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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

A 38 year-old laborer experienced solvent intoxication during each of two spray paintings of a dump truck and other heavy equipment in an enclosed, unventilated garage. The paint base consisted primarily of toluene and methyl ethyl ketone. Nausea, headaches, dizziness, respiratory difficulty and other symptoms began after exposures. Over the next several days he developed impaired concentration, memory loss and cerebellar signs including an intention tremor, gait ataxia and dysarthria. MRI of the brain and EGG early in the work-up were normal, although later MRIs demonstrated fluid collection over the left parietal area. Examination by a toxicologist and neurologist revealed likely toxic encephalopathy with dementia and cerebellar ataxia. Three formal neuropsychological assessments over 2 1/2 years quantified cognitive, motor and behavioral changes. Despite similar findings in chronic exposure to these solvents, lasting sequelae following acute exposure have not been widely reported.
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PMID:Chronic neuropsychological and neurological impairment following acute exposure to a solvent mixture of toluene and methyl ethyl ketone (MEK). 174 49

The nervous system is particularly susceptible to the harmful effects of alcohol. These include Wernicke-Korsakoff syndrome, which is related to thiamine deficiency secondary to chronic alcohol abuse. Other neurotoxic effects of alcohol with cognitive impairments include delirium tremens, alcoholic seizures or "rum fits," and alcoholic neuropathies. It has become recognized in recent years that alcohol and its metabolites directly damage the nervous system even in the absence of nutritional deficiencies. Cerebral blood flow (CBF) measurements provide a noninvasive indirect monitor of cerebral metabolic activity. It has been shown conclusively that CBF measured by the 133Xe inhalation method is decreased in chronic alcoholism, correlating well with the amount of alcohol consumed. With abstinence, CBF returns toward normal levels provided the neurotoxic effects of chronic alcoholism are of recent onset. Clinical and pathological studies show significant loss of brain volume with ventricular dilatation after alcohol abuse even among young "social" drinkers. This toxic effect of alcohol is accompanied by varying degrees of cognitive impairments ranging from slight memory loss to frank dementia. Both the decrease in brain volume and the cognitive impairments, which occur with or without nutritional deficiency, are to a large extent reversible with abstinence and nutritional supplementation. Alcohol appears to accelerate age-related declines in CBF while nutritional deficiencies enhance the neurotoxic effects of alcohol. Measurements of local CBF (LCBF) and partition coefficients (L lambda) in deep cerebral structures, including the hypothalamus, thalamus, forebrain nuclei, and limbic system, can be achieved utilizing three-dimensional methods after inhalation of stable xenon as a contrast medium combined with serial computed tomographic imaging of the brain. Among chronic alcoholics, there are significant and diffuse reductions in cortical and subcortical gray matter CBF that are especially remarkable in hypothalamus and substantia innominata, which includes the nucleus basalis of Meynert, a major source of cholinergic input to neocortex and hippocampus. Reductions in LCBF are measurable in cognitively impaired patients with and without Wernicke-Korsakoff syndrome. Reductions of CBF include white matter and are more severe in patients with Wernicke-Korsakoff syndrome. Both types of encephalopathy improve with treatment, but recovery is usually more rapid and complete if nutritional deficiency is absent. Alcohol also appears to be a risk factor for stroke, possibly by depleting neuronal reserves and unfavorably influencing cardiovascular risks.
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PMID:Cerebral hemodynamic and metabolic effects of chronic alcoholism. 270 68

D-Lactate-associated encephalopathy is a rare clinical syndrome characterized by dizziness, ataxia, confusion, headaches, memory loss, lethargy, and aggressiveness which may progress to frank but reversible coma. It occurs in patients with profound dysfunction of the short-bowel syndrome and is believed to result from massive carbohydrate malabsorption with resultant over-production of D-lactate and other organic anions by the colonic flora. Extremely elevated serum levels of D-lactate (but not L-lactate) confirm the diagnosis, but currently D-lactate is not clearly established as the putative neurotoxin. We describe a patient who repeatedly developed D-lactate encephalopathy after surgical removal of nearly the entire jejunum and ileum. Markedly elevated D-lactate serum levels were documented during an encephalopathic episode. Potential pathophysiologic mechanisms and the treatment rationale are discussed.
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PMID:D-lactate-associated encephalopathy after massive small-bowel resection. 276 Apr 34

Ninety-four patients with limited stage small cell lung cancer treated between 1981 and 1985 with a regimen including prophylactic brain irradiation (PBI) after combination chemotherapy were assessed for compliance with PBI, brain relapse, and neurologic morbidity. Seventy-seven percent of patients had PBI and of these, 22% developed brain metastases after a median time of 11 months post treatment. The brain was the apparent unique initial site of relapse in 10% of PBI cases but more commonly brain relapse was preceded or accompanied by failure at other sites, especially the chest. Brain metastases were the greatest cause of morbidity in 50% of PBI failures. Twelve of 14 PBI patients alive 2 years after treatment had oncologic, neurologic, and neuropsychological evaluation, and brain CT. All long-term survivors were capable of self care and none fulfilled diagnostic criteria for dementia, with three borderline cases. One third had pretreatment neurologic dysfunction and two thirds post treatment neurologic symptoms, most commonly recent memory loss. Fifty percent had subtle motor findings. Intellectual functioning was at the 38th percentile with most patients having an unskilled occupational history. Neuropsychologic impairment ratings were borderline in three cases and definitely impaired in seven cases. CT scans showed brain atrophy in all cases with mild progression in those having a pre-treatment baseline. Periventricular and subcortical low density lesions identical to the CT appearance of subcortical arteriosclerotic encephalopathy were seen in 82% of posttreatment CT studies, and lacunar infarcts in 54%. Neuropsychologic impairment scores and the extent of CT periventricular low density lesions were strongly associated (rank correlation 0.7, p less than .05). Overall, PBI after intensive combination chemotherapy did not induce gross dementia or neurologic dysfunction but its risk/benefit ratio is not overwhelmingly favorable, with failure to prevent brain relapse in 1/5 patients and subtle but detectable motor findings and neuropsychologic impairment in the majority.
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PMID:The role of prophylactic brain irradiation in limited stage small cell lung cancer: clinical, neuropsychologic, and CT sequelae. 283 43

Eight patients with acquired immune deficiency syndrome (AIDS) presented complications affecting the nervous system. The complaints were headache, seizure, confusion or hallucination. Neurologic manifestations included meningitis, focal deficits, cranial nerve palsy, and dementia. Cerebrospinal fluid exhibited a decrease in the percentage of T helper lymphocytes with an inverted helper-to-suppressor cell ratio. The neurologic manifestations of AIDS may depend on multiple factors, such as HIV infection of the central nervous system, concomitant infections with other agents or meningeal invasion by systemic lymphoma or Kaposi's sarcoma. Many patients develop a diffuse encephalopathy which characteristically begins with impaired concentration and mild memory loss, and progresses to severe global cognitive impairment and dementia. Perivascular infiltrates and scattered microglial nodules, consisting of aggregates of microglia and astrocytes, are the most common findings in these patients.
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PMID:[Neurologic complications accompanying acquired immunodeficiency syndrome (AIDS): study of a group of 8 cases]. 295 8

Although organic solvents are essential components of an industrial economy, they are not used without risk. The relationship between excessive exposure to organic solvents and subsequent development of chronic encephalopathy has been recognized for nearly 100 years. Fifteen industrial painters who underwent evaluation in an occupational health clinic for symptoms that they related to their work were found to have a high prevalence of neurasthenic symptoms, most frequently, memory loss and personality change. Although neurologic and screening laboratory examinations showed no consistent abnormalities, psychological tests documented poor short-term memory and an array of neuropsychologic deficits. Personality profiles revealed depression, anxiety, and preoccupation with somatic concerns. These findings agree well with previous reports of "chronic painter's syndrome." Heightened awareness among industrial physicians and prospective studies to evaluate existing threshold limit values and personal protective equipment requirements are indicated.
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PMID:Organic solvent-induced encephalopathy in industrial painters. 395 Jul 85

During an epidemic of dengue type 2 virus in the rural community of Charters Towers, North Queensland, Australia, in 1993, 210 cases presented to the local hospital with signs and symptoms of classic dengue fever. Two cases were noteworthy because of neurologic complications, which included drowsiness, short term memory loss, agitation, and seizure. The cases are presented in detail because they are the first cases of dengue-associated encephalopathy to be documented in Australia. An increasing number of cases of encephalopathy associated with classic dengue fever is being reported world wide, but the etiology of this clinical syndrome remains unknown.
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PMID:Dengue fever with encephalopathy in Australia. 860 Jul 60

Semi-quantitative neuropathological analysis and morphometric evaluations of the brains of 5 elderly people (63-85 years old) dying following a 5-27-year history of dementia reveal that, despite exhaustive survey of all major brain regions, 4 of these cases show virtually no histopathological lesions of Alzheimer's disease. Instead their CNS manifests a severe, bilateral, neuronal depletion, and astrogliosis afflicting the lateral temporal neocortex, highly compatible with a previous herpetic viral encephalitis. In the fifth case unilateral neocortical temporal lobe sclerosis is accompanied by Alzheimer's disease, but with much more dense Alzheimer lesions throughout the contralateral cerebral hemisphere. Three of these 5 individuals had a history either of herpes zoster of the skin or of a single episode of viral meningoencephalitis, roughly concomitant with the onset of memory loss. This clinical and pathological evidence that a remote herpes virus encephalopathy (when bilateral) "protects" that brain against Alzheimer's disease strengthens our growing suspicion that incomplete replication cycles of herpes simplex or zoster virus, following repeated reactivation within neurons of the trigeminal ganglia, may link these viruses to the pathogenetic cascade underlying dementia of the Alzheimer type.
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PMID:Neocortical temporal lobe sclerosis masquerading as Alzheimer dementia: does herpes virus encephalopathy protect against Alzheimer's disease? 902 Mar 87

A mild chronic encephalopathy may be the most common neurologic symptom in patients with late stage Lyme disease. The symptoms tend to be diffuse and nonspecific, and patients typically report memory loss, sleep disturbance, fatigue, and depression. Among patients with these symptoms, it is generally felt that those with abnormal cerebral spinal fluid (CSF) have a neurological basis to their illness. A comparison of Lyme patients, with and without abnormal CSF, revealed that only the abnormal CSF group had lower memory test scores than normal controls. However, most patients in both Lyme groups complained of memory loss and also reported significantly more symptoms of depression and fatigue than controls. Thus, while depressive symptoms may not be a factor in objective memory performance, they may indeed play a role in perceived memory loss. A survey of the neuropsychological literature suggests that active neurologic involvement, the psychological consequences of chronic illness, and possibly residual neurologic deficits from past infection with Lyme disease all may affect the patient's perception of cognitive dysfunction.
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PMID:Lyme encephalopathy: a neuropsychological perspective. 916 57


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