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. Patients with delirium often have symptoms of memory loss, but have symptoms of inattention and altered consciousness as well. 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 casue memory loss.
- Frontotemporal dementia
- Semantic dementia
- Creutzfeldt-Jakob disease (CJD)
- Progressive supranuclear palsy
- Corticobasal syndrome
- Normal pressure hydrocephalus
- HIV dementia
- Limbic encephalopathy
- Hashimoto encephalopathy
- Brain tumor
- Transient global amnesia
- Wernicke-Korsakoff syndrome
Rajesh Tampi, MD, MS, DFAPA
Professor of Psychiatry
Case Western Reserve University School of Medicine
RT declares that he has no competing interests.
Dr Rajesh Tampi would like to gratefully acknowledge Dr Michael D. Geschwind, Dr Mee-Ohk Kim, Dr Michael H. Rosenbloom, Dr Steven Z. Chao, and Dr Julie N. Thai, previous contributors to this topic.
MDG is an author of a number of references cited in this topic. He serves on the board of directors for San Francisco Bay Area Physicians for Social Responsibility, on the editorial board of Dementia & Neuropsychologia, and serves or has served as a consultant for Best Doctors, Inc; the Gerson Lehrman Group, Inc; Guidepoint Global, LLC; Biohaven Pharmaceuticals, Inc; Lewis Brisbois Bisgaard & Smith LLP; Lundbeck; MEDACorp; NeuroPhage Pharmaceuticals; and Quest Diagnostics. He receives research support from CurePSP, the Michael J. Homer Family Fund, the National Institute on Aging (R01 AGAG031189), Quest Diagnostics, and the Tau Consortium. He receives honorarium from various medical centers for lectures in the field of dementia. M-OK, MHR, SZC, and JNT declare that they have no competing interests.
Olakunle Ashaye, MD
Consultant Psychiatrist and Visiting Professor
University of Hertfordshire
Mental Health Unit
OA declares that he has no competing interests.
Asif Bhutto, MD
Assistant Professor of Internal Medicine
Division of Geriatric Medicine
St Louis University
AB declares that he has no competing interests.
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