Transient Global Amnesia
Jill C. Cash
Definition
A.Amnesia is a partial or complete loss of memory. There are two forms of amnesia—retrograde and antegrade. Retrograde amnesia is a state in which the individual is unable to recall past events. Antegrade amnesia is a state in which the individual has a profound amnesia to recent events and is unable to create new memories.
B.Transient global amnesia (TGA) is a spontaneous, reversible syndrome of significant antegrade amnesia and a milder reduction in retrograde episodic long-term memory. During the event, individuals have a profound amnesia to recent events, are disoriented as to time, have somewhat diminished executive function but maintain self-awareness, have no clouding of consciousness or loss of personality, and exhibit no agitation. There are no focal neurologic signs or symptoms. Individuals are able to perform complex tasks previously learned such as driving or playing a musical instrument but are unable to learn a new task or lay down new memory during the attack. After the attack resolves, there is amnesia of the events during the episode and a few minutes to prior to the beginning of the episode.
Incidence
C.The incidence of TGA is approximately 5.2 to 10 per 100,000 persons a year. The incidence increases with age so that episodes of TGA with persons 50 years and older increase to approximately 23.5 to 30 persons per 100,000 per year. The majority of TGA episodes occur between the age of 50 and 80 with the mean onset occurring in the seventh decade of life. Some studies report that TGA occurs slightly more in males than females while others report no difference between the genders.
Pathogenesis
A.The primary site of neurologic involvement causing TGA is the hippocampus, particularly the CA-1 and Sommer sector and the mediobasal temporal lobe. The hippocampus is critical in making new memories and converting short-term memory into long-term memory. The pathogenesis of TGA or what triggers the episode has not yet been clearly established but several hypotheses have been suggested. A vascular etiology such as transient ischemic attack (TIA) was thought to be a contributing cause except that TGA episodes last longer than TIA episodes.
B.Venous congestion has also been suggested as another cause based on observations that specific maneuvers such as Valsalva that increase intrathoracic pressure or venous return have preceded TGA episodes.
C.Another suggested cause is a migrainous phenomenon or cortical spreading depression (CSD; self-propagating wave of neuronal and glial depolarization that spreads across the cerebral cortex) that is thought to occur with migraine headaches.
D.Epileptic seizures have been suggested as a contributing cause but EEGs taken during episodes of TGA do not show epileptic electrical discharges, Finally, TGA was thought to be psychogenic but most experts believe that TGA has an organic cause even though stressors and/or psychogenic predisposition may have a role.
Predisposing Factors
A.Definite risks:
1.Advancing age.
2.Migraine headaches.
B.Possible risks:
1.Arterial ischemia (ischemic heart disease and carotid artery sclerotic changes).
2.Hyperlipidemia.
3.Significant emotional event.
4.Psychiatric disorders (posttraumatic stress disorders [PTSDs] and dissociative disorders).
Common Complaints
A.Significant antegrade amnesia and lesser retrograde amnesia.
Others Signs and Symptoms
A.Cognitive impairment limited to amnesia.
B.No loss of personality or clouding of consciousness.
C.Repetitive questioning.
D.Absence of neurologic signs or symptoms.
E.Absence of epilepsy.
F.Attacks resolve within 1 to 10 hours.
G.Associated symptoms: Headache, nausea, and vomiting immediately prior to attack.
Subjective Data
A.Determine onset, course, and duration of symptoms.
B.Note the extent and depth of loss of past memory.
C.Note repetitive questioning and ability to remember new information.
D.Note the individual’s ability to perform previous learned complex tasks.
E.Note level of self-awareness, consciousness, and mood.
F.Determine if any signs and symptoms preceded the amnesic event such as headache, nausea, or vomiting.
G.Significant life event stressors, psychiatric disorders, head injury, or epilepsy.
H.Review medication history including prescribed drugs, over-the-counter (OTC) drugs, and herbal remedies.
Physical Examination
A.Obtain vital signs: Blood pressure (BP), pulse, and respirations.
B.Inspect:
1.Observe overall appearance.
C.Auscultate:
1.Heart and lungs.
2.Carotid arteries bilaterally.
D.Neurologic examination:
1.Evaluate level of consciousness (LOC) and ability to perform cognitive testing.
2.Perform cognitive assessment screening tests:
a.Mini-Mental State Examination (MMSE). Available at www.uml.edu/docs/mini%20Mental%20State%20Exam_tcm18-169319.pdf.
b.Montreal Cognitive Assessment (MOCA). Available at www.Mocatest.org
c.Saint Louis University Mental Status (SLUMS) Examination. Available at echo.unm.edu/wp-content/uploads/2014/07/clinic-dementia-mental-status.pdf.
d.Check deep tendon reflexes (DTRs); assess for hyperreflexia
e.Assess muscle strength/tone, testing upper and lower extremities for increased tone (spasticity), tremors, and/or decreased tone.
f.Assess sensory response, testing perception for sharp versus dull stimulus, heat versus cold stimulus, local pain perception, and proprioception, and evaluate sense of vibration with tuning fork.
g.Note gait, posture, coordination, and balance.
Diagnostic Tests
A.CT and/or MRI.
B.EEG—if epilepsy suspected.
C.Complete blood count (CBC).
D.Chemistry profile.
E.Lipid levels.
F.Toxicology screen.
Differential Diagnoses
A.TGA.
B.Transient epileptic amnesia.
C.TIA.
D.Dissociative amnesia.
E.Migraine headache.
F.Hypoxic states (such as aortic dissection).
G.Hypoxic states (ischemic events).
H.Drug or alcohol withdrawal.
I.Hypoglycemia.
J.Psychogenic amnesia.
K.Metabolic derangements.
L.Wernicke’s encephalopathy.
Plan
A.General interventions:
1.Admit to hospital for duration of episodic event.
2.General supportive care during the amnesic event.
3.Provide ongoing treatment for comorbidities.
4.Thiamine 1,000 mg intravenous (IV; for possible Wernicke’s encephalopathy).
5.Ensure emotional support and reassurance.
B.Patient teaching:
1.Help the individual and significant others to understand the circumstances surrounding TGA.
2.Advise the individual and significant others that TGA does reoccur rarely but most have a single episode.
3.Memory that has been lost during the episode is permanent.
C.Pharmaceutical therapy:
1.Thiamine 1,000 mg given IV during hospitalization (for possibility of Wernicke’s encephalopathy).
2.No other medication needed for episode once resolved.
3.Treatment for comorbid conditions should continue as usual.
Follow-Up
A.Follow-up is not usually required once the TGA episode is resolved because most do not have a recurrence.
Consultation/Referral
A.Referral for follow-up care depends upon the findings of diagnostic studies that were conducted in the hospital setting.
B.Refer to a neurologist for long-term deficits.
Individual Considerations
A.Geriatrics:
1.TGA is a disorder occurring in older persons. Comorbidities occur with greater frequency in this age group. However, experts report no significant morbidity or mortality associated with this disorder.
2.In the geriatric population, distinguishing between TIA and TGA could be challenging. Both are identified with transient memory loss that is reversible, and both occur within similar age onset (60–79 years). Statistical analysis from research has shown:
a.TGA has significantly lower profiles of coronary artery disease (CAD), hypertension (HTN), diabetes mellitus (DM), and embolic disease than TIA/stroke.
b.The absence of lateralizing weakness and visual field deficits do not usually occur with TGA events.
c.Ninety-seven percent (97%) of TGA episodes last more than 1 hour (mean duration 4–8 hours).
d.In contrast, majority of TIA last less than 60 minutes and often only a few minutes.
3.Multiple studies consistently indicate that history of TGA does not increase risk for strokes.
4.Healthcare providers’ coaching and interventions to TGA geriatrics must include the following:
a.Support grief expressions.
b.Offer contact information of support groups.
c.Assist family members with positive coping strategies.
d.Emphasize a progressive pace unique to the older adult, acknowledge pleasant activities, and praise success of each memory restoration no matter how small it may seem.
e.Refer to individual/family counseling and encourage family discussions.
f.Introduce cognitive behavioral therapy (CBT) that assists patients with irrational thoughts, assumptions, filling in the blanks,
and negative beliefs. Learn about CBT: www.goodtherapy.org/learn-about-therapy/types/cognitive-behavioral-therapy.