Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cognitive speed, inhibitory function, and memory decline with age while crystallised, particularly verbal, abilities remain largely intact. Poor health, fewer years of education, lower activity, the presence of the APOE E4 allele, and high BP appear to predict faster cognitive decline. Dementia is diagnosed in the presence of objective cognitive impairment, both long- and short-term memory, plus at least one additional (cortical) cognitive deficit, such as dysphasia, dyspraxia, agnosia, or disturbance in executive functioning. In addition, patients have to show significant impairment in social or occupational functioning and a significant decline from previous levels. Both smoking and diabetes increase the risk of all types of dementia, not smoking or even stopping smoking reduces this risk, but better control of type 2 diabetes does not appear to have a measurable effect. Drinking small to moderate amounts of alcohol appears to confer some benefit in ameliorating cognitive decline. There is some evidence that HRT, DHEA, BP lowering in patients without prior cerebrovascular disease, statins, vitamin B6 and procaine are NOT helpful. There is insufficient evidence to establish or refute a beneficial effect for exercise, treatment of type 2 diabetes, omega-3 fatty acids, folic acid with/without vitamin B12, antioxidant vitamins, or ginkgo biloba. Depressive symptoms are more prevalent than dementia. Clinical (major) depression can present with cognitive deterioration, often associated with subjective complaints. Patients with subjective or objective memory impairment, but without functional deterioration, can be referred to the local memory clinic, while demented patients eligible for acetylcholinesterase inhibitor treatment, patients whose diagnosis is unclear and who may need some specific investigations, as well as patients who may benefit from a combined approach with psychotropic drugs and behavioural support should be referred to the local mental health team.
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PMID:Normal cognitive decline or dementia? 2019 32

The goal of this report is to review periodic lateralized epileptiform discharges (PLEDs), particularly their associated symptoms, the possibility that the pattern represents a focal status epilepticus, and finally the usefulness of antiepileptic drugs (AEDs). The associated symptoms often include an "altered state of consciousness" or "confusional state," but also more specific symptoms have been noted, such as nystagmus retractorius, cortical blindness, depression, apraxia, amnesia, hemianopsia, hemiparesis, gaze preference or deviation, dysphasia, and speech impediment. PLEDs have often been referred to as an ictal pattern, and many investigators have viewed the condition an example of subclinical status epilepticus. The intense hypermetabolism and increased blood flow revealed by PET and SPECT scans have been considered to support the ictal nature of this waveform. Although the pattern is difficult to treat, the AEDs that have been reported as successful include carbamazepine, midazolam, pentobarbital, sodium valproate, and felbamate. As only subtle symptoms are, at times, present and therefore may be missed and the pattern is known to be difficult to treat, epileptologists who view the PLED pattern as only an EEG curiosity and decide against treatment may wish to reevaluate the electroclinical evidence related to this interesting and significant pattern.
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PMID:Periodic lateralized epileptiform discharges: Do they represent an ictal pattern requiring treatment? 2055 51

The term "dyspraxia" was coined by Julian de Ajuriaguerra and Mira Stambak in 1964. This clinical term was treated very differently according to which explanatory model was adopted. Nowadays, it is used to refer to developmental coordination disorder in view of its neuro-developmental origin. In any case, the actual clinical situations vary and are often complex. In our opinion, it is first necessary to examine the differential diagnosis: apraxia in children caused by lesions, dysgraphia, simply delayed motor development, non-verbal learning disability syndrome, hemispheric specialisation deficits, pervasive developmental disorders (autisms, Asperger syndrome, atypical autism and other pervasive developmental disorders), mixed specific developmental disorders, multiple developmental disorder, and children with high potential. Next we focus on co-morbidity. Firstly, we look at psychopathological disorders associated with dyspraxia: autism and pervasive developmental disorders, dyscalculia/math disability, dyslexia/reading difficulties, dysphasia accompanied by verbal dyspraxia, intelligence deficiency, anxiety disorders, and attention-deficit hyperactivity disorder (ADHD). Secondly, we examine psychopathological disorders associated with dyspraxia. Children with developmental coordination disorder are less inclined to participate in collective games. As a result, there is a greater risk of them becoming lonely and isolated. They have higher child behaviour checklist (CBCL) scores in the somatic problems scale as well as for anxiety, depression and social withdrawal. They have low self-perception in sports as well as at school, which is related to their physical appearance and their self-esteem, attention deficit and externalized behaviour. These children are often at risk of academic failure and they suffer from oppositional defiant disorder and functional disorders. And finally, we believe that it is important to touch on the impact of these disorders on the family.
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PMID:[Psychopathology in children with dyspraxia]. 2061 74

Common causes of memory loss in older people are mild cognitive impairment, the various types of dementia, and psychiatric illness, mainly depression. Around 10% of patients with mild cognitive impairment progress to dementia each year. Alzheimer's disease accounts for 60-80% of cases. Other common types of dementia are vascular, fronto-temporal, Lewy body, Parkinson's, and mixed type dementia. There is evidence to suggest that dementia pathology is established before the onset of symptoms, and thus mild cognitive impairment can be considered as a predementia stage. NICE guidance suggests examination of: attention, concentration, short- and long-term memory, praxis, language and executive function. Particular attention should be paid to any signs of neglect, state of dress, agitation or poor attention. Dysphasia and difficulty in naming objects is often present. Mood symptoms (including suicidal ideation) may be primary or comorbid. Abnormal thoughts and perceptions should be probed for, as psychotic symptoms are common. Primary care options for cognitive testing include the General Practitioner Assessment of Cognition or the Abbreviated Mental Test Score. Physical examination should include observation of gait, inspection for tremor; examination for rigidity, bradykinesia, frontal release signs, upper motor neurone lesions, pulse and BP. Structural brain imaging can improve diagnostic accuracy, exclude other pathologies and act as a prognostic marker of dementia progression but the overlap in structural changes between the dementias makes imaging alone insufficient for diagnostic purposes. NICE guidelines recommend referral to a memory clinic for patients with mild cognitive impairment, those at high risk of dementia, such as patients with learning disabilities, Parkinson's disease, or patients who have had several strokes.
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PMID:Establishing the cause of memory loss in older people. 2572 16


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