Author:
Editor(s):
Updated:
ULY CLINIC
ULY CLINIC
19 Mei 2025, 07:03:22
Amnesia

Amnesia is a pathological disturbance in memory function that can manifest as partial or complete, and can affect memory for events either before (retrograde amnesia) or after (anterograde amnesia) the causative event. It may be transient or permanent, sudden or gradual in onset, and may be of organic (neurological) or psychogenic (functional) origin.
Classification
Based on temporal orientation
Anterograde Amnesia: Inability to form new memories following the onset of the causative event. Commonly affects short-term memory and is typical in hippocampal damage.
Retrograde Amnesia: Loss of pre-existing memories formed before the causative event. May show a temporal gradient, with more distant memories preserved.
Based on Etiology
Organic Amnesia: Resulting from identifiable structural or biochemical brain abnormalities (e.g., head trauma, encephalitis).
Functional (Psychogenic) Amnesia: No identifiable structural lesion; typically associated with emotional or psychological stress (e.g., dissociative amnesia).
Pathophysiology
Memory formation and retrieval involve the hippocampus, fornix, mammillary bodies, and prefrontal cortex. Disruption at any level can impair memory processes. For example:
Hippocampal lesions: Disrupt encoding and consolidation of new memories (anterograde amnesia).
Thalamic/mammillary body damage (e.g., Wernicke-Korsakoff): Affects memory retrieval and formation.
Temporal lobe epilepsy or encephalitis: May cause transient or permanent memory loss.
History Taking
Patient History
Often unreliable due to the nature of memory impairment. Collateral history is critical.
Focus on:
Onset: Sudden or gradual?
Duration: Temporary or persistent?
Type: Anterograde, retrograde, or both?
Precipitating factors: Trauma, seizure, substance use, psychological stress.
Associated symptoms: Confusion, LOC, focal neurologic deficits, psychiatric symptoms.
Functional Inquiry
Activities of daily living
Orientation to person, place, time
Behavioral or personality changes
Occupational or academic performance
Physical and Neurological Examination
General Examination
Vital signs: Fever (encephalitis), hypotension (cerebral hypoperfusion)
General appearance and behavior
Mood and affect
Neurological Examination
Level of Consciousness (LOC)
Cranial nerves: Visual disturbances, pupillary responses
Motor and Sensory Systems: Hemiparesis, ataxia, paresthesias
Gait: Suggestive of cerebellar or frontal lobe pathology
Memory Testing:
Immediate memory: Recall three unrelated items immediately
Short-term memory: Recall same items after 3–5 minutes
Intermediate memory: Historical events (e.g., last meal, last holiday)
Remote memory: Personal history (birthplace, school attended)
Differential diagnosis and associated features
Cause | Type(s) of Amnesia | Onset & Duration | Associated Clinical Findings |
Alzheimer’s Disease | Retrograde → progresses to anterograde | Gradual onset, chronic, progressive over months/years | Agitation, poor concentration, poor hygiene, confusion, irritability, emotional lability, later aphasia, dementia, incontinence, muscle rigidity |
Cerebral Hypoxia | Often total amnesia for the hypoxic event | Sudden onset, variable duration | Numbness, tingling, other sensory disturbances following recovery from CO poisoning or respiratory failure |
Head Trauma | Retrograde and anterograde (anterograde usually longer) | Immediate onset post-trauma, may last minutes to permanent | Altered LOC/respirations, headache, dizziness, confusion, blurred/double vision, hemiparesis, paresthesia contralateral to injury |
Herpes Simplex Encephalitis | Severe, potentially permanent amnesia | Develops during/after acute phase | Headache, fever, altered LOC, seizures, motor/sensory deficits (e.g., paresis, numbness, tingling), signs of meningeal irritation |
Hysteria (Dissociative Amnesia) | Retrograde (psychogenic, generalized) | Abrupt onset and resolution | Confusion, typically no neurological deficits, memory loss may cover identity and life history |
Temporal Lobe Seizures | Transient anterograde/retrograde | Sudden onset, lasts seconds to minutes | Aura (possible), confusion, impaired LOC, hallucinations (visual, auditory, olfactory), oral automatisms, laterality of focus affects verbal (left) vs. visual (right) memory |
Wernicke-Korsakoff Syndrome | Retrograde and anterograde, potentially permanent | Gradual in alcoholics, worsens without treatment | Confabulation, apathy, poor concentration/sequencing, diplopia, ataxia, headache, decreased LOC, peripheral neuropathy (numbness, tingling) |
Drug-Induced (e.g., anesthetics, sedatives) | Primarily anterograde | Immediate, dose-dependent, usually transient | Varies by drug; commonly seen with fentanyl, halothane, isoflurane, pentobarbital, thiopental, triazolam; drowsiness, confusion possible |
Electroconvulsive Therapy (ECT) | Retrograde and/or anterograde | Onset with each session, duration: minutes to hours; prolonged with repeated sessions | Memory gaps, confusion post-treatment; rare long-term deficits with intensive/frequent treatment |
Temporal Lobe Surgery | Retrograde and anterograde (depends on extent) | Immediate onset post-op | Brief/slight memory loss with unilateral resection; permanent global amnesia if bilateral medial temporal lobes removed |
Investigations
Neuroimaging:
CT/MRI: Rule out structural lesions (tumor, hemorrhage, atrophy)
Diffusion-weighted MRI: May reveal hippocampal changes in transient global amnesia
EEG: Evaluate for seizure activity
CSF Analysis: If infectious cause suspected (e.g., HSV encephalitis)
Blood Tests: CBC, LFTs, thiamine levels (Wernicke’s), toxicology screen
Neuropsychological Testing: Memory assessment and differentiation between organic and functional causes
Management
General Principles
Treat underlying cause (e.g., antivirals for HSV, thiamine for Wernicke’s)
Ensure patient safety, particularly if disoriented
Optimize orientation: Clocks, calendars, family photos
Structured environments and routines
Involve caregivers in management
Condition-Specific Interventions
Alzheimer’s Disease: Cholinesterase inhibitors, memantine
Wernicke-Korsakoff: Immediate IV thiamine before glucose
Seizures: Antiepileptic drugs; lifestyle counseling
Psychogenic Amnesia: Psychotherapy, cognitive-behavioral therapy
Nursing anda llied health considerations
Fall prevention
Monitoring for behavioral changes
Support with activities of daily living
Documenting patterns of memory loss
Patient education tailored to cognitive capacity
Patient and family education
Use written instructions for patients with anterograde amnesia
Encourage use of memory aids (e.g., diaries, apps, labels)
Provide realistic expectations regarding recovery
Discuss safety, especially for patients living alone
For pediatric cases: Involve school personnel and clarify that memory loss is not equivalent to intellectual disability
Pediatric cnsiderations
Children with epilepsy may have transient amnesia postictally
Risk of misdiagnosis as learning disability
Importance of adherence to anticonvulsant therapy
Collaboration with educators to support learning strategies
Prognosis
Prognosis depends on the etiology:
Transient global amnesia: Good recovery within 24 hours
Trauma or encephalitis: Variable, may result in permanent deficits
Degenerative diseases: Progressive and irreversible
Psychogenic amnesia: Reversible, but may recur
References
Liang, J. F., Shen, A. L., & Lin S. K. (2009). Bilateral hippocampal abnormalities on diffusion-weighted MRI in transient global amnesia: Report of a case. Acta Neurologica Taiwan, 18(2), 127–129.
Yang, Y., Kim, J. S., Kim, S., Kim, Y. K., Kwak, Y. T., & Han, I. W. (2009). Cerebellar hypoperfusion during transient global amnesia: An MRI and oculographic study. Journal of Clinical Neurology, 5(2), 74–80.
Sadock BJ, Sadock VA, Ruiz P. Kaplan & Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry. 11th ed. Philadelphia: Wolters Kluwer; 2015.
Blumenfeld H. Neuroanatomy through Clinical Cases. 2nd ed. Sunderland: Sinauer Associates; 2010.
Waxman SG. Clinical Neuroanatomy. 28th ed. New York: McGraw-Hill Education; 2020.
Mesulam MM. Principles of Behavioral and Cognitive Neurology. 2nd ed. New York: Oxford University Press; 2000.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-5. 5th ed. Arlington: American Psychiatric Publishing; 2013.
Victor M, Ropper AH, Samuels MA, Klein JP. Adams and Victor's Principles of Neurology. 11th ed. New York: McGraw-Hill Education; 2019.
Squire LR, Stark CE, Clark RE. The medial temporal lobe. Annu Rev Neurosci. 2004;27:279–306.
Kopelman MD. Disorders of memory. Brain. 2002;125(Pt 10):2152–2190.
Park NW, Ingles JL, Fisk JD. Memory complaints after concussion: relationships with postconcussive symptoms and neuropsychological functioning. J Clin Exp Neuropsychol. 2001;23(6):770–781.
Harding A, Halliday G, Caine D, Kril J. Degeneration of anterior thalamic nuclei differentiates alcohol-related dementia from Korsakoff's syndrome—A clinicopathological study. Brain. 2000;123(1):141–154.