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Diseases

Evaluation of memory deficit

OVERVIEW

  • Summary
  • Urgent Considerations
  • Etiology

DIAGNOSIS

  • Differential Diagnosis
  • Diagnostic Approach

IMAGES

  • Library

REFERENCES

  • Citations
  • Credits

Summary

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Memory is the tie that binds together thoughts, impressions, and experiences. Memory function is dependent on several mental or cognitive abilities using several brain systems. Many disease processes can lead to compromise of these systems.
When evaluating a patient with a concern of memory loss, the following questions should be considered:
  • Does the patient truly have memory loss or is there another cognitive problem causing the memory disorder?

  • What is the localization within the brain of the memory problem?

  • What is the temporal profile for the memory loss: acute (seconds/minutes/hours), subacute (days/weeks), or chronic (many months to years)?

  • What etiologies could be responsible for the memory disorder?

The first consideration is to determine whether the patient truly has memory loss or another cognitive problem. Depression may present with similar symptoms to dementia, particularly in older people.[1] Patients with delirium often have symptoms of memory loss, but have symptoms of inattention and altered consciousness as well.[2] Patients with vision or hearing problems may appear to have dementia.
Memory dysfunction can affect episodic, working, semantic, or procedural memory. It may result from lesions in the hippocampus, limbic circuits, prefrontal cortex, angular gyrus, temporal lobes, cerebellum, basal ganglia, or supplementary motor area. In many cases, memory is encoded properly in the hippocampus, but patients have trouble retrieving the stored memory. This retrieval deficit is typically due to problems with frontal lobe function, often caused by white matter disease.
The temporal profile of memory loss is an essential part of the history that can rapidly refine the differential diagnosis. For example, neurodegenerative disease typically causes chronic symptoms, inflammatory disease usually causes subacute symptoms, and neurologic conditions such as seizure or migraine cause acute symptoms.
Neurodegenerative, neurologic, inflammatory, infectious, traumatic, endocrine, vascular, neoplastic, and metabolic conditions may all cause memory loss.
content by BMJ Group
Last updated

Library

  • Diagnostic algorithm for acute onset memory deficit. 1: changes in signal intensities, structural le

    Diagnostic algorithm for acute onset memory deficit. 1: changes in signal intensities, structural lesions on brain MRI; 2: sometimes increased signal intensities on diffusion-weighted imaging; EEG, electroencephalogram; MRI, magnetic resonance imaging

  • Diagnostic algorithm for subacute onset memory deficit. 1: changes in signal intensities, structural

    Diagnostic algorithm for subacute onset memory deficit. 1: changes in signal intensities, structural lesions on brain MRI; 3: MRI in CJD shows cortical ribboning and/or deep nuclei restricted diffusion on diffusion-weighted imaging/apparent diffusion coefficient map; CSF biomarkers might be elevated; ADC, apparent diffusion coefficient; CJD, Creutzfeldt-Jakob disease; CSF, cerebrospinal fluid; DWI, diffusion-weighted imaging; HSV, herpes simplex virus; MRI, magnetic resonance imaging; NSE, neuron-specific enolase

  • Diagnostic algorithm for chronic onset memory deficit; bvFTD, behavioral variant frontotemporal deme

    Diagnostic algorithm for chronic onset memory deficit; bvFTD, behavioral variant frontotemporal dementia; CBD, corticobasal degeneration; FDG-PET, fluorodeoxyglucose - positron emission tomography; FTD, frontotemporal degeneration; LP, lumbar puncture; PIB-PET, Pittsburgh compound B - positron emission tomography; PNFA, progressive nonfluent aphasia; PSP, progressive supranuclear palsy

  • MRI brain: shows diffuse cortical atrophy with predominant hippocampal atrophy (red arrows) in patie

    MRI brain: shows diffuse cortical atrophy with predominant hippocampal atrophy (red arrows) in patient with Alzheimer dementia. Parietal atrophy and neocortical involvement is evident in more advanced disease (blue arrows)

  • MRI brain (T2 weighted): demonstrates symmetric hyperintensity of the bilateral medial temporal lobe

    MRI brain (T2 weighted): demonstrates symmetric hyperintensity of the bilateral medial temporal lobes (hippocampi; outlined by arrows pointing to anterior and middle of hippocampi) consistent with active inflammation in limbic encephalitis and encephalopathy. Note that hippocampi are brighter than other gray matter regions, particularly posterior cortex

Citations

    Key Articles

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    • National Institute for Health and Care Excellence. Dementia: assessment, management and support for people living with dementia and their carers. Jun 2018 [internet publication].[Full Text]

    • Galvin JE, Sadowsky CH. Practical guidelines for the recognition and diagnosis of dementia. J Am Board Fam Med. 2012 May-Jun;25(3):367-82.[Abstract][Full Text]

    Other Online Resources

    • Montreal Cognitive Test
    • Cognitive impairment: recognition, diagnosis and management in primary care

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