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)

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

Two unusual cases of cerebral toxoplasmosis in AIDS patients are presented. Two homosexual males aged 33 and 52 years in CDC stage IV C1 complained of memory loss during the past 6 months, as well as weight loss and mild fever. They showed severe intellectual deterioration and discrete basal ganglia dysfunction. Motor performance and cognitive function as well as the conventional EEG findings were grossly abnormal. MRI was normal in the younger patient but showed signal-intensive zones in the basal ganglia and cortical atrophy in the older one. CSF and serological antibody tests were normal; immunological function was severely impaired. The patients were diagnosed as late "HIV-related dementia". Both deteriorated rapidly and died within a few weeks. Neuropathological examination revealed histologically severe Toxoplasma gondii encephalitis, involving the basal ganglia in particular. It is concluded that in AIDS patients with a severely impaired immune status cerebral opportunistic infection may present as dementia with mild basal ganglia impairment in the absence of other focal neurological signs or the characteristic radiological findings.
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PMID:Two cases of cerebral toxoplasmosis in AIDS patients mimicking HIV-related dementia. 177 50

Neurologic manifestations, afflicting up to 70% of SLE patients, include psychosis, seizures, chorea, neuropathies, and stroke. MRI is useful in evaluation of lupus patients and several reports have documented cerebral atrophy or focal hyperintensities. We report an unusual MRI appearance in a 56-year-old woman with SLE, diagnosed on the basis of pleuritis, lymphopenia, anti-DNA antibodies, and neurologic involvement. She reported recent onset of Raynaud's phenomenon and generalized macular rash. She presented after two months of gradual deterioration with memory loss, flattened affect, dysphagia, dysarthria, anomia, and somnolence, without focal neurologic signs. Investigations included elevated ESR, reduced complement, normal CSF without oligoclonal bands, negative viral serology, normal hormone and vitamin levels, normal renal and hepatic function. Neuropsychologic testing showed widespread impairment (WAIS-R: FSIQ-63; WMS-69; DRS-98; RCPM-14; WAB AQ-78.8). CT was normal but MRI showed strikingly symmetric, confluent hyperintensities extensively involving cerebral and cerebellar white matter on T1 and T2 weighted scans. Basal ganglia and subependymal and subcortical white matter were spared. Treated with prednisone, the patient made a gradual, but incomplete, recovery. These MRI findings may reflect widespread vasculopathy or direct immunologic brain insult with or without immunologic blood-brain barrier disruption.
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PMID:Dementia with leukoencephalopathy in systemic lupus erythematosus. 191 71

Six patients with small cell lung cancer developed a slowly progressive neurologic syndrome characterized by apathy, abulia, memory loss, gait ataxia, and corticospinal tract signs 26 to 50 months (mean, 35.2 months) after prophylactic cranial irradiation and systemic chemotherapy. In each case this was accompanied by CT and/or MRI evidence of changes in the periventricular white matter. These patients are long-term survivors (41 to 69 months) and do not have CNS metastases.
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PMID:Delayed leukoencephalopathy in survivors with small cell lung cancer. 303 38

Among 39 cases with acute-onset amnestic syndrome having unilateral localized infarct, 8 cases with anteromedial thalamic infarct ("thalamic" amnesia), and 18 cases with medial temporal lobe infarct including hippocampus in the posterior cerebral artery territory ("PCA" amnesia) were studied in terms of X-CT and MRI findings and neuropsychological examinations. Results were as follows: 7 out of 8 cases with thalamic amnesia (88%), and 15 of 19 cases with PCA amnesia (78%) showed left side lesions on CT scan. All groups showed a prolonged recent memory loss with little loss of immediate recall and remote memory, and disorientation and dyscalculia. In both types of amnesia, patients having a left sided lesion showed recent memory loss with new learning disabilities of verbal materials. Patients having a right sided lesion showed recent memory loss with new learning disabilities of both verbal and visuospatial materials. Judging from the X-CT and MRI findings, the lesions most probably causing amnesia in these cases seemed to be the anterior and dorsomedial nuclei of the thalamus in thalamic amnesia and hippocampus in PCA amnesia. Differential diagnosis in amnestic syndrome with localized infarct is also discussed.
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PMID:Acute-onset amnestic syndrome with localized infarct on the dominant side--comparison between anteromedial thalamic lesion and posterior cerebral artery territory lesion. 357 4

Retrograde amnesia for autobiographical material in the absence of anterograde amnesia or other memory disturbances was found in a patient with acute viral encephalitis. Memory loss showed a temporal gradient, but new learning was spared. Both brain perfusion imaging with 99mTc-HMPAO SPECT, and EEG localized the lesion in the left temporal lobe while CT and MRI were normal. This observation supports the anatomical differentiation between the different memory functions. The uncommon combination of isolated retrograde amnesia without other neuropsychological findings may raise the doubt of psychogenic aetiology, which in this case was refuted.
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PMID:Isolated retrograde amnesia for autobiographical material associated with acute left temporal lobe encephalitis. 779 57

The patient was a right-handed 59-year-old female technician who was admitted to our hospital with a complaint of memory loss. Clinical examination revealed pure anterograde amnesia regarding episodic memory, while semantic and procedural memory was intact. Radiological procedures (CT scan and MRI) revealed a tumor of the septum pellucidum, which localized from the lower part of the corpus callosum to the anterior parts of the bilateral fornices. Transcallosal total removal was performed (pathological examination revealed that it was astrocytoma). Radiological and operative findings showed that the thalamus, the mammillary bodies, the hippocampus, and the basal forebrain, which are closely related to memory, were spared. After the operation, she reported no further memory disturbance. Preoperative neuropsychological tests revealed anterograde amnesia for verbal and visual stimuli, but postoperatively the former disappeared and the latter improved. Pre- and postoperatively, she was nonaphasic, and her immediate memory, intelligence, and frontal functions were intact. Cases of amnesia due only to fornix lesions are rare, and have not been reported yet in Japan. Our case is valuable in terms of showing that only the fornix lesion was responsible for memory disturbance. The main symptom resulting from fornix lesion is thought to be anterograde amnesia.
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PMID:[Pure anterograde amnesia due to bilateral fornix lesions]. 783 48

This paper describes a patient whose amnesia for an offence (fraud) and two fugue episodes occurred against the background of an underlying organic amnesia. The fugue states conformed in their duration and precipitating factors to previous accounts in the literature. The organic, anterograde memory impairment was attributed to multiple small infarcts and a larger infarction in the left medial temporal lobe, which were evident on MRI and PET scans after the patient had developed transient neurological signs. At follow-up, the anterograde amnesia had persisted, and the patient also showed some difficulty in retrieving autobiographical memories of past incidents or events, although other aspects of his retrograde memory were intact (including his knowledge of facts about his past life and his general knowledge of public events). The difficulty in retrieving autobiological incidents may have resulted from the presence of a moderate degree of frontal lobe dysfunction or, just possibly, from ischaemia in the left anterior temporal lobe. The persistence of the organic memory impairment and the importance of both the clinical history and neuropsychological testing in assessment are discussed, as well as the need to examine for possible organic factors in patients who may initially appear to manifest purely 'psychogenic' memory loss.
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PMID:The case of the amnesic intelligence officer. 789 49

The first comprehensive in vivo documentation of the long term profile of pathological and spared tissue is described in a group of 10 patients with a diagnosis of herpes simplex encephalitis, who were left with memory difficulties as a major residual sequel of their condition. With a dedicated MRI protocol, which included high resolution images of temporal lobe and limbic system areas, data are provided on structures that have recently gained importance as anatomical substrates for amnesia. The major features of the lesion profile were: (1) unilateral or bilateral hippocampal damage never occurred in isolation, and was often accompanied by damage to the parahippocampus, the amygdala, specific temporal lobe gyri, and the temporal poles; (2) the insula was always abnormal; (3) neocortical temporal lobe damage was usually unilateral or asymmetric. It never occurred in isolation, and was invariably associated with more medial pathological changes; (4) anterior and inferior temporal lobe gyri were damaged more often and more severely than posterior and superior temporal lobe gyri; (5) pronounced abnormality was often present in the substantia innominata (region of the basal forebrain/anterior perforated substance); (6) there was evidence of significant abnormality in the fornix; (7) there was evidence of damage to the mammillary bodies; (8) thalamic nuclei were affected in around 50% of cases, with damage usually unilateral; (9) frontal lobe damage was present in a few patients, and affected medial areas more than dorsolateral areas; (10) there was some involvement of the striatum, although this was usually unilateral and mild; (11) there was usually limited involvement of the cingulate gyrus and of the parietal and occipital lobes; (12) the cerebellum and brain stem were never damaged. Lesion covariance analysis indicated a close relation between the presence of abnormalities in temporal lobe and limbic-diencephalic regions. Unlike severe head injury, lesions in the temporal pole were not associated with the presence of lesions in the orbitofrontal cortex. Long term neuropsychological impairments were characterised by a dense amnesia in 60% of cases, and a less serve but noticeable anterograde memory impairment in the others. Naming and problem solving deficits were found in a small number of cases. Only two patients were able to return to open employment. Severity of amnesia showed a significant relation with severity of damage to medical limbic system structures such as the hippocampus, with bilateral damage being particularly important. By contrast, there was a minimal relation between memory loss and severity of damage to the thalamus, to lateral temporal lobe areas, or to the frontal lobes.
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PMID:Herpes simplex encephalitis: long term magnetic resonance imaging and neuropsychological profile. 796 8

A patient had repeated episodes of transient loss of memory, which had been attributed to psychogenic causes. Preservation of his sense of personal identity and the presence of repetitive questioning indicated an organic basis, however, and the multiplicity of the attacks and their brief duration suggested an epileptic aetiology. Although three standard EEGs, CT and MRI were all normal, two sleep EEGs confirmed bilateral foci in the temporal lobes. The attacks responded to an anticonvulsant. A fluoro-deoxyglucose PET scan, performed a few months after the most recent attack, was normal. The patient also had impaired anterograde memory that persisted six months after recovery from the acute attacks.
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PMID:Transient epileptic amnesia differentiated from psychogenic "fugue": neuropsychological, EEG, and PET findings. 805 91


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