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Transient Global Amnesia, Emergency Medicine

Basics

Description

- Temporary short-range retrograde amnesia: - More recent memories at more risk - Previously encoded memories unavailable only temporarily

- Often precipitated by stressful condition: - Cough, Valsalva - Physical exertion - Sexual intercourse - Extreme fright or shock - Intense heat or cold

- May have other subtle transient symptoms at onset, such as headache, dizziness, nausea - Historical features helpful in excluding other diagnoses are: - Onset of attack witnessed, with no seizure activity or epileptiform features noted - No history of seizures in prior 2 mo - No history of recent traumatic brain injury - Acute anterograde amnesia with relatively preserved remote memory

- Marked anterograde amnesia - Most cases ( ≥90% in case series) will demonstrate repetitive questioning - Neurologic and general exam normal - TGA patient WILL NOT be: - Somnolent - Inattentive - Globally confused - Confabulate

- Acute confusional state/Korsakoff syndrome/metabolic disorder: - Alcohol, medication, or toxin ingestion - Decreased attention or other findings of an encephalopathy - Impairment with serial 7s or spelling "world " backward - Able to lay down new memory if allowed time to encode

- Complex partial seizures/epileptic amnestic attacks: - Witnessed epileptiform activity or features (e.g., blank stares, automatisms, lip-smacking, olfactory hallucinations) - Short duration (typically <30 min; TGA lasts hours) - No repetitive questioning - Frequent and rapid recurrences

- Psychogenic amnesia: - Younger patient with a known psychiatric stressor - Prominent retrograde amnesia - Psychogenic memory loss for personal identification, name, birth date, etc.

  • Transient global amnesia (TGA) has the following features:Episode of amnesia with abrupt onsetNo focal neurologic signs or symptomsTemporary, severe, anterograde amnesia:Acute inability to form new memoriesPermanent memory gap after the episodeTemporary short-range retrograde amnesia:More recent memories at more riskPreviously encoded memories unavailable only temporarilyGradually improves until only remaining memory deficit is the gap induced by the anterograde amnesia
  • Incidence between 3 and 8 per 100,000 people:75% occur in people of 50 " 70 yr oldTGA rare <40 yr
  • Most attacks last between 1 and 8 hr (range 15 min " 7 days)

Etiology

  • Multimodal MRI, SPECT, and PET have shown some abnormalities of regional blood flow in selectively vulnerable hippocampal structures
  • The exact etiology of TGA is unknown; speculation is controversial
  • Speculated causes:Vasoconstriction due to hyperventilation:Psychogenic hyperventilation in setting of age-related cerebrovascular autoregulatory dysfunctionHippocampal venous congestion with Valsalva:Ultrasonography has suggested internal jugular vein incompetenceMigraine (in younger patients)
  • No correlation between TGA and thromboembolic cerebrovascular disease has been found

Diagnosis

Signs and Symptoms

Diagnostic criteria:

  • Attack must be witnessed
  • Acute onset of anterograde amnesia
  • No alteration in consciousness
  • No cognitive impairment except amnesia
  • No loss of personal information (e.g., name, birth date, address, etc.)
  • No focal neurologic symptoms
  • No epileptic features
  • No recent history of head trauma or seizures
  • Attack must resolve within 24 hr
  • Other causes of amnesia excluded

History

  • Often precipitated by stressful condition:Cough, ValsalvaPhysical exertionSexual intercourseExtreme fright or shockIntense heat or cold
  • Patient will likely feel something is wrong:May ask "how did I get here? "May be repetitive in questionsWill be generally aware of attack
  • May have other subtle transient symptoms at onset, such as headache, dizziness, nausea
  • Historical features helpful in excluding other diagnoses are:Onset of attack witnessed, with no seizure activity or epileptiform features notedNo history of seizures in prior 2 moNo history of recent traumatic brain injuryAcute anterograde amnesia with relatively preserved remote memory

Physical Exam

  • Marked anterograde amnesia
  • Most cases ( ≥90% in case series) will demonstrate repetitive questioning
  • Neurologic and general exam normal
  • TGA patient WILL NOT be:SomnolentInattentiveGlobally confusedConfabulate
  • TGA patient WILL be:Oriented to name, birth date, address, phone number, dateAble to perform complex tasks and following complex commands
  • Aphasia, apraxia, and agnosia are NOT findings consistent with TGA

Essential Workup

  • True TGA can be diagnosed with a careful history and physical exam alone
  • If clinical diagnosis is certain, no other workup is essential

Diagnosis Tests & Interpretation

Testing indicated only when the diagnosis is uncertain

Lab

  • CBC, comprehensive chemistries including glucose, LFTs, NH3, thyroid studies, and UA for organic " metabolic etiologies were implicated
  • Tox screen, alcohol level for toxic etiologies were suspected

Imaging

  • Consider MRI if indicated.In true TGA, MRI may show a focal hippocampal DWI or T2 lesion that resolves over time
  • Head CT for intracranial mass if indicated

Diagnostic Procedures/Surgery

  • EEG for seizure or nonconvulsive status if suspected
  • Lumbar puncture and CSF analysis for encephalitis if suspected

Differential Diagnosis

  • Other entities may present somewhat similarly but will likely have historical or physical exam features that readily distinguish them from TGA:Anterior choroidal artery or posterior cerebral artery or TIA:Additional related neurologic signs such as hemianopiaAcute confusional state/Korsakoff syndrome/metabolic disorder:Alcohol, medication, or toxin ingestionDecreased attention or other findings of an encephalopathyImpairment with serial 7s or spelling "world " backwardAble to lay down new memory if allowed time to encodeComplex partial seizures/epileptic amnestic attacks:Witnessed epileptiform activity or features (e.g., blank stares, automatisms, lip-smacking, olfactory hallucinations)Short duration (typically <30 min; TGA lasts hours)No repetitive questioningFrequent and rapid recurrencesPsychogenic amnesia:Younger patient with a known psychiatric stressorProminent retrograde amnesiaPsychogenic memory loss for personal identification, name, birth date, etc.Temporal lobe brain lesion or encephalitis affecting the temporal lobe:Has other associated neurologic symptoms (e.g., visual field cut, confusion)Progressive and permanent amnesiaPreviously unrecognized Alzheimer dementia:Memory loss for personal information such as date, phone number, addressSigns of additional global cognitive impairment

Treatment

Pre-Hospital

There are no considerations in true TGA that are specific to the pre-hospital environment

Initial Stabilization/Therapy

There is no known effective therapy for TGA

Ed Treatment/Procedures

  • TGA is a self-limited, relatively benign entity
  • Observe the patient for improvement
  • Assuming a true diagnosis of TGA, no acute treatment beyond reassurance of patient and family is indicated

Medication

First Line

Not applicable

Second Line

Not applicable

Follow-Up

Disposition

Admission Criteria

  • Admission for further observation for patients without significant improvement at the time of disposition
  • Patients with uncertain diagnosis
  • Patients showing a trend toward resolution but who have suboptimal social support at home

Discharge Criteria

  • A clear diagnosis of TGA
  • Resolving or resolved amnesia
  • Good social support

Issues for Referral

  • Recurrence rate of TGA is 8%
  • Refer patients with recurrent episodes of TGA to a neurologist:May benefit from ambulatory EEG to workup epilepsy

Followup Recommendations

Given median age of TGA patients (60 yr), follow-up with primary care provider for general cardiovascular risk factor modification may be beneficial:

  • No follow-up specific to TGA is indicated
  • See "Issues for Referral " for patient with recurrent episode of TGA

Pearls and Pitfalls

  • TGA is a distinct and relatively benign entity:Acute onset of isolated anterograde amnesiaResolves spontaneously
  • Be aware of subtle features that may suggest a more pathologic alternative diagnosis:Short, recurrent episodes or automatisms in epilepsyCognitive impairment with encephalopathySubtle neurologic signs in encephalitis or TIA
  • If there is uncertainty regarding the diagnosis, the highest yield tests are multimodal MRI and EEG

Additional Reading

  • Bartsch T, Deuschl G. Transient global amnesia: Functional anatomy and clinical implications. Lancet Neurol. 2010;9:205 " 214.
  • Hunter G. Transient global amnesia. Neurol Clin. 2011;29:1045 " 1054.
  • Kirshner HS. Transient global amnesia: A brief review and update. Curr Neurol Neurosci Rep. 2011;11:578 " 582.
  • Markowitsch HJ, Staniloiu A. Amnesic disorders. Lancet. 2012;380:1429 " 1440.

See Also (Topic, Algorithm, Electronic Media Element)

Codes

ICD9

  • 437.7 Transient global amnesia
  • 780.93 Memory loss

ICD10

  • G45.4 Transient global amnesia
  • R41.1 Anterograde amnesia
  • R41.2 Retrograde amnesia

SNOMED

  • 230736007 Transient global amnesia
  • 88822006 Anterograde amnesia (finding)
  • 51921000 Retrograde amnesia (finding)