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Transient Global Amnesia

  • Author: Roy Sucholeiki, MD; Chief Editor: Helmi L Lutsep, MD  more...
 
Updated: Apr 22, 2016
 

Background

Transient global amnesia (TGA) has been a well-described phenomenon for more than 40 years. Clinically, it manifests with a paroxysmal, transient loss of memory function. Immediate recall ability is preserved, as is remote memory; however, patients experience striking loss of memory for recent events and an impaired ability to retain new information. In some cases, the degree of retrograde memory loss is mild.

Many patients are anxious or agitated and may repeatedly ask questions concerning transpiring events. Upon mental status examination, language function is preserved, which indicates a preservation of semantic and syntax memory. Attention is spared, visual-spatial skills are intact, and social skills are retained. Symptoms typically last less than 24 hours. As the syndrome resolves, the amnesia improves, but the patient may be left with a distinct lapse of recollection for events during the attack.

Generally, TGA is a solitary event, however, patients can experience more than one event with very similar symptoms and recovery.

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Pathophysiology

The precise pathophysiology of transient global amnesia is not clear. The findings reported with positron emission tomography (PET), diffusion-weighted MRI (DWI), single photon emission computed tomography (SPECT) and MR spectroscopy (MRS) have indicated various brain regions that are affected in TGA.

  • On PET and DWI, blood flow to specific brain areas that involve memory appears to be disrupted transiently during TGA. This includes the thalamus and/or mesial temporal structures (in particular the amygdala and hippocampus).
  • Hakan et al demonstrated tiny increases in signal in the left parahippocampal gyrus and splenium of the corpus callosum on DWI in one patient. This method of imaging allows detection of hyperacute ischemic change. Liang et al and Yang et al have also recently used DWI to document tiny lesions in the hippocampus of patients with acute TGA. [1, 2] However, Eustache et al reported a PET study consistent with a spreading depression in the left lateral frontal cortex. This case also featured oligemia in the left occipital cortex. [3] Strupp et al found mainly medial temporal changes on DWI in 7 of 10 patients with TGA. They suggested that cellular edema or spreading depression could be responsible, not just ischemia. [4]
  • Winbeck et al found a significant incidence (10/28) of acute DWI changes in patients with TGA, which is comparable to the TIA group (21/74). Although the patients who presented with a TIA had a higher prevalence of vascular risk factors, those in the TGA group (who had DWI changes) were found to have significantly more carotid atherosclerosis. [5]
  • Nakada et al demonstrated via high-resolution T2-reversed MRI a high incidence of hippocampal cavities compared with their normal or disease controls. The authors conclude that their findings may indicate that TGA can be associated with neuronal loss in the CA1 region of the hippocampus. [6]
  • Generally, the territory of the vertebrobasilar system is most often rendered ischemic and dysfunctional. However, since ischemia typically does not progress to infarction, symptoms are expected to resolve completely.
  • Yamane et al reported rather diffuse cerebral hypoperfusion on SPECT that improved months later upon repeating the test in a patient with TGA. [7] Yang et al also reported hypoperfusion in the cerebellar vermis that recovered by the time of follow-up examination. [1]
  • Bartsch et al found that in 7 patients with TGA, 4 had a diffusion abnormality corresponding with a T2 lesion in the CA-1 sector of the hippocampus. In 3 of these patients, MRS revealed a lactate peak. The authors suggest that this represents an acute stress reaction of this particular area and indicates the pathological substrate of TGA. [8]

Overall, the variety of findings on functional imaging studies may support the notion that TGA is a syndrome with not only a variety of precipitating causes but also of differing mechanisms.

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Epidemiology

Frequency

United States

Based on data from Rochester, Minnesota, Miller et al determined an incidence of 5.2 cases per 100,000 population. However, among individuals older than 50 years, the incidence was 23.5 cases per 100,000 population per year.[9]

International

Estimates vary, but Matiea-Guiu et al found a lower incidence in Alcoi, Spain, of 2.9 cases per 100,000 population.[10] On the other hand, Lauria et al found an incidence of 10 cases per 100,000 population in Belluno, Italy.[11]

Mortality/Morbidity

As the name implies, transient global amnesia symptoms are transient.

The mean annual recurrence rate is thought to be low (approximately 4-5%). However, in the study by Miller et al, the calculated recurrence rate could be as high as 24% over a lifetime depending on inclusion criteria.[9] These occasional recurrences usually involve no long-term morbidity or death.

If transient ischemic attack (TIA) is suspected, then the patient should be evaluated for stroke risk factors. Likewise, if a seizure is suspected, appropriate testing should be initiated.

Age- and sex-related demographics

The typical age of occurrence is older than 50 years.

No sex predilection has been observed. However, one study found that particular triggers may be associated with men and women. For men, transient global amnesia occurs more often after a physical precipitating event. In women, episodes may be more associated with emotional precipitating events, a history of anxiety, or pathological personality.

 

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Contributor Information and Disclosures
Author

Roy Sucholeiki, MD Director, Comprehensive Seizure and Epilepsy Program, The Neurosciences Institute at Central DuPage Hospital

Roy Sucholeiki, MD is a member of the following medical societies: American Academy of Neurology, American Neuropsychiatric Association, American Epilepsy Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Additional Contributors

Carmel Armon, MD, MSc, MHS Chair, Department of Neurology, Assaf Harofeh Medical Center, Tel Aviv University Sackler Faculty of Medicine, Israel

Carmel Armon, MD, MSc, MHS is a member of the following medical societies: American Academy of Neurology, Massachusetts Medical Society, American Academy of Sleep Medicine, American Stroke Association, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American College of Physicians, American Epilepsy Society, American Medical Association, American Neurological Association, Sigma Xi

Disclosure: Received research grant from: Neuronix Ltd, Yoqnea'm, Israel.

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