Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0233794 (memory impairment)
 7,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 58-year-old laboratory-glassware manufacturer was referred to hospital because of coarse "tremor" of the upper extremities of 16-months-duration. Examination showed severe intention and action myoclonus, confirmed by electromyographic recording, slight memory impairment but was otherwise normal. Mercury levels were high in blood and urine (not in CSF) and, as other causes of myoclonus were excluded, inorganic mercury poisoning, was diagnosed. Only slight unilateral intention tremor persisted after dimercaprol treatment. Inhalation of mercury vapor was the mode of contamination. Myoclonus is the hallmark of severe inorganic mercury intoxication, the main clinical and pathological aspects of which are briefly discussed.
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PMID:[Intention and action myoclonus disclosing occupational mercury poisoning]. 669 24

A 70 year-old-man with recurrent herpetic keratitis had a meningo-encephalitis with transient left hemiplegia and disorders of consciousness. EEG disclosed periodic slow waves on the right temporal region. Isotope and CT scans showed focal abnormalities in the same region. Antibodies to herpes simplex virus were demonstrated by complement fixation in serum and specific antiherpes IgG and IgM by immunofluorescence assay in serum and CSF. A year later the patient had a status epilepticus. CT scan showed a large right temporal hypodense area. CSF was abnormal with pleiocytosis, increased protein and IgG levels. High titers of antiherpes IgG persisted in serum and CSF. Neuropsychological tests did not demonstrate any memory impairment. The occurrence of persistent inflammation after herpes simplex encephalitis is discussed. The unusual benign course without antiviral therapy, may be related to the reactivation of a latent infection with an efficient immunological response. The unilateral temporal necrosis may explain the absence of amnestic sequelae.
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PMID:[Acute necrotizing herpetic encephalitis with a spontaneously improving clinical course]. 669 26

Postinfectious encephalomyelitis is a kind of demyelinating disease with pathological characteristics and a monophasic clinical course. Herein, we describe a patient who had the symptoms of binge eating, fatigue, memory impairment, hypotalkativeness, hypoactivity, lethargy, incoherent speech, dysphoric mood, and episodic disorientation. Only elevation of CSF protein was noted upon initial admission; however, blurred vision of the eyes developed progressively after discharge. A magnetic resonance image (MRI) scanning of the brain demonstrated scattered lesions of low signal intensity on T1-weighted images and high areas on T2-weighted images in the left thalamus, bilateral hypothalamus and midbrain. The findings of MRI image, CSF, and clinical course all suggested postinfectious encephalomyelitis. After a treatment of prednisolone, a follow-up MRI revealed evidence of improvement, and the binge eating also improved.
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PMID:The binge eating and emotional change in a patient with postinfectious encephalomyelitis. 909 51

We report a 6-year-old girl with Japanese B encephalitis. The initial symptoms were high fever, headache and vomiting. On the second day of illness, she developed hemiconvulsion and was admitted to our hospital. Physical examination demonstrated a stiff neck. C-reactive protein elevated to 22.7 mg/dl. CSF examination showed a marked increase in the cell count (10,896/3 mm3). During the course of the treatment, she showed transient hemiparesis and dysphagia, followed by akinetic mutism lasting for about a month. The patient was left with severe cognitive and memory impairment and complex partial seizures but no motor dysfunction. Japanese B encephalitis was diagnosed by means of serological examination. Magnetic resonance imaging revealed cystic lesions in the medial and posterior thalamus and substantia nigra and severe atrophy of the hippocampus. Despite the involvement of substantia nigra, the patient had no parkinsonism. The cognitive impairment may in part be explained by the lesions in the medical and posterior thalamus.
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PMID:[A case of Japanese B encephalitis with lesions of thalamus and substantia nigra revealed by MRI]. 969 26

A 70-year-old man presented to us in 1994 with a three-year history of worsening dementia. With the exceptions of a Mini-Mental State exam score of 20 and an inability to tandem walk, his physical and neurological examinations were normal. His past medical history revealed that in 1992 he had been evaluated at another institution for memory impairment and bifrontal headaches. A spinal tap had been done in 1992 showing elevated protein, reduced glucose, and a pleocytosis; his CSF fungal culture and cryptococcal antigen test were negative. He subsequently was lost to follow-up, and although his headaches had resolved, his mental status had continued to worsen. In 1994 his CSF cryptococcal antigen was positive, and his CSF fungal culture grew C. neoformans. He gradually improved with treatment for cryptococcal meningitis (CM). With the exception of mild memory impairment, in 2003 he and his family thought that his mental status had returned to normal. This case emphasizes that: 1) CM should always be kept in the differential diagnosis of dementia; 2) CM may be extremely insidious and difficult to diagnose; and 3) if one is to rule out unequivocally all possible reversible causes of dementia, one should perform a spinal tap.
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PMID:Reversible dementia: a case of cryptococcal meningitis masquerading as Alzheimer's disease. 1585 46

Limbic encephalitis affects the mesial temporal lobes and is characterized by subacute onset of memory impairment, personal change, temporal seizures and autonomic nervous disorders. It can occur as viral infections, especially caused by Herpes simplex, paraneoplastic syndrome as a remote effect of cancer, CNS complication of well defined autoimmune diseases. Recently acute reversible limbic encephalitis which probably autoimmune mediated disorders has been reported. Anti-immunotherapy including steroids, plasma exchange and intravenous immunoglobulin often improves this condition and anti-voltage gated potassium channel (VGKC) antibody or anti-glutamate receptor epsilon2 antibody has been detected in some patients. Establishing the means of early detection of these antibodies as well as other characteristic paraneoplastic antibodies should now be the aim. Detection of neurotropic viral genomes in CSF by PCR is also important for differential diagnosis. As complete recovery of higher cerebral function is generally difficult, immunotherapy and anti-convulsants in addition to vitamin B, and acyclovir should be considered in an early stage of disease.
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PMID:[Limbic encephalitis: etiology, pathogenesis, diagnosis and therapy]. 1565 Dec 95

Paraneoplastic limbic encephalitis (PLE) is a rare neurological consequence of a variety of cancers, most commonly originating from lung, breast and testis. The aetiology is believed to be immune-mediated, caused by tumour-induced autoimmunity launching an attack against one's own central nervous system. The patient may present with amnesia, depression, anxiety, seizures and/or personality changes. The onset of these symptoms may precede the diagnosis of malignancy by a period of up to 2 years. The malignancy may be occult and unless the syndrome is recognised, it may fail to be detected. The diagnosis of PLE is suggested by the clinical picture, MRI evidence of mesial temporal lobe abnormality and CSF abnormalities such as the presence of oligoclonal bands. It may be further supported by the presence of paraneoplastic antibodies in the serum. Immunosuppression has been tried in some cases but memory impairment is often irreversible. There are several case reports in the literature of paraneoplastic limbic encephalitis but few emphasise the resulting impact that this may have on the patient's quality of life and their carers. The accompanying amnesia is often far more distressing to the carers, who are aware of the limitations of treatment of the underlying malignancy. Hospices offer the appropriate palliative environment for such patients as well as physical and psychological respite to the carers.
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PMID:Paraneoplastic limbic encephalitis. 1570 28

We report the case of a 79-year-old woman who developed a rapidly progressive dementia (RPD) with severe memory impairment, early visual hallucinations and extrapyramidal signs. Symptoms started suddenly after hip replacement surgery following an accidental fall. Motor epileptic seizures appeared at the end of the illness. Dementia worsened gradually leading to akinetic mutism. She died five and a half months after the onset of symptoms. MRI showed cerebral atrophy but failed to detect any other lesion. Results of all laboratory tests performed were negative. After the most frequent treatable diseases were excluded, the diagnosis of dementia with Lewy bodies was initially considered. CJD was also suggested based on the rapid evolution of the disease and the positivity of 14-3-3 protein in CSF. Neuropathological examination revealed an extensive miliary metastatic dissemination from an unknown primary adenocarcinoma. Pulmonary origin was suggested according to the immunohistochemical profile. Histopathological changes of Alzheimer's disease were also observed in the cerebral cortex and hippocampus. Neither Lewy bodies nor PrP deposits were found. The sudden onset of the dementia just after the hip replacement surgery raises the possibility of a pathological fracture with secondary tumoral microembolic dissemination. Despite its rarity, this entity should be included in the differential diagnosis of RPD. This case illustrates the definite importance of neuropathological post-mortem examination in order to elucidate the different types of dementia.
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PMID:Miliary brain metastases presenting as rapidly progressive dementia. 1587 9

Infusion of Fe2+, Abeta42, and buthionine-sulfoximine (FAB), but not Abeta42 alone or in combination with Fe2+, into the left cerebral ventricle of Long-Evans rats for 4 weeks induced memory impairment that was accompanied by increased hyperphosphorylated Tau protein levels in the CSF. FAB-infused animals displayed thioflavin-S-positive amyloid deposits, hyperphosphorylated Tau protein, neuronal loss, and gliosis. Animals treated with Abeta42, Fe2+, or buthionine-sulfoximine alone or in combination failed to show the histological modifications seen with FAB. This data suggests that Abeta42 is not sufficient to induce an Alzheimer's disease-like symptomatology, and it supports a model whereby a decrease in the brain's antioxidant defense system leads to the Abeta42-independent oxidative stress necessary for the peptide to induce histopathological changes and memory loss.
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PMID:Beta-amyloid and oxidative stress jointly induce neuronal death, amyloid deposits, gliosis, and memory impairment in the rat brain. 1622 1

In humans, age-related memory impairments begin in mid-life and cognitive weakening continues with advancing age. An important aspect of defining memory decline is the distinction between dementia as a result of neurological diseases, such as Alzheimer's disease, and memory loss not specifically associated with disease. Within the population of elderly without dementia, there is considerable variability in memory. This variability is likely to be a result of the interaction of genetic make-up and environment, which influences several processes for cell maintenance and repair including oxidative damage and cholesterol metabolism, leading to disruption of Ca(2+) homeostasis, and ultimately Ca(2+)-dependent processes that underlie memory. In humans, several methods have been employed to distinguish biological markers of aging that may predict cognitive decline. Memory deficits associated with normal aging and Alzheimer's disease have been linked to a decrease in the volume of brain structures, such as the hippocampus and to genetic markers, such as apolipoprotein E. In this regard, examination of CSF for biomarkers of disease can help in differentiating normal aging from Alzheimer's disease. Measures of oxidative stress and cholesterol in plasma correlate with memory deficits; research suggests that treatments that reduce oxidative stress or cholesterol through exercise, diet or the use of antioxidant vitamins may delay cognitive decline.Nevertheless, to date, very little treatment is available to reverse memory deficits in later life. In this regard it is important to identify individuals at risk for memory deficits in order to discriminate different mechanisms of brain aging and develop treatments. Considerable effort is driving research to develop accurate biological markers of brain aging. In turn, these markers will provide information on mechanisms of aging and cognitive decline and point to potential treatments. Accordingly, the effectiveness of treatment needs to be verified for both cognitive changes and biological markers that are specific for age-related memory deficits.
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PMID:Biological markers of age-related memory deficits: treatment of senescent physiology. 1647 90


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