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)

Cyanocobalamin (vitamin B12) deficiency can cause polyneuropathy, myelopathy, blindness, confusion, psychosis and dementia. Nonetheless, its deficiency as the sole cause of dementia is infrequent. We report a 59 years old man with a 6 months history of progressive loss of memory, disorientation, apathy, paranoid delusions, gait difficulties with falls, and urinary incontinence. He had suffered a similar episode 3 years before, with a complete remission. On examination there was frontal type dementia with Korsakoff syndrome, a decrease in propioception and ataxic gait. Cerebrospinal fluid examination showed a protein of 0.42 g/L. Brain computed tomography showed sequelae of a frontal left trauma. Brain single photon computed tomography (SPECT) was normal. Complete blood count showed a macrocytic anemia with a hematocrit 29% and a mean corpuscular volume of 117 micron3. Plasma vitamin B12 levels were undetectable, erythrocyte folate levels were 3.9 ng/ml and plasma folate was normal. The myelogram showed megaloblastosis and the gastric biopsy showed atrophic gastritis. Treatment with parenteral B12 vitamin and folic acid reverted the symptoms, with normalization of the neuropsychological tests and reintegration to work.
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PMID:[Dementia caused by vitamin B12 deficiency. Clinical case]. 1455 47

We report seven patients, six from a single institution, who developed subacute limbic encephalitis initially considered of uncertain aetiology. Four patients presented with symptoms of hippocampal dysfunction (i.e. severe short-term memory loss) and three with extensive limbic dysfunction (i.e. confusion, seizures and suspected psychosis). Brain MRI and [(18)F]fluorodeoxyglucose (FDG)-PET complemented each other but did not overlap in 50% of the patients. Combining both tests, all patients had temporal lobe abnormalities, five with additional areas involved. In one patient, FDG hyperactivity in the brainstem that was normal on MRI correlated with central hypoventilation; in another case, hyperactivity in the cerebellum anticipated ataxia. All patients had abnormal CSF: six pleocytosis, six had increased protein concentration, and three of five examined had oligoclonal bands. A tumour was identified and removed in four patients (mediastinal teratoma, thymoma, thymic carcinoma and thyroid cancer) and not treated in one (ovarian teratoma). An immunohistochemical technique that facilitates the detection of antibodies to cell surface or synaptic proteins demonstrated that six patients had antibodies to the neuropil of hippocampus or cerebellum, and one to intraneuronal antigens. Only one of the neuropil antibodies corresponded to voltage-gated potassium channel (VGKC) antibodies; the other five (two with identical specificity) reacted with antigens concentrated in areas of high dendritic density or synaptic-enriched regions of the hippocampus or cerebellum. Preliminary characterization of these antigens indicates that they are diverse and expressed on the neuronal cell membrane and dendrites; they do not co-localize with VGKCs, but partially co-localize with spinophilin. A target autoantigen in one of the patients co-localizes with a cell surface protein involved in hippocampal dendritic development. All patients except the one with antibodies to intracellular antigens had dramatic clinical and neuroimaging responses to immunotherapy or tumour resection; two patients had neurological relapse and improved with immunotherapy. Overall, the phenotype associated with the novel neuropil antibodies includes dominant behavioural and psychiatric symptoms and seizures that often interfere with the evaluation of cognition and memory, and brain MRI or FDG-PET abnormalities less frequently restricted to the medial temporal lobes than in patients with classical paraneoplastic or VGKC antibodies. When compared with patients with VGKC antibodies, patients with these novel antibodies are more likely to have CSF inflammatory abnormalities and systemic tumours (teratoma and thymoma), and they do not develop SIADH-like hyponatraemia. Although most autoantigens await characterization, all share intense expression by the neuropil of hippocampus, with patterns of immunolabelling characteristic enough to suggest the diagnosis of these disorders and predict response to treatment.
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PMID:Treatment-responsive limbic encephalitis identified by neuropil antibodies: MRI and PET correlates. 1603 Jan 81

Pellagra is a systemic disturbance caused by a cellular deficiency of niacin, resulting from inadequate dietary nicotinic acid and/or its precursors, the essential amino-acid tryptophan. In Europe and North America cases of pellagra are rarely encountered, but in some developing countries this disease is frequent, and is the most frequent clinical feature of nutritional deficiency of adult. The principal causes of pellagra are: nutritional niacin deficiency; chronic alcoholism; gastro-intestinal malabsorption; some medications (5-fluoro-uracil, isoniazid, pyrazinamide ehtionamide, 6-mercaptopurine, hydantoins, phenobarbital and chloramphenicol). The diagnosis of pellagra is based on the patient's history and the presence of "3 D syndrome": dermatitis, diarrhea, and dementia. The dermatitis caused by pellagra is a bilaterally symmetrical erythema at the sites of solar exposure. The dermatitis begins in the form of an erythema with acute or intermittent onset gradually changing to an exsudative eruption on the dorsa of the hand, face, neck, and chest with pruritus and burning. Acute dermatitis of pellagra resembles sunburn in the first stages, sometimes with vesicles and bullae. The gastro-intestinal disturbances are: anorexia, nausea, epigastric discomfort and chronic or recurrent diarrhea. Anorexia and malabsorbative diarrhea lead to a state of malnutrition and cachexia. Stools are typically watery, but occasionally can be bloody and mucoid. Neuropsychologic manifestation included photophobia, asthenia, depression, hallucinations, confusions, memory loss and psychosis. As pellagra advances, patient become disoriented, confused and delirious; then stuporous and finally die. Pathological changes in the skin is non-specific, there are no chemical tests available to definitively diagnose pellagra. However low levels of urinary excretion of N-methylnicotinamide and pyridone indicates niacin deficiency. The treatment of pellagra consisted to exogenous administration of niacin or nicotinamide cures. Topical management of skin lesions with emollients may reduce discomfort. The therapy should also include other B vitamins, zinc and magnesium as well as a diet rich in calories. The prevention is based in the nutritional education (food sources of niacin: eggs, bran, peanuts, meat, poultry, fish, red meat, legumes and seeds), and the eviction of alcohol.
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PMID:[Pellagra]. 1620 85

The case of HM, a man with intractable epilepsy who became amnesic following bilateral medial temporal lobe surgery nearly half a century ago has instigated ongoing research and theoretical speculation on the nature of memory and the role of the hippocampus. Neuropsychological testing showed that although HM had extensive anterograde memory loss he could still acquire motor and cognitive skills implicitly, but could not remember the context of this learning. This has lead to declarative and procedural descriptions of the memory process. Cholinergic and monoaminergic neurotransmitter systems have also been implicated in the memory process and anticholinergic drugs traditionally have been associated with impairment of declarative memory. The cholinergic hypothesis of Alzheimer's disease is a classic example of an application of these neuropharmacological findings. In schizophrenia, preattentive deficits have been amply demonstrated by unconscious priming studies. Memory processes are also impaired in these patients. Dopamine, glutamate and even cholinergic dysfunction has been implicated in the clinical picture of schizophrenia. The present paper will attempt to bring together both the anatomical and pharmacological data from these disparate fields of research under a cohesive theory of cognition and memory. A hypothesis is presented for an inverse relationship between monoaminergic and cholinergic systems in the modulation of implicit (unconscious) and explicit (conscious) cognitive processes. It is postulated that muscarinic cholinergic receptors and monoaminergic systems facilitate unconscious and conscious processes, respectively, and they disfacilitate conscious and unconscious processes, respectively (the purported inverse relationship). In fact, the muscarinic and monoaminergic modulations of a neural network are proposed to be finely balanced such that, if, the activity of one receptor system is modified then this by necessity has effects on the other system. It takes into account receptor subtypes and their effects mediated through excitatory and inhibitory G-protein complexes. For example, m1/D2 and D1/m4 paired receptor subtypes, colocalized on separate neurons would have opposing functional effects. A theory is then presented that the critical underlying pathophysiology of schizophrenia involves a hypofunctional muscarinic cholinergic system, which induces abnormal facilitation of monoaminergic subsystems such as dopamine (e.g., a decrease in m1R function would potentiate D2R function). This extends the idea of an inverted U function for optimal monoaminergic concentrations. Not only would this impair unconscious preattentive processes, but according to the hypothesis, explicit cognition as well including memory deficits and would underlie the mechanism of psychosis. Contrary to current thinking a different view is also presented for the role of the hippocampus in the memory process. It is postulated that long-term explicit memory traces in the neocortex are laid down by phasic coactivation of forebrain projecting monoaminergic systems above some basal firing rate, such as the rostral serotonergic raphe, which projects diffusely to the cortex and according to a modified Hebbian principle. This is the proposed principal function of the hippocampal theta rhythm. The phasic activation of the cholinergic basal forebrain is mediated by projections from a separate cortical structure, possibly the lateral prefrontal cortex. Phasic muscarinic receptor activation is proposed to strengthen implicit memory traces (at a synaptic level) in the neocortex. Thus, the latter are spared by medial temporal surgery explaining the dissociation of explicit from implicit memory.
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PMID:Neuropharmacology of cognition and memory: a unifying theory of neuromodulator imbalance in psychiatry and amnesia. 1630 Sep 5

Carbon monoxide (CO) poisoning is an important cause of mortality and late neurological sequelae such as memory loss, personality changes, psychosis, dementia, and so on. The benefits of hyperbaric oxygen (HBO) therapy are still discussed, but the majority of trials recommend it in severe cases with coma and/or hemodynamic instability, irrespective of carboxyhemoglobin (COHb) level, to prevent permanent neurological deficits. We present a 35-yr-old woman who underwent accidental CO poisoning. Although breathing 100% oxygen by mask during transfer to the hospital, she was in deep coma, hypotensive, cyanotic, and hypoxic (arterial pO(2) 7,41 kPa, HbO(2) 87.8%), with serum COHb 26.7% on hospital admission. Orotracheal intubation, mechanical ventilation, iv fluids, dobutamin, and norepinephrine were administered. COHb level decreased to 17.2% within 1 h. To prevent severe neurological sequelae, the patient was transferred as soon as possible to an HBO center 60 km distant to perform HBO therapy twice at 3.0 and once at 2.2 atm within 24 h. After the second HBO session, the patient regained consciousness, and respiratory failure and shock resolved. She was transferred to our hospital and discharged few weeks later with discrete paresis of peripheral nerves, discrete ischemic brain lesions on computed tomography (CT) scan, and moderately abnormal electroencephalogram (EEG) without cognitive disturbances. She was able to resume her daily activities. We conclude that in severe CO poisoning, normobaric oxygen therapy and resuscitation by fluids, inotropic agents, and catecholamines is essential for survival, but additional HBO therapy seems to prevent major neurological sequelae.
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PMID:Severe carbon monoxide poisoning treated by hyperbaric oxygen therapy--a case report. 1639 63

Paraneoplastic limbic encephalitis is a rare disorder that can cause memory loss, confusion, personality change, cognitive dysfunction, and psychosis. We present a case of an 11-year-old girl who was successfully treated with electroconvulsive therapy for a catatonic state associated with paraneoplastic limbic encephalitis caused by an ovarian teratoma.
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PMID:Electroconvulsive therapy in a pediatric patient with malignant catatonia and paraneoplastic limbic encephalitis. 1714 59

Beriberi is a disease caused by thiamine (vitamin B1) deficiency. Peripheral and central nerve involvement causes psychosis and memory loss as well as cardiocirculatory effects. We report the case of a 35-year-old woman 8 weeks pregnant who came to the emergency department after bouts of nausea and vomiting over a period of 6 days, with intolerance of both solids and liquids. The initial diagnosis of gastroenteritis was later changed to hyperemesis gravidarum. Episodes of vomiting and nausea continued 48 hours after admission, accompanied by vertical nystagmus, ataxia, and diminished osteotendinous reflexes. Evaluation of the clinical picture confirmed vitamin B1 deficiency, leading to a diagnosis of Wernicke-Korsakoff syndrome. Symptoms improved with thiamine therapy but did not entirely disappear. The patient was admitted for elective cesarean section at 37 weeks' gestation. Examination revealed neurological involvement (horizontal and vertical nystagmus) and general anesthesia was therefore chosen to assure adequate hemodynamic control given the possibility of cardiocirculatory alteration.
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PMID:[Anesthetic management for elective cesarean section for a woman with beriberi]. 1739 Jun 94

A strong correlation was frequently observed between memory complaints and the scores obtained on anxiety and depression scales. This paper contributes to explore the psychopathological basis of the experience of decreased memory efficiency. Our research, based on a clinical psychopathological methodology, rests upon semi-directed interviews associated with a psychological examination combining neuropsychological tests and projective methodology. The population consists of 31 subjects aged 53 to 85 years, who presented with memory complaint upon their own initiative in a memory clinic and for whom the neuropsychological examination ruled out the hypothesis of the onset of cerebral deterioration. The patients exhibited more or less mild neurotic, borderline and narcissistic psychic modes of functioning. There was no patient exhibiting psychotic functioning. We have been able to verify among the neurotic patients how the emphasis of anxiety of memory loss correspond to a revival of the anxiety of castration, that of being dispossessed of capacities which guarantee autonomy, judgement, power of decision and action. Furthermore, in the contemporary context of cerebral pathologies which can transform every intelligent man in a dependent, indeed bedridden being, this complaint jointly betrays an anxiety triggered by the risk of a violated intimacy due to the care which could be given as well as an anxiety linked to eviction, dispossession and to acts of mistreatment which are greatly apprehended. In patients exhibiting borderline functioning, the complaint of memory decline betrayed anxiety of fracture and dissolution of the self, and of lack of object-support. In narcissistic patients, the weakness of memory mobilisation eradicated the illusion that time does not pass, does not cause damage and that objects neither leave nor die.
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PMID:[Diversity of the psychopathology of memory complaints in the aging adult]. 1787 29

Regardless of their origin, neuroactive steroids are capable of modifying neural activities by modulating different types of membrane receptors. Neurosteroids are synthesized de novo in neurones and glia. Steroidogenic enzymes are found in the central nervous system. Classical steroid receptors are localized in the cytoplasm, they exert regulatory actions on the genome, and their activation causes medium- and long-term effects. Non-classical receptors are located within the membrane and act as mediators of short-term effects. Other important players are co-repressors and co-activators that can interfere with or enhance the activity of steroid receptors. Beyond their function in stress, corticosteroids play a very important role in fear, anxiety, and memory functions. Patients with Cushing's syndrome frequently develop mood disorder, reversible brain atrophy with transient memory loss, rarely delirium or psychosis. Well-known peripheral symptom is steroidal myopathy. In patients with Addison's disease the main signs are weakness of muscles, lack of energy, decreased mental functions and reduced quality of life. Estrogen and progesterone have their own respective hormone receptors, whereas allopregnanolone acts via the GABA receptors. These hormones have significant role in the development of brain, the architecture of neural circuits and dendrites, density of axonal connections, and the number of neurons. They influence maturation, neuroprotection, seizures, cognitive functions, mood, anxiety, pain, and restitution of peripheral nerves. Androgens also affect cognitive functions, pain, anxiety, mood, and additionally aggression.
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PMID:[Neurological and psychiatric aspects of some endocrine diseases. The role of neurosteroids and neuroactive steroids]. 1792 Nov 20

Alzheimer's disease (AD) is the most common cause of cognitive impairment in older patients, and its prevalence is expected to soar in coming decades. Neuropathologically, AD is characterized by beta-amyloid-containing plaques, tau-containing neurofibrillary tangles, and cholinergic neuronal loss. In addition to the hallmark of memory loss, the disease is associated with other neuropsychiatric and behavioral abnormalities, including psychosis, aggression, and depression. Although cholinergic cell loss is clearly an important attribute of the pathological process, another well-described yet underappreciated early feature of AD pathogenesis is degeneration of the locus coeruleus (LC), which serves as the main source of norepinephrine (NE) supplying various cortical and subcortical areas that are affected in AD. The purpose of this review is to explore the extent to which LC loss contributes to AD neuropathology and cognitive deficits.
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PMID:Functional consequences of locus coeruleus degeneration in Alzheimer's disease. 1853 47


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