Mr. E, aged 51 years, presented to the emergency department (ED) with confusion and altered mental status. He was confused as to time and situation. He had been asymptomatic at 7:30 am. At 9:30 am, after Mr. E packed his truck, his daughter noticed him constantly staring at his watch and repeatedly asking what day it was. Mr. E admitted to feeling confused and could not remember anything about the morning. He was brought to the ED at 10:30 am.


The patient had a medical history of hypertension and hyperlipidemia. Mr. E was taking carvedilol (Coreg) and fenofibrate (Lipofen). He had no history of head trauma, headaches, seizures, or thyroid disease and had not experienced periodic confusion or memory loss before. No recent hospitalizations or surgeries were noted. Mr. E did not use tobacco and drank one to two drinks on the weekends. Although there was no family history of stroke or heart attack, there was a significant family history of diabetes.


Mr. E was afebrile. His BP was 155/97 mm Hg with a heart rate of 74 beats per minute. He appeared agitated and confused. He repeatedly asked the same chain of questions over several hours. The patient was able to recognize family members but could not recall the year or name of the current president. Mr. E was able to read sentences clearly and identify objects and scenarios in pictures.

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His neurologic examination was otherwise unremarkable. No abnormality in language, visual-spatial, or attention skills was noted. No abnormality in the motor or sensory system was found. Reflexes and coordination were intact. All cranial nerves were intact.


Mr. E was sent for a CT scan to rule out a hemorrhagic stroke. The CT showed no areas of increased density, ruling out acute intracranial hemorrhage. There was no extra-axial fluid collection. No abnormalities of the ventricles, gray or white matter, sulci, or basilar cisterns were seen. An ECG showed normal sinus rhythm.

Blood work consisted of a comprehensive metabolic profile, international normalized ratio, prothrombin time, lipid panel, cardiac enzymes, and a thyroid panel. All lab values were within normal limits except the lipid panel.

A chest x-ray showed no radiographic abnormalities. An MRI and magnetic resonance angiogram (MRA) were done to show intracranial arterial circulation and to identify areas that have suffered from ischemia. This patient’s MRI showed no foci of restricted diffusion, which ruled out recent infarction.

The MRA showed strong antegrade flow through all the arteries of the circle of Willis other than the right vertebral artery. The right vertebral artery appeared to be congenitally hypoplastic; however, no significant stenosis was seen. A carotid Doppler ultrasound showed no evidence of significant atherosclerosis or stenosis.

Mr. E was admitted to the hospital and observed overnight. As the hours progressed, his symptoms began to resolve. By 7:00 pm, the patient’s confusion had subsided. His ability to retain information was re-established; however, he could not recall that day’s events.

Once the imaging tests ruled out a cerebral vascular accident (CVA), Mr. E was diagnosed with transient global amnesia (TGA). After overnight observation, he was discharged with instructions to take a daily aspirin and to follow up with a neurologist in two weeks.


TGA, a form of temporary amnesia, typically lasts two to eight hours. Patients with TGA usually present with short-term amnesia, which renders them unable to retain new information. Long-term memory and immediate recall are spared. Patients appear agitated and confused, with the attack lasting no more than 24 hours. They will often repeat the same questions until the attack subsides and memory retention is regained. Other associated symptoms include headache, dizziness, and nausea.1 The neurologic examination of a patient with TGA will be without abnormalities, and diagnostic imaging is usually normal. This presentation differs from that of a stroke, in which the patient usually has an abnormal neurologic examination, and imaging often shows acute ischemic changes. Therefore, TGA is a diagnosis of exclusion.

TGA has an incidence rate of 5.2 cases per 100,000 per year. Incidence increases significantly after age 50 years.2 Gender and race do not show predominance. Diagnostic criteria, which were first presented in 1990, consist of the following:

Attacks must be witnessed and information made available by a capable observer who was present for most of the attack.There must be clear-cut anterograde amnesia during the attack.Clouding of the consciousness and loss of personal identity must be absent, and the cognitive impairment limited to amnesia (for example, no aphasia or apraxia).There should be no accompanying focal neurologic symptoms during the attack and no significant neurologic signs afterwards.Epileptic features must be absent.Attacks must resolve within 24 hours.Patients with a recent head injury or known active epilepsy (that is, patients remaining on medication or who have had one seizure in the past two years) are excluded.3

Exact etiology of TGA is unknown, but several theories have been proposed. Probable causes include migraine, seizure, transient ischemic attack, anatomical anomalies, and venous congestion. It has been theorized that glutamate release during a migraine causes a spreading cortical depression in the brain, leading to dysfunction of the hippocampus. Migraines have shown to be a higher risk factor in younger patients.1

In a study consisting of 277 patients with TGA, 14.1% had a history of migraine, 11.2% had a history of cerebrovascular disease, and 33.4% had a prior incident of physical exertion.2 Other common precipitating factors include overwhelming stress, pain, cold-water submersion, sexual intercourse, and Valsalva maneuver. The Valsalva maneuver leads to an increase in intrathoracic pressure and reflex bradycardia. The maneuver is done by forcefully exhaling while keeping the glottis closed (without releasing air). Studies now show that patients with jugular insufficiency are at increased risk of venous pressure elevations during a Valsalva maneuver. This increase in pressure causes venous congestion, which leads to impaired blood flow to the structures in the brain related to memory.4

Positron emission tomography (PET) and diffusion-weighted imaging (DWI) scans conducted during an attack of TGA have shown impaired blood flow to the areas of the brain that involve memory function. The areas of the brain responsible for memory include the thalamus, amygdala, and hippocampus. Researchers used DWI and single photon-emission computed tomography scans to show abnormalities during TGA attacks. Their study demonstrated that the patients with TGA had cerebellar hypoperfusion with ischemic insults to the lateral hippocampus.5

TGA is a diagnosis of exclusion. It is most important during patient evaluation to rule out a stroke. Although no treatment is necessary, a follow-up appointment with a neurologist is advised. Patients make a full recovery with the exception of amnesia of the actual attack. Recurrence is uncommon, with only 10% of patients experiencing a second attack of TGA.6 Patients with a history of TGA are not at an increased risk for cerebrovascular disorders. In fact, TGA patients have similar vascular profiles to healthy individuals.7 Because TGA has a good prognosis, reassurance to the patient and family members should be provided.

Ms. Euler is a second-year student in the physician assistant program at Georgia Health Sciences University in Augusta, where Ms. Haddow is an assistant professor and the director of education.


1. Quinette P, Guillery-Girard B, Dayan J, et al. What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases. Brain. 2006;129:1640-1658. 

2. Miller JW, Petersen RC, Metter EJ, et al. Transient global amnesia: clinical characteristics and prognosis. Neurology. 1987;37:733-737.

3. Hodges JR, Warlow CP. Syndromes of transient amnesia: towards a classification. A study of 153 cases. J Neurol Neurosurg Psychiatry. 1990;53:834-843.

4. Nedelmann M, Eicke BM, Dieterich M. Increased incidence of jugular valve insufficiency in patients with transient global amnesia. J Neurol. 2005;252:1482-1486.

5. Yang Y, Kim JS, Kim S, et al. Cerebellar hypoperfusion during transient global amnesia: an MRI and oculographic study. J Clin Neurol. 2009;5:74-80.

6. Berli R, Hutter A, Waespe W, Bachli EB. Transient global amnesia—not so rare after all. Swiss Med Wkly. 2009;139:288-292.

7. Enzinger C, Thimary F, Kapeller P, et al. Transient global amnesia: diffusion-weighted imaging lesions and cerebrovascular disease. Stroke. 2008;39:2219-2225.

All electronic documents accessed June 15, 2011.