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)

We describe a patient with amyotrophic lateral sclerosis with dementia (ALS-D) displaying a long clinical course. A 68-year-old Japanese male with no family history of note was admitted complaining of severe dysarthria and dysphagia. At 63 years old, Pick's disease was diagnosed on the basis of abnormal behavior, such as "Denkfaulheit" and moria, and temporal lobe atrophy observed on magnetic resonance imaging (MRI). Five years after onset, dysarthria and dysphagia emerged, and gradually worsened. On admission, muscular weakness of the upper extremities, fasciculation, and exaggerated tendon stretch reflexes were noted. Needle electromyography performed on the left upper and lower extremities revealed neurogenic pattern changes. Based on these findings and clinical course, ALS-D was diagnosed. Due to severe bulbar palsy, verbal communication was impossible. However, neither specific symptoms of dementia nor abnormal behavior was demonstrated, although this latter had been observed 5 years ago, with only short-term memory impairment apparent. MRI disclosed severe knife-edge atrophy of bilateral temporal lobes, most prominently in the anterior regions. SPECT images revealed decreased uptake of tracer in bilateral inferior temporal lobes, predominantly on the left side. The patient died suddenly 4 months after admission, and post-mortem examination was not conducted. Total clinical course was about 8 years. Several cases of ALS-D have displayed similar clinical courses to the presented case. Some of these would also have initially been diagnosed as Pick's disease. We speculate that cases displaying psychiatric symptoms for several years and initially diagnosed as Pick's disease may finally be diagnosed as ALS-D upon the eventual emergence of motor symptoms(bulbar palsy).
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PMID:[A case of amyotrophic lateral sclerosis with dementia presenting long clinical course]. 1268 97

The partial androgen deficiency of aging males (PADAM) is responsible for a variety of behavioral symptoms, such as weakness, fatigue, decreased libido, depressive mood, lack of motivation and energy, lower psychological vitality, anxiety, irritability, insomnia, decreased work and sport performances, difficulty in concentrating, memory impairment and low dominance. Psychological and behavioral aspects of PADAM overlap with signs and symptoms of major depression. The evidence of the association between testosterone (T) level and male depression comes from studies that have assessed: 1) depression in hypogonadal subjects; 2) the relationship between T level and male depressive illness, and 3) the antidepressant action of androgen replacement. In humans, the role of androgens has been described, albeit inconsistently, in the regulation of sexuality, aggression, emotion and personality. These direct effects appear to be greatly influenced by social factors as well. Sex hormones are important for the development and maintenance of acquired cognitive abilities. Hormonal changes in androgen levels in older men modulate, at least in part, the cognitive changes of aging. Treatment with androgen hormones in hypogonadal men has shown an improvement in cognitive, verbal and visual memory, mental status, visuomotor scanning and attention, verbal knowledge/language, spatial abilities and memory for both verbal and visual information. The etiology of the behavioral symptoms of PADAM is multifactorial, being the result of the interaction of biological and social changes, and of the personal ability to adapt to the numerous individual and social changes that take place during mid-life transition.
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PMID:Partial androgen deficiency and neuropsychiatric symptoms in aging men. 1676 Jun 26

Hashimoto's encephalopathy is a rare complication of autoimmune thyroiditis not associated with thyroidal function decline. We report a 50-year-old man presenting with lower motor neuron symptoms evolving over 3 years and changes in behavior associated with attentive and cognitive impairment occurring in the last few months. Memory deficits, emotional instability, marked dysarthria, mild symmetric weakness of the lower extremities and fasciculations were the most striking clinical features. EEG was diffusely slow, cranial MRI revealed multiple subcortical white matter lesions, CSF protein was slightly elevated, electromyographic recordings showed acute and chronic denervation and extremely high TPO antibody titers were found in the serum. Hashimoto's encephalopathy and lower motor neuron disease were diagnosed. As repeated high-dose intravenous methylprednisolone administration followed by oral tapering improved both central nervous system and lower motor neuron symptoms, the question was raised whether there was a common autoimmune pathogenesis of both clinically distinct diseases.
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PMID:Hashimoto's encephalopathy and motor neuron disease: a common autoimmune pathogenesis? 1693 96

While both neuronal intermediate filament inclusion disease (NIFID) and basophilic inclusion body disease (BIBD) show frontotemporal lobar degeneration and/or motor neuron disease, it remains unclear whether, and how, these diseases differ from each other. Here, we compared the clinicopathological characteristics of four BIBD and two NIFID cases. Atypical initial symptoms included weakness, dysarthria, and memory impairment in BIBD, and dysarthria in NIFID. Dementia developed more than 1 year after the onset in some BIBD and NIFID cases. Upper and lower motor neuron signs, parkinsonism, and parietal symptoms were noted in both diseases, and involuntary movements in BIBD. Pathologically, severe caudate atrophy was consistently found in both diseases. Cerebral atrophy was distributed in the convexity of the fronto-parietal region in NIFID cases. In both BIBD and NIFID, the frontotemporal cortex including the precentral gyrus, caudate nucleus, putamen, globus pallidus, thalamus, amygdala, hippocampus including the dentate gyrus, substantia nigra, and pyramidal tract were severely affected, whereas lower motor neuron degeneration was minimal. While alpha-internexin-positive inclusions without cores were found in both NIFID cases, one NIFID case also had alpha-internexin- and neurofilament-negative, but p62-positive, cytoplasmic spherical inclusions with eosinophilic p62-negative cores. These two types of inclusions frequently coexisted in the same neuron. In three BIBD cases, inclusions were tau-, alpha-synuclein-, alpha-internexin-, and neurofilament-negative, but occasionally p62-positive. These findings suggest that: (1) the clinical features and distribution of neuronal loss are similar in BIBD and NIFID, and (2) an unknown protein besides alpha-internexin and neurofilament may play a pivotal pathogenetic role in at least some NIFID cases.
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PMID:Basophilic inclusion body disease and neuronal intermediate filament inclusion disease: a comparative clinicopathological study. 1808 Jan 29

Cystic glioblastoma multiforme (GBM) is a rare disease. Its exact prevalence has not yet been reported. Also, the mechanism of cyst formation remains to be elucidated. We report a case of GBM with a large peripheral cyst. A 43-year-old woman visited our clinic with a 3-month history of severe headache, memory impairment and general weakness. T1-weighted gadolinium-enhanced magnetic resonance (MR) image revealed a midline enhanced solid mass and bilateral symmetric banana-shaped peripheral cysts. A centrally enhanced mass was measured 2x4 cm in size and both mass and cysts as 7x7 cm. Both the frontal lobe and the frontal horn were severely compressed inferiorly and posteriorly. We resected a midline solid tumor and cysts via the bilateral interhemispheric transcortical approach. Histopathologic examination revealed GBM. The patient was subsequently treated with fractionated conventional brain radiation therapy, followed by temozolomide chemotherapy. Eighteen months later, there was no tumor recurrence and no neurological deficits were noted. Our patient showed no tumor recurrence and a long survival at a long follow-up.
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PMID:Midline glioblastoma multiforme with bilateral symmetric cysts. 1909 13

This study provides a critical review of the literature on depressive symptoms of partial androgen deficiency (PADAM) and their treatment with Testosterone (T). PADAM in aging males is responsible for a variety of behavioral symptoms, such as weakness, decreased libido and erectile dysfunction, lower psychological vitality, depressive mood, anxiety, insomnia, difficulty in concentrating, and memory impairment. The psychological and behavioural aspects of PADAM may overlap with signs and symptoms of major depression. Evidence of the relationship between androgen deficiency and male depression comes from studies that have assessed depression in hypogonadal subjects, the association between low T level and male depressive illness, and the antidepressant action of androgen replacement. The etiology of depressive symptoms of PADAM is multifactorial, and results from the interaction of the biological and psychosocial changes that take place during the mid-life transition. Although data derived from androgen treatment trials and androgen replacement do not support T treatment or replacement as more efficacious than placebo for major depressive disorder (MDD), the clinical impression is that, in some sub-threshold depressive syndromes, T may lead to antidepressant benefits.
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PMID:Partial androgen deficiency, depression and testosterone treatment in aging men. 1922 62

We report the rare case of a 59-year-old man with motor neuron disease and semantic dementia (SD-MND); SD-MND was in a very early stage, and its clinical progression, especially with regard to language impairment, and abnormalities on neuroimages were evaluated for 3 years. The patient complained only of difficulties in recalling names of acquaintances and in writing kanji characters. After 1 year, he experienced difficulty in describing common objects. He developed two-way anomia only in some words, which varied from day to day. His anomia was not category-specific and was noted even with respect to words that describe color. In addition to experiencing difficulty in writing kanji characters, he experienced difficulty in writing kana characters. Muscle atrophy was observed, and he experienced weakness in his limbs, especially in the right upper limb; however, bulbar symptoms were not observed. At this point, he fulfilled the diagnostic criteria for MND. In the next year, semantic memory impairment became apparent, and he was subsequently diagnosed with SD. Deterioration in his ability to name objects in all categories, except body parts, was noted. Further, the ability of writing both kana and kanji characters was increasingly impaired. He developed bulbar symptoms and experienced increased muscle weakness. The characteristics of this patient differed from those of SD patients without MND with regard to the difficulty in writing kana characters and naming colors even though the SD-MND was in the early stage. Further, the pattern of brain hypoperfusion was different from that observed for SD patients without MND. In the case of this patient, brain hypoperfusion was found not only in the left anterior temporal lobe but also in the frontal lobe. The characteristics of his language symptoms might be related to the specific pattern of brain hypoperfusion, which might be commonly observed in patients with dementia and MND.
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PMID:[Language and semantic memory impairment in a patient with motor neuron disease and semantic dementia: a case report]. 2054 24

The ultimate goal of rehabilitation research is to improve the lives of people with disabilities; yet, little research is implemented into clinical practice. The objectives of the current article are to serve as a guide for rehabilitation researchers regarding factors that contribute to translation of the evidence base in clinical practice, to highlight some common problems encountered by clinicians when trying to implement evidence-based treatments, and to provide tips that researchers can use to enhance the likelihood of their research products being used in clinical practice. The impact of clinician and environmental factors on use of evidence-based medicine are reviewed. Practical issues encountered by clinicians when attempting to translate evidence-based findings into practice are highlighted by discussing 2 areas of research: compensatory strategies for memory impairment after brain injury and use of electrical stimulation for weakness and paralysis in persons with spinal cord injury. The article closes with a series of tips to assist researchers in translating findings to clinicians.
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PMID:Maximizing usability of evidence in rehabilitation practice: tips for researchers. 2312 79

We report an autopsy case of dementia associated with amyotrophic lateral sclerosis (ALS) in a 73-year-old female. She developed memory impairment at the age of 68 years. Atrophy of her hand muscles was noted at the age of 71 years. She was not aware of her memory impairment or muscle weakness, and was loquacious and euphoric. She was clinically diagnosed as having Alzheimer disease (AD) complicated by ALS with dementia/frontotemporal lobar degeneration with motor neuron disease (ALS-D/FTLD-MND). A neuropathological study confirmed the presence of features of sporadic ALS. Furthermore, severe neuronal loss involving the subiculum and the rostral portion of the medial side of the temporal pole cortex was detected, and TAR DNA-binding protein-43-positive-neuronal cytoplasmic inclusions were identified in the granule cells of the dentate gyrus. These findings were compatible with the pathological features of ALS-D/FTLD-MND. Although many pretangles, neuropil threads and senile plaques were revealed in the degenerated areas, there were few neurofibrillary tangles and typical plaques (Braak stage III, C). Further discussion is required to determine whether AD with ALS-D/FTLD-MND is different from typical AD. This case might be helpful for diagnosing similar cases in the future.
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PMID:[Autopsy case of frontotemporal lobar degeneration with motor neuron disease associated with numerous diffuse plaques, pretangles and neuropil threads]. 2480 77

We report a 46-year-old woman with a nine-year history of obesity; chronic diffuse pain in the adipose tissue of her medial upper arms, lower trunk, and thighs; multiple biopsy-proven lipomas and angiolipomas; and a lipomatous pseudomass of the breast. Her systemic symptoms included generalized weakness, fatigue, memory impairment, and arthralgias. Although some of the lesions were tender, most were only appreciated with palpation. Her clinical history and histopathologic data suggested adiposis dolorosa (Dercum's disease). Owing to the chronic pain, an interdisciplinary approach with the use of analgesics and doxycycline has been initiated.
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PMID:Adiposis dolorosa. 2552 45


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