin gene. Ferguson, J.N., Young, L.J., Hearn, E.F., Matzuk, M.M., Insel, T.R., Winslow, J.T. Nat. Genet. (2000) [Pubmed]
  12. Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nader, K., Schafe, G.E., Le Doux, J.E. Nature (2000) [Pubmed]
  13. Retrograde amnesia produced by several treatments: evidence for a common neurobiological mechanism. Gold, P.E., Sternberg, D.B. Science (1978) [Pubmed]
  14. Memory: modification of anisomycin-induced amnesia by stimulants and depressants. Flood, J.F., Bennett, E.L., Orme, A.E., Rosenzweig, M.R., Jarvik, M.E. Science (1978) [Pubmed]
  15. Attenuation of amnesia in rats by systemically administered enkephalins. Rigter, H. Science (1978) [Pubmed]
  16. Vasopressin in amnesia. Oliveros, J.C., Jandali, M.K., Timsit-Berthier, M., Remy, R., Benghezal, A., Audibert, A., Moeglen, J.M. Lancet (1978) [Pubmed]
  17. Desmopressin in post-traumatic amnesia. Jenkins, J.S., Mather, H.M., Coughlan, A.K., Jenkins, D.G. Lancet (1979) [Pubmed]
  18. Neurohypophyseal hormones, analogs, and fragments: their effect on puromycin-induced amnesia. Walter, R., Hoffman, P.L., Flexner, J.B., Flexner, L.B. Proc. Natl. Acad. Sci. U.S.A. (1975) [Pubmed]
  19. Synaptic plasticity and learning: selective impairment of learning rats and blockade of long-term potentiation in vivo by the N-methyl-D-aspartate receptor antagonist AP5. Morris, R.G. J. Neurosci. (1989) [Pubmed]
  20. Reminder effects: the molecular cascade following a reminder in young chicks does not recapitulate that following training on a passive avoidance task. Salinska, E., Bourne, R.C., Rose, S.P. Eur. J. Neurosci. (2004) [Pubmed]
  21. Effects of four non-cholinergic cognitive enhancers in comparison with tacrine and galanthamine on scopolamine-induced amnesia in rats. Chopin, P., Briley, M. Psychopharmacology (Berl.) (1992) [Pubmed]
  22. Effects of high-dose fentanyl anesthesia on the electroencephalogram. Sebel, P.S., Bovill, J.G., Wauquier, A., Rog, P. Anesthesiology (1981) [Pubmed]
  23. Reversal of scopolamine-induced amnesia and alterations in energy metabolism by the nootropic piracetam: implications regarding identification of brain structures involved in consolidation of memory traces. Piercey, M.F., Vogelsang, G.D., Franklin, S.R., Tang, A.H. Brain Res. (1987) [Pubmed]
  24. Aniracetam augments, and midazolam inhibits, the long-term potentiation in guinea-pig hippocampal slices. Satoh, M., Ishihara, K., Iwama, T., Takagi, H. Neurosci. Lett. (1986) [Pubmed]
  25. Human amnesia and the medial temporal region: enduring memory impairment following a bilateral lesion limited to field CA1 of the hippocampus. Zola-Morgan, S., Squire, L.R., Amaral, D.G. J. Neurosci. (1986) [Pubmed]
  26. Double dissociation of short-term and long-term memory for nonverbal material in Parkinson's disease and global amnesia. A further analysis. Sullivan, E.V., Sagar, H.J. Brain (1991) [Pubmed]
  27. Brain energy metabolism in bilateral paramedian thalamic infarcts. A positron emission tomography study. Levasseur, M., Baron, J.C., Sette, G., Legault-Demare, F., Pappata, S., Mauguière, F., Benoit, N., Tran Dinh, S., Degos, J.D., Laplane, D. Brain (1992) [Pubmed]
  28. Contributions of the left intralaminar and medial thalamic nuclei to memory. Comparisons and report of a case. Mennemeier, M., Fennell, E., Valenstein, E., Heilman, K.M. Arch. Neurol. (1992) [Pubmed]
  29. Cholecystokinin-related peptides, after systemic or central administration, prevent carbon monoxide-induced amnesia in mice. Maurice, T., Hiramatsu, M., Kameyama, T., Hasegawa, T., Nabeshima, T. J. Pharmacol. Exp. Ther. (1994) [Pubmed]
  30. Phosphorylation of extra-nuclear ERK/MAPK is required for long-term memory consolidation in the crab Chasmagnathus. Feld, M., Dimant, B., Delorenzi, A., Coso, O., Romano, A. Behav. Brain Res. (2005) [Pubmed]
  31. Memory consolidation in day-old chicks requires BDNF but not NGF or NT-3; an antisense study. Johnston, A.N., Rose, S.P. Brain Res. Mol. Brain Res. (2001) [Pubmed]
  32. Neurokinin A and senktide attenuate scopolamine-induced impairment of spontaneous alternation performance in mice. Ukai, M., Shinkai, N., Kameyama, T. Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology. (1996) [Pubmed]
  33. Amyloid precursor protein expression in the rat hippocampal dentate gyrus modulates during memory consolidation. Conboy, L., Murphy, K.J., Regan, C.M. J. Neurochem. (2005) [Pubmed]
  34. Metabolic impairment in human amnesia: a PET study of memory networks. Fazio, F., Perani, D., Gilardi, M.C., Colombo, F., Cappa, S.F., Vallar, G., Bettinardi, V., Paulesu, E., Alberoni, M., Bressi, S. J. Cereb. Blood Flow Metab. (1992) [Pubmed]
  35. Reduced dorsal hippocampal glutamate release significantly correlates with the spatial memory deficits produced by benzodiazepines and ethanol. Shimizu, K., Matsubara, K., Uezono, T., Kimura, K., Shiono, H. Neuroscience (1998) [Pubmed]
  36. Testing cyclic AMP mediation of memory: reversal of alpha-methyl-p-tyrosine-induced amnesia. Chutae, D.L., Villiger, J.W., Kirton, N.F. Psychopharmacology (Berl.) (1981) [Pubmed]
  37. Subjective and psychomotor effects of subanesthetic doses of propofol in healthy volunteers. Zacny, J.P., Lichtor, J.L., Coalson, D.W., Finn, R.S., Uitvlugt, A.M., Glosten, B., Flemming, D.C., Apfelbaum, J.L. Anesthesiology (1992) [Pubmed]
  38. Dexmedetomidine does not improve patient satisfaction when compared with propofol during mechanical ventilation. Corbett, S.M., Rebuck, J.A., Greene, C.M., Callas, P.W., Neale, B.W., Healey, M.A., Leavitt, B.J. Crit. Care Med. (2005) [Pubmed]
 
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