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Query: UMLS:C0751295 (memory loss)
3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A clinical and neuropsychological syndrome for early recognition of occult hydrocephalus and cerebral atrophy is described. Five illustrative patients are reported. The main features of the syndrome are (i) subjective non-specific complaints (headaches, depression and loss of memory); (ii) the tonic foot response of the sole and the grasp reflex of the foot in the absence of the grasp reflex of the hand; (iii) attacks of sudden and transient loss of muscle tone in both lower limbs leading to falls without warning while standing or while walking. These attacks indistinguishable from drop-attacks are termed chalastic fits; (iv) a dissociation between the satisfactory performances on the Ottawa-Wechsler scale and the poor performances on Kohs Block Design test. Clinical and neuropsychological findings could not differentiate between occult hydrocephalus and cerebral atrophy; only radionuclide cisternography and computerized tomography were able to delineate the final diagnosis.
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PMID:A syndrome of early recognition of occult hydrocephalus and cerebral atrophy. 91 52

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

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

Nephropathic cystinosis is associated with end-stage renal failure, retinal damage, and hypothyroidism. Patients may now survive past the first decade of life with the use of dialysis and renal transplantation. Examination of a 24-year-old woman with this disorder revealed ovarian failure, mildly abnormal results on a glucose tolerance test, intermittent confusion, short-term memory loss, and cerebral atrophy on computerized axial tomography. Autopsy examination at age 25 years revealed cystine storage in multiple tissues including the atrophic ovaries, pancreatic islet cells, the aorta, and the brain. Dysfunction of multiple organ systems may develop in patients with cystinosis who survive into adulthood. This emphasizes the need for a systemic therapy for cystinosis.
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PMID:Nephropathic cystinosis with central nervous system involvement. 367 1

Both patients 1 and 2 were males 73 and 77 years old, respectively, and over the past several years, both had gradually developed progressive loss of vigor, paucity speech, personality changes, and anosognosia, in addition to memory loss and disorientation. Patient 1 experienced emotional lability, mild pyramidal signs and parkinsonian features. The various diseases causing secondary dementia were ruled out. The Mini Mental Scale scores were 13 and 21, respectively. Brain CT scans and MRI showed cerebral atrophy, most prominent in the frontal and the temporal lobes. There were few lesions suggestive of cerebrovascular disease. The EEGs showed nonspecific diffuse slowing, and the cerebrospinal fluid was normal. 123I-amphetamine SPECT, which provided the most valuable diagnostic findings in these two cases, demonstrated selective hypoperfusion of the frontal and the temporal lobes in both patients. Frontal lobe dementia of the non-Alzheimer type (Gustafson, Neary), progressive subcortical gliosis (Neumann), Pick's disease, and Alzheimer's disease with frontal lobe predominance were considered the most likely of the various diseases causing frontal lobe dementia. The usefulness of SPECT in diagnosing and elucidating the pathophysiology of dementia are discussed.
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PMID:[Frontal lobe dementia--two cases diagnosed by SPECT]. 812 6

Patients with Alzheimer's disease (AD) show loss of memory and cognitive deficits the molecular mechanisms of which are not completely known. We examined age-related changes in the expression levels of beta-amyloid precursor protein (beta APP) in the brain of the senescence accelerated mouse (SAM) P/10, which shows age-dependent brain atrophy and impairment in learning and memory, and in the senescence resistant mouse (SAM)-R/1 using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Levels of both beta APP mRNA and protein increased with age, reaching a peak at 8 months of age in the hippocampus of SAM-P/10. In contrast, beta APP protein level decreased with age in the hippocampus of SAM-R/1 while beta APP mRNA level did not change significantly. Levels of beta APP mRNA and protein showed no change with ageing in other brain regions, including cerebral cortex, thalamus/midbrain and cerebellum brain stem. These results suggest that the beta APP over-expression in the hippocampus might be related to the characteristic memory loss in SAM-P/10.
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PMID:Age-related changes in the expression of Alzheimer's beta APP in the brain of senescence accelerated mouse (SAM)-P/10. 918 23

Although mild progressive memory impairment is commonly associated with normal human aging, it is unclear whether this phenomenon can be explained by specific structural brain changes. In a research sample of 54 medically healthy and cognitively normal elderly persons (ages 55-87, x = 69.0 +/- 7.9), magnetic resonance imaging (MRI) was used to derive head-size-adjusted measurements of the hippocampal formation (HF) (dentate gyrus, hippocampus proper, alveus, fimbria, subiculum), the superior temporal gyrus (STG), and the subarachnoid cerebrospinal fluid (CSF) (to estimate generalized cerebral atrophy). Subjects were administered tests of primary memory (digit span) and tests of secondary memory with immediate and delayed recall components (paragraph, paired associate, list recall; facial recognition). Separate composite scores for the immediate and delayed components were created by combining, with equal weighting, the subtests of each category. The WAIS vocabulary subtest was used as a control measure for language and intelligence. A highly significant correlation (P < 0.001), independent of age, gender, and generalized cerebral atrophy was found between HF size and delayed memory performance. No significant correlations were found between HF size and primary or immediate memory performance. STG size was not significantly correlated with any of the composite memory variables. These results suggest that HF atrophy may play an important independent role in contributing to the memory loss experienced by many aging adults.
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PMID:Hippocampal formation size in normal human aging: a correlate of delayed secondary memory performance. 1046 85

We describe a Polish family with Alzheimer's disease in some of its members. Two sisters were observed and examined--also neuropathologically in the Institute of Psychiatry and Neurology in Warsaw. The disease onset was in our patients at 32 and 33 years. The first symptoms were memory loss and disorientation. Later on myoclonus and extrapyramidal stiffness were noted in both cases. Neurovisualizing examinations performed in both sisters showed diffuse brain atrophy. The symptoms increased rapidly and in short time (several months) the patients became mute and bedbound. They died at age 35 and 37 years. We were informed that the father of the patients suffered from very similar illness and died at age of 37 years and their older brother had the some symptoms and died at the age of 28 years. Post-mortem brain examination disclosed in the both hospitalized cases diffuse atrophy of the cerebral hemispheres, particularly severe in the temporal lobes. Microscopically senile plaques of various types were found in the cortex. The density of the plaques was very high but Alzheimer's fibrillary degeneration was found occasionally only. The amyloid burden in cortex of the examined brains, estimated as the measure of parenchymal amyloidosis beta, was two to six-fold higher in most areas compared with changes in sporadic AD and Down-syndrome cases. DNA was isolated from blood and tissue of both cases and from blood of their 8 children as well. In both patients mutation in presenilin 1 (PS1) gene of Prol 117 Leu was found and it was discovered that 4 persons of their progeniture were carriers of this mutation. The described mutation causes one of the earliest so far reported onset and death in FAD kindreds. Presenilin isolated from both cases and transfected into cultures of murine neuroblastoma and human kidneys provoked production of beta amyloid with increased A-beta 42/40 ratio.
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PMID:[Familial Alzheimer's disease connected with mutation in presenilin gene 1 (P117L)]. 1159 21

Patients presenting with subacute amnesia are frequently seen in acute neurological practice. Amongst the differential diagnoses, herpes simplex encephalitis, Korsakoff's syndrome and limbic encephalitis should be considered. Limbic encephalitis is typically a paraneoplastic syndrome with a poor prognosis; thus, identifying those patients with potentially reversible symptoms is important. Voltage-gated potassium channel antibodies (VGKC-Ab) have recently been reported in three cases of reversible limbic encephalitis. Here we review the clinical, immunological and neuropsychological features of 10 patients (nine male, one female; age range 44-79 years), eight of whom were identified in two centres over a period of 15 months. The patients presented with 1-52 week histories of memory loss, confusion and seizures. Low plasma sodium concentrations, initially resistant to treatment, were present in eight out of 10. Brain MRI at onset showed signal change in the medial temporal lobes in eight out of 10 cases. Paraneoplastic antibodies were negative, but VGKC-Ab ranged from 450 to 5128 pM (neurological and healthy controls <100 pM). CSF oligoclonal bands were found in only one, but bands matched with those in the serum were found in six other patients. VGKC-Abs in the CSF, tested in five individuals, varied between <1 and 10% of serum values. Only one patient had neuromyotonia, which was excluded by electromyography in seven of the others. Formal neuropsychology testing showed severe and global impairment of memory, with sparing of general intellect in all but two patients, and of nominal functions in all but one. Variable regimes of steroids, plasma exchange and intravenous immunoglobulin were associated with variable falls in serum VGKC-Abs, to values between 2 and 88% of the initial values, together with marked improvement of neuropsychological functioning in six patients, slight improvement in three and none in one. The improvement in neuropsychological functioning in seven patients correlated broadly with the fall in antibodies. However, varying degrees of cerebral atrophy and residual cognitive impairment were common. Over the same period, only one paraneoplastic case of limbic encephalitis was identified between the two main centres. Thus, VGKC-Ab-associated encephalopathy is a relatively common form of autoimmune, non-paraneoplastic, potentially treatable encephalitis that can be diagnosed by a serological test. Establishing the frequency of this new syndrome, the full range of clinical presentations and means of early recognition, and optimal immunotherapy, should now be the aim.
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PMID:Potassium channel antibody-associated encephalopathy: a potentially immunotherapy-responsive form of limbic encephalitis. 1496 Apr 97

Stroke is an important risk factor for dementia, but the exact mechanisms involved in cognitive decline remain unclear. In this study, we related baseline MRI brain measures with later cognitive decline. Seventy-nine stroke survivors aged 75+ years without dementia were recruited 3-month post-stroke. They underwent yearly neuropsychological assessments and had an MRI at baseline and 2 years. Medial temporal lobe atrophy (MTA) was scored and volume of white matter hyperintensities (WMH) was measured at baseline. The rate of ventricular enlargement was measured by comparing the baseline and repeat images. Linear regression indicated that memory loss was related to both baseline memory and MTA (p=0.001; standardized regression coefficient beta=-0.35) but not WMH volume. The only independent predictor of ventricular enlargement was MTA (p=0.003; beta=0.47). However, no baseline MRI variable differed between those who did (18%) and did not (82%) develop dementia. The association of MTA but not WMH with subsequent cognitive decline and increasing brain atrophy suggests a greater role for Alzheimer type than vascular pathology in delayed cognitive impairment after stroke.
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PMID:Medial temporal atrophy rather than white matter hyperintensities predict cognitive decline in stroke survivors. 1693 70


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