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ULY CLINIC

ULY CLINIC

19 Mei 2025, 07:03:22

Amnesia

Amnesia
Amnesia
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
  1. 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.

  2. 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.

  3. Sadock BJ, Sadock VA, Ruiz P. Kaplan & Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry. 11th ed. Philadelphia: Wolters Kluwer; 2015.

  4. Blumenfeld H. Neuroanatomy through Clinical Cases. 2nd ed. Sunderland: Sinauer Associates; 2010.

  5. Waxman SG. Clinical Neuroanatomy. 28th ed. New York: McGraw-Hill Education; 2020.

  6. Mesulam MM. Principles of Behavioral and Cognitive Neurology. 2nd ed. New York: Oxford University Press; 2000.

  7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-5. 5th ed. Arlington: American Psychiatric Publishing; 2013.

  8. Victor M, Ropper AH, Samuels MA, Klein JP. Adams and Victor's Principles of Neurology. 11th ed. New York: McGraw-Hill Education; 2019.

  9. Squire LR, Stark CE, Clark RE. The medial temporal lobe. Annu Rev Neurosci. 2004;27:279–306.

  10. Kopelman MD. Disorders of memory. Brain. 2002;125(Pt 10):2152–2190.

  11. 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.

  12. 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.

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