Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors present a 60-year-old patient undergoing periodic hemodialysis who, 3 years after beginning the treatment, developed a clinical picture consisting of disturbances of language, motor dispraxia, loss of memory and concentration, irritability, great change of personality, myoclonias and asterixis. This led progressively to a total loss of motor coordination, including speech. He died 5 months later in a state of dementia, psychosis and incontinence of sphincters. The symptomatology increased after hemodialysis sessions. The normal analytical studies carried out in these cases (electrocardiogram, electromyography, complete roentgenologic study) and also Zn, Cu, and ceruloplasmin measurements were normal. The electroencephalogram showed only a slow tracing with delta waves. Various etiopathogenic possibilities are commented on, as for example alterations in the dialysis water, the use of detergents in cleaning the artificial kidney, a syndrome of imbalance, a decrease in the body potassium and poisoning caused by certain metals such as tin, zinc and aluminium or by drugs which contain benzodiazepine derivatives. The authors conclude that the picture corresponds to a metabolic encephalopathy.
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PMID:[Dementia and hemodialysis (author's transl)]. 43 Nov 64

The hypothalamus, in addition to regulating the anterior and posterior pituitary, controls water balance through thirst, regulates food ingestion and body temperature, influences consciousness, sleep, emotion and other behaviors. Much has been learned of these effects in human disease through the clinical manifestations that occur with hypothalamic lesions. This study reviews the clinical pathologic correlations that have been made in recent years showing that regions of the hypothalamus exert functions in humans that are similar to those identified in experimental animals. Clinical pathologic correlations have not always provided precise analysis of hypothalamic function. The hypothalamus is small and often lesions that come to clinical attention achieve considerable size before their recognition, making local anatomic dissections of the effects of the lesions difficult. Nevertheless, the use of modern non-invasive techniques including CT scans and magnetic resonance imaging (MRI) have provided new information not previously available. This paper reviews several cases of hypothalamic disorder recognized recently. (1) A 33-year-old black man with hypothalamic sarcoidosis. Manifestations of hypothalamic dysfunction included panhypopituitarism, aggressive hyperphagia, polydipsia (partially due to hyperglycemia secondary to diabetes mellitus), drowsiness, depression, and irritability. (2) A 37-year-old woman with a large intrahypothalamic tumor (biopsy showed pituitary adenoma), with drowsiness, poikilothermia, lack of satiety, confusion, and memory loss. She becomes depressed when she is transiently more alert (as after hypertonic contrast-dye infusion). (3) A 60-year-old man with hypothalamic compression by a pituitary tumor, associated with syndrome of inappropriate ADH (SIADH), severe anorexia, memory loss, but preserved thirst. After surgical decompression of the tumor his appetite acutely recovered, but he developed severe hypo(poikilo)thermia. (4) A 45-year-old woman with a suprasellar craniopharyngioma presented with severe drowsiness, hyperphagia, depression, and memory loss post-operatively, which responded to antidepressants (except for the memory loss). She had extremely labile blood pressures and serum Na for about 1 week post-operatively.
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PMID:Neurologic manifestations of hypothalamic disease. 148 Jul 55

Previous studies have shown that following an acute bout of pyrithiamine-induced thiamine deficiency (PTD) rats are impaired in learning appetitively and aversively motivated T-maze tasks. The present study examined if PTD-treated rats exhibit both anterograde and retrograde memory loss of an aversively motivated spatial navigation task. Histological examination revealed two consistent lesions in the PTD treated rats: a bilateral, symmetrical destruction of medial thalamus centered on the internal medullary lamina (IML), and a lesion of the medial nucleus of the mammillary body. In Experiment 1, control and recovered PTD rats were trained to find a hidden platform in a Morris water maze. PTD rats with the IML lesion were impaired in learning the water maze task but were eventually able to perform as well as controls and PTD animals without the IML lesion. In Experiment 2, half of the pretrained CT animals underwent thiamine deficiency (PTD2), were recovered, and subsequently were tested for retention of the platform location. The remaining CT animals and the PTD1 group were also tested for retention. No significant group differences were observed on any of the four postretention trials. When compared to their performance on the last four preretention trials, the performance of PTD1 and PTD2 animals with IML lesions were similar to those of the controls. These results demonstrate that acute thiamine deficiency in rats produces damage of medial thalamic and mammillary body nuclei, a mild anterograde learning deficit, but no loss of retrograde memory of the Morris water maze task.
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PMID:Diencephalic lesions, learning impairments, and intact retrograde memory following acute thiamine deficiency in the rat. 161 8

While the cause of Parkinson's disease (PD) remains unknown, recent evidence suggests that certain external factors, ie, environmental agents, may act as neurotoxins, initiating the chain of oxidative reactions that ultimately destroy neurons in the substantia nigra. Young-onset PD might result from greater exposure to a putative neurotoxin. This hypothesis has rekindled interest in the epidemiology of PD. We therefore conducted a detailed analysis of various environmental exposures and early life experiences in 80 patients with old-onset PD (at an age older than 60 years), 69 young-onset patients (younger than 40 years), and 149 age- and sex-matched control subjects. Contrary to previous reports, we were unable to implicate well water or exposure to herbicides, pesticides, or industrial toxins as significant PD risk factors. A residential history of rural living was reported by more patient cases than control subjects and was marginally significant. On the other hand, at least one episode of head trauma "severe enough to cause vertigo, dizziness, blurred or double vision, seizures or convulsions, transient memory loss, personality changes, or paralysis" occurred significantly more often prior to disease onset in patients with both young-onset and old-onset PD than in control subjects (odds ratio = 2.7). When adjusted for head trauma and rural living, smoking was inversely associated with PD, as has been previously reported (odds ratio = 0.5). There were no significant differences in early life experiences or environmental exposures between young-onset and old-onset patients. We suggest that the risk of developing PD is influenced by a variety of factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The epidemiology of Parkinson's disease. A case-control study of young-onset and old-onset patients. 195 12

Alzheimer's disease is characterized by the loss of cholinergic neurons in the nucleus basalis of Meynert and by a primary loss of memory function. Since staurosporine has been reported to induce differentiation in human neuroblastoma cells in vitro, we studied the effects of staurosporine on the amnesia induced by basal forebrain-lesion in rats. Staurosporine (0.05 and 0.1 mg/kg intraperitoneal) attenuated the impaired performance of water maze and passive avoidance tasks, even though the drug administration began 2 weeks after the lesion. Moreover, staurosporine (0.1 mg/kg) partially reversed the decrease of choline acetyltransferase activity in the fronto-parietal cortex induced by basal forebrain-lesion. These results suggest that staurosporine attenuates impairment of learning through reversal of damage to cholinergic neurons induced by basal forebrain-lesion. This evidence indicates that neurotrophic factor-like substances may be used in novel therapeutic approaches to Alzheimer's disease.
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PMID:Staurosporine facilitates recovery from the basal forebrain-lesion-induced impairment of learning and deficit of cholinergic neuron in rats. 203 5

Trimethyltin (TMT) produces behavioral and cognitive deficits resulting, in part, from limbic system toxicity. To determine whether these effects result from learning deficits or accelerated memory loss, the present experiment examined two delay conditioning paradigms in rats previously treated with either saline or TMT. Saline-treated Long-Evans rats receiving injections of lithium after consuming saccharin-flavored water later avoided saccharin ingestion: the degree of avoidance varied inversely with the time (0.5, 3 or 6 h) separating initial saccharin availability and lithium injection. Rats treated with TMT (8 mg/kg IV, 30 days prior) showed impaired conditioning at the long but not the short or intermediate delay conditions, suggesting that the deficits were mnemonic and not associative. Similar delay-dependent deficits in rats treated with TMT were observed in a passive avoidance task that arranged one of two delays between response emission and shock delivery during training. The effects of TMT on delay conditioning were accompanied by reduced bodyweight and hippocampal pathology. In summary, TMT appears to alter the temporally dependent association of events (entering darkened compartment versus saccharin consumption) and consequences (foot shock versus lithium administration) during acquisition. Furthermore, the observed deficits in delay conditioning produced by TMT did not appear to be task specific, with similar effects determined with tests of both somatosensory and gustatory avoidance learning designed to distinguish between functional alterations due to deficits in memorial processes from those due to altered sensory, motor, or associative processes.
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PMID:Time-dependent deficits in delay conditioning produced by trimethyltin. 249 48

Acute peripheral administration of physostigmine inhibits cortical acetylcholinesterase (AChE) for about 1 hr in the rat and improves performance on learning and memory paradigms after excitotoxic lesions of the nucleus basalis magnocellularis (NBM) in rats. This study examined the effects of continuous systemic infusion of physostigmine using osmotic minipumps. One week of continuous physostigmine infusion in normal animals inhibited cortical AChE activity in a dose-dependent manner. Doses causing near maximal (0.06 mg/kg/hr) and ED50 (0.0075 mg/kg/hr) inhibition of cortical AChE activity were used to determine the effects of continuous physostigmine administration on spatial learning in the water maze in rats with bilateral ibotenic acid lesions of the NBM. Physostigmine had no effect on the acquisition of the maze task but prevented the retention deficit measured in untreated NBM-lesioned rats. Physostigmine treatment also improved the search strategy during the spatial probe trial compared to the untreated NBM-lesioned rats. The two doses of physostigmine examined did not produce differential responses on behavioral measures. Although NBM lesions significantly depleted cortical AChE activity, physostigmine treatment reduced the activity further in a dose-dependent manner. Whereas neither the lesion nor the low dose of physostigmine altered cortical receptor binding, the higher dose of physostigmine significantly down-regulated cortical muscarinic receptor binding by 28%. These data demonstrate that enhancement of acetylcholine neurotransmission can improve memory loss and spatial strategy associated with excitotoxic NBM lesions.
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PMID:Continuous physostigmine infusion in rats with excitotoxic lesions of the nucleus basalis magnocellularis: effects on performance in the water maze task and cortical cholinergic markers. 281 Jan 14

Posttraumatic hydrocephalus is a treatable complication of head injury and can present with several different clinical syndromes. These include obtundation; simple failure to improve; a tetrad of psychomotor retardation, memory loss, gait trouble, and incontinence; and unusual symptoms including emotional disorder. Posttraumatic hydrocephalus seems to result from a blockage of cerebrospinal fluid (CSF) flow around the cerebral convexities. When the lumbar CSF pressure is consistently above 180 mm H2O, the hydrocephalus should be treated unless a contraindication to operation exists. Underlying brain injury from the trauma itself, however, may prevent recovery. When the typical symptoms of normal pressure hydrocephalus (NPH) are present, a shunt is also indicated. Decision-making is difficult when the patient has normal pressure, but is too injured to display the symptoms of NPH or has atypical symptoms. Overnight pressure recording, lumboventricular infusion testing, or cisternography may clarify whether a shunt is needed in this situation, but there is still considerable uncertainty about shunt prediction in this setting.
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PMID:Posttraumatic hydrocephalus. 638 12

A 59-y-old with a history of chronic renal failure on hemodialysis was diagnosed with herpes zoster and begun on 800 mg acyclovir 5 times daily. Two days later the patient developed visual hallucinations, ataxia, confusion and memory loss along with focal myoclonus, nausea and vomiting. No fever, elevated WBC count or significant electrolyte imbalance was found. CT scan of the brain was unremarkable. The patient was then dialyzed for presumed acyclovir toxicity. Her acyclovir level was later found to have been 3.4 micrograms/ml (normal peak range 0.4-2 micrograms/ml) prior to dialysis. After 3 h of hemodialysis, her post-dialysis acyclovir level was 1.9 micrograms/ml. After a second course of hemodialysis the next day the patient's mental status improved, and she was discharged 5 d later. Due to its low volume of distribution (0.6 L/kg), low protein binding (about 15%) and water solubility, acyclovir is an example of the ideal drug that can be removed by hemodialysis. About 45% of the total body amount can be extracted through a 3-h course of hemodialysis with resultant improvement in symptoms.
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PMID:Hemodialysis removal of acyclovir. 757 52

To examine the role of nitric oxide (NO) in the maintenance of working memory of rats, the effects of chronic administration (in drinking water) of the NO synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), on this behavior was examined with a simple test of remembering recently explored objects. Unlike other working memory tasks that require a subject to perform for a reward such as food or water or to avoid shock, our task measured spontaneous exploration of novel and familiar objects and has been described as a "pure" working memory task [9]. Normal subjects spend significantly more time in contact with new environmental components and less time with familiar objects. A subject that extensively reexplores a stimulus with which it has previous experience is presumed to exhibit some memory loss associated with the object. Memory changes were evaluated by measuring the relative time subjects explored familiar versus new stimulus objects. Rats (n = 15) that chronically drank L-NAME (approximately 90 mg/kg/day) for 14 days spent significantly less time exploring a novel object than did rats (n = 13) that drank only tap water (p < .05). This effect of L-NAME was abolished by concurrent administration of L-Arginine (approximately 4.5 g/kg/day). Total object exploration was not affected by our drug treatments, suggesting that our object discrimination task is not activity dependent. These data are consistent with the hypothesis that NO is required for some forms of working memory.
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PMID:Chronic administration of L-NAME in drinking water alters working memory in rats. 758 48


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