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Transient global amnesia presenting in primary care: A case report

Ammerman, Beth Anne, DNP, FNP-BC

doi: 10.1097/01.NPR.0000534940.19843.e4
Department: Clinical Case Report

Beth Anne Ammerman is a clinical instructor at the University of Michigan, Ann Arbor, Mich., and a family NP in Linden, Mich.

The author has disclosed no financial relationships related to this article.

Transient global amnesia (TGA) is a benign, transitory condition in which patients present with severe anterograde amnesia and disorientation. Onset of TGA occurs without warning in an intense manner and can mimic fatal conditions. Because many primary care providers are not aware of this condition, TGA can be misdiagnosed as stroke, seizure, drug misuse, or intoxication. Therefore, it is essential for primary care providers to be cognizant of TGA when diagnosing and treating patients with sudden acute memory disruption.

TGA is a single, abrupt, temporary episode of severe memory loss with disorientation that lasts fewer than 24 hours.1 During an episode of TGA, a patient experiences severe anterograde amnesia, often accompanied by retrograde amnesia.1,2 While patients experiencing TGA exhibit disorientation and repetitive questioning, they maintain their identity and their ability to communicate.3 Although the presentation is alarming, TGA is considered a benign disorder with an excellent prognosis for full recovery and no lasting deficits.1

Patients who present with TGA can be challenging for primary care providers (PCPs) to treat. Because most patients affected by TGA present to EDs, most case reports target providers who work in neurology or emergency medicine. However, some patients have presented to primary care settings experiencing sudden memory loss and have been misdiagnosed with cerebrovascular, cardiovascular, or epileptic conditions.1,4 Therefore, PCPs need to be aware of TGA.

This case report specifically explores the events during the assessment, diagnosis, and treatment of a female patient who suddenly experienced memory loss and disorientation while in a primary care practice. Because the signs and symptoms of TGA are similar to urgent and life-threatening conditions, it is crucial to distinguish between TGA and its differentials. Being able to recognize the signs and symptoms of TGA is imperative for PCPs to expedite proper diagnosis and management. This case is presented within the CARE guidelines for clinical case reporting.5

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Although medical literature as early as the 1950s described an unknown syndrome of sudden but temporary anterograde memory loss, it was not until 1964 that TGA was officially named by two physicians, C. Miller Fisher and Raymond Adams.6-8 Fisher and Adams focused on retrospective chart reviews and case studies, noting that this form of amnesia followed a distinct pattern with intense onset and complete resolution within 24 hours.7 In 1990, Hodges and Warlow developed criteria for diagnosing TGA.2,4,8,9 Their criteria are still used today (see Hodges and Warlow criteria for diagnosing TGA).

The symptoms of TGA include a sudden onset of amnesia with repetitive questioning and confusion, but without loss of consciousness or personal identity.9 No speech or motor deficits are associated with TGA. Accompanying signs and symptoms can also include nausea, vomiting, headache, dizziness, chills, shaking, cold extremities, and increased anxiety.2,4,6,9

Because TGA appears quickly, without warning, and can mimic life-threatening diseases, immediate medical attention is usually sought to rule out fatal illnesses and to ensure a proper diagnosis. However, most patients experience a costly, yet negative, medical workup for this diagnosis.8 Arena and Rabinstein challenged such methods by proposing that a TGA diagnosis can be made based on health history, cognitive evaluation, and physical assessment.1

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TGA occurs with a reported incidence of 3 to 30 cases per 100,000 indviduals.10 It usually occurs in individuals ages 50 to 80, with the median age of affliction being 61.5.4 TGA episodes occur randomly, though most often during the morning or early afternoon, which correspond with times when primary care offices are often seeing patients.6,10 While an attack of TGA usually lasts between 1 and 10 hours, most average between 4 and 5 hours, with the first 8 hours showing the most acute symptoms.5,11,12 While TGA usually occurs just once in most patients, a 5-year recurrence has been reported in approximately 3% to 20% of patients.4

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Stress has been associated with triggering attacks of TGA.8,13 While TGA affects both genders at a similar rate, common triggers appear to be physical and emotional stress for men and women, respectively.14 Suspected emotional stress triggers include receiving bad news, witnessing an accident, participating in an argument, anxiety, and bereavement, whereas physical exertion triggers include sports and exercise, sexual intercourse, and, especially, swimming in cold water.2,6,9,13,15

Additional triggers include medical procedures, anesthesia, pain, Valsalva maneuvers, and migraine headaches.6,9,14,15 Obstructive sleep apnea has also been thought to contribute to some episodes of TGA.8 TGA episodes are not associated with an increased incidence of stroke, seizure, malignancy, or cognitive impairment risks.10



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The etiology of TGA is unknown, but the triggers seem to point toward ischemic episodes within the recent memory centers of the brain, namely the hippocampus and the mesial temporal lobes.6 Diffusion-weighted magnetic resonance imaging (DW-MRI) in some patients with TGA has shown transient lesions in the hippocampus within hours of the attacks, which later completely resolve.6,10 The cause of these temporary lesions is unknown but is thought to be related to increased venous congestion, migraine headaches, and cerebrovascular factors.14

In addition, because some studies have shown an increase of TGA in patients with jugular vein incompetence, it is thought a Valsalva maneuver may be one trigger for TGA.11 None of these possible causes fully explain all TGA cases, and TGA may have several different causes.

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Because of its dramatically abrupt presentation, TGA is sometimes initially mistaken for other, more life-threatening conditions including stroke, seizure, myocardial infarction (MI), or substance abuse (see Differential diagnoses of amnesia). DW-MRI of the brain has shown hippocampal changes in some patients who have TGA, but not in all; therefore, while DW-MRI may help with the diagnosis, not all patients with TGA show changes on the imaging.16

Although there are no blood tests to confirm TGA, the diagnosis is often made by ruling out other conditions. Blood testing such as toxicology screening, troponin levels, complete blood cell (CBC) counts, electrolytes, blood glucose, blood urea nitrogen, and creatinine are key to ruling out life-threatening differentials.

While patients experiencing stroke exhibit symptoms such as changes in cognition, coordination, and cerebral functioning, patients with TGA exhibit an inability to make new memories while retaining their cognition and coordination.4 On computerized tomography (CT) imaging, a stroke presents as an obstruction or hemorrhage, whereas TGA does not.

Transient shadowing on MRI in the hippocampus has been seen in some patients experiencing TGA but not in others. Carotid Doppler studies are also normal in TGA and may show narrowing of the carotid artery and plaque buildup in patients with a stroke.16

While patients with seizures present with generalized or partial seizure activity, patients with TGA are usually alert and talkative.2 Electroencephalographic (EEG) changes, which are prevalent in patients with seizures, are not noted in those with TGA.2 Elevated prolactin levels may indicate epileptic seizure but not TGA.12

MI is associated with elevated troponin tests and ECG changes, both of which are normal in patients with TGA.17 Although both conditions can present with anxiety, patients with TGA generally do not encounter pain or appear to be ill, whereas patients with MI often do. Those experiencing an MI often suffer symptoms of pain (chest, arm, or jaw), dyspnea, nausea, weakness, or loss of consciousness.



Patients experiencing an overdose will have positive drug or alcohol levels and may present with delirium, agitation, anxiety, hallucinations, loss of consciousness, or other changes in mental status.

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There are no medications or interventions to hasten the recovery or improve patient outcomes.2,4 Resolution of the episode comes predictably within 24 hours; therefore, the only treatment for TGA patients is observation and supportive reassurance.2 Care for the family of the affected patient is also a concern for staff and providers.

Due to TGA's rapid onset and obviously unusual patient behavior, it is common for families and significant others to become anxious about the patient's condition, particularly regarding the amnesia and repetitive questioning. Offering emotional support and providing education about the patient's condition are key to helping the patient and family.

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A case study

Mrs. G, 65, walked into her PCP's office requesting that a nurse check her BP. She reported that she had been feeling mildly dizzy, lightheaded, and “not quite right” all that morning. Other than these vague symptoms, her review of systems was negative.

Mrs. G's social history was unremarkable. She was retired, but occasionally worked a few hours at a local retail store. On that day, she had been doing light housework at home. While she usually walked for exercise a few times a week, she had not that day. She lived alone in her house and her adult children lived nearby. She had been widowed several years prior.

Mrs. G's medical history included coronary artery disease (CAD) with stent placement 2 years earlier, hypertension, hyperlipidemia, gastroesophageal reflux, and occasional bouts of situational anxiety. Her surgical history included an appendectomy and bilateral cataract extraction with lens implant. Mrs. G's family medical history included maternal hypertension, and her father died in an accident years prior.

Mrs. G's daily medications included baby aspirin, losartan, pantoprazole, and simvastatin. She also took nitroglycerin sublingual as needed for chest pain (used rarely, with the last dose being over 1 year prior), and occasionally took alprazolam (used rarely and not on the day described in this case study).

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While Mrs. G's BP was normal during her visit to her PCP's office that day, she seemed worried enough for the staff to alert a provider to assess her. Although Mrs. G was alert, oriented, and pleasant with an unremarkable physical exam, her stated fear of impending doom concerned the NP.

She was fearful and said, “Something does not feel right in my body.” Because of her history of CAD, an ECG was attempted but aborted when Mrs. G experienced a sudden change in mental status and could not hold still for the procedure. She began with rapid speech, asking where she was and how she got there, where her family was, and who the healthcare workers were. Her questions were answered in a reassuring manner, and she seemed to momentarily understand before she began repeating the same questions again within seconds.



During this time, Mrs. G was unable to recall driving to the office or any events from that morning. She accurately recalled the name of her medications, health history, family members, and her daughter's work phone number. She had normal sensation, reflexes, and movement in all extremities. Mrs. G did not display weakness or deficits in speech.

Emergency medical services were summoned, and Mrs. G's daughter was notified of her condition via phone. Mrs. G was transported to the nearby ED and was subsequently hospitalized for evaluation. Her altered mental status with rapid questioning continued at the hospital through the first night. She could eat, drink, and did not have any bowel or bladder difficulties, but she remained forgetful.

Her speech and mobility remained intact throughout the hospitalization, and her family stayed with her. Her workup included a CT scan of the brain, an EEG, carotid Doppler ultrasound, chest radiography, and ECG, all of which were unremarkable. Her lab test results for troponin levels, drug screen, urinalysis, blood cultures, CBC count, and blood chemistry were all within normal limits. Mrs. G's vital signs remained normal throughout her hospitalization, and she remained pain-free.

On the second day, symptoms resolved, and Mrs. G began to remember again. Upon resolution of all symptoms, she had no memory of the previous day's events, but her memories prior to the attack were intact. (See Timeline of Mrs. G's symptoms during the TGA episode.) Mrs. G was released home on day 3 with a diagnosis of TGA and was given instructions to follow up with a neurologist and her PCP later that week.

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Implications for practice

TGA is an important differential to consider when assessing and treating patients with sudden onset of amnesia. Although TGA has an excellent prognosis, it is sometimes misdiagnosed in primary care. PCPs should become aware of TGA's signs and symptoms to accurately diagnose and treat affected individuals and provide support to their families. A calm approach is necessary to help the patients and family understand the diagnosis.

Because TGA can be difficult to diagnose and because symptoms can mimic other serious health conditions, patients presenting with sudden memory loss should be evaluated and monitored in the hospital to exclude other possible and life-threatening causes. By becoming familiar with TGA, PCPs can better care for patients with this diagnosis.

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