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Transient Global Amnesia

By Rohit Vinay


 

Case

HISTORY: 61year old male with past medical history of Type 2 Diabetes, Hyperlipidemia, presents to the Emergency Department with memory loss. The family stated that patient had an acute onset of confusion at 7:00 pm prior to which he had been outside chopping wood and doing household activities and seemed normal when he came inside. Patient showered prior to dinner and was noted shortly after by the family to be confused and repetitive and unable to recall recent events. He repetitively kept asking about whether he had done his normal daily activities. He was brought to the emergency department where he was found to be aware of his identity and orientation was intact. However, he was unable to recall anything prior including the reason why he had been brought to the emergency department.

PHYSICAL EXAM:

Vitals on arrival: BP 137/70 mmHg, P 63/min, RR 15/min, T 36.6°C, O2 Sat 99% RA.

Constitutional: No apparent distress and is comfortable at rest.

HEENT: Atraumatic. Normocephalic. PERRL. EOMI without nystagmus. Normal sclera without injection, normal pinnae without drainage, no nasal deformity. Neck supple.

No remarkable findings on cardiovascular, respiratory, abdominal or MSK examinations.

Neurological Exam: Glasgow Coma Scale was 15/15. He was oriented to person, time, place. His cranial and peripheral nerves were normal. No focal neurological deficits. Motor: Tone Normal, Strength 5/5, Reflexes 2+ in upper and lower limbs. Sensory: light touch, temperature, pin sensation, vibration and position sense are normal. Co-ordination normal. Romberg sign absent.

ED COURSE:

Non-Contrast Head CT: No evidence of hemorrhage. No evidence of ischemic infarct.

Chest x-ray normal

CBC normal; Blood sugar 126 mg/dl

Negative sequential high-sensitivity troponin

Electrolyte, RFT, LFT, TSH - Normal

Urine analysis and toxicology: Normal

DIAGNOSIS & MANAGEMENT: After discussion with a Neurology consultant, the diagnosis of TGA was confirmed and patient was observed, reassured and advised to follow up on an outpatient basis.

Clinical Question: What is Transient Global Amnesia? Is it a Transient Ischemic Attack?

Transient Global Amnesia (TGA) is a syndrome in which there is transient but complete anterograde amnesia and a period of retrograde amnesia. It presents as sudden and temporary loss of the ability to form new memories, usually lasting for several hours.

The patient frequently asks repetitive stereotyped questions, sometimes several times at irregular intervals such as — “How did I get here?,” “Where am I?,” “What happened?,” “What time is it?”. Retrograde memory loss comprises of a period of many hours before the event, which gradually decreases during recovery. The individual is able to recall distant memories several hours or days prior to the onset of symptoms and is able to recall personal identity. Patient can state their own name, date of birth, recognize and recall names of their spouse and relatives. No abnormalities in neurologic examination is found during and after the incident. (1,2)

TGA episodes occur around the mean age of 61-67 years with an incidence of 3-10/100000 (3). TGA is a clinical diagnosis first described in 1956 as an “isolated episode of confusion with amnesia” not associated with other neurological deficits, which was later coined as TGA by Fisher and Adams in 1958 (4). Caplan initially established the criteria and classification (5) followed by Hodges and Warlow in 1990 (6) who reviewed 153 patients by dividing them into three categories (pure TGA, probably epileptic amnesia, and probably TIA) based on exclusionary criteria for pure TGA namely focal neurological symptoms, such as ataxia, limb weakness, and sensory disturbances. Based on their studies the following criteria were established and have been followed ever since. Proposed Diagnostic Criteria for TGA Adapted from Caplan

  • Attack is witnessed.

  • Dysfunction limited to repetitive queries and amnesia.

  • No other major neurological signs

  • Memory loss is transient, usually lasting hours to a day

Adapted from Hodges and Warlow

  • The attack was witnessed and reported.

  • There was obvious anterograde amnesia during the attack.

  • There was an absence of clouding of consciousness.

  • There were no focal neurological signs or deficits during or after the attack.

  • There were no features of epilepsy.

  • The attack resolved within 24 h.

  • The patient did not have any recent head injury or active epilepsy.

TGA may be precipitated by a physical or mental shock or extreme exertion, such as news of a death, assault, sudden exposure or shower in cold water, sexual intercourse, invasive medical procedures (e.g., endoscopy), or severe pain. (1) TGA recurrence is not rare, reoccurring 10% to 15% within 5 years. Recurrent TGA was associated with earlier age at the time of first TGA episode and higher prevalence of both personal/family history of migraine compared with isolated cases. (7) DIAGNOSTIC IMAGING:



TGA is often normal or associated with a punctate hyperintense lesion in the CA1 region of the hippocampus on diffuse weight imaging (DWI) obtained within 24–96 hours of the TGA episode. Though these acute lesions in TGA are considered to be transient in nature and are believed to “vanish” on imaging performed more than 30 days after the onset of TGA, there are other studies that report persisting radiological changes up to 8 months (8,9)

Is TGA a Transient Ischemic Attack (TIA)?

Transient global amnesia is not a Transient ischemic attack. Sudden memory loss is the main and generally the only sign of TGA, whereas TIA has the same symptoms as stroke- difficulty seeing from one or both eyes, numbness or weakness in the face, arms or legs (especially on one side), acute onset aphasia (either receptive or expressive) or may affect balance presenting with isolated central vertigo. (10)

TGA occurs in patients aged 50 years and above (3), whereas TIA can occur at all ages but more common in elderly. The etiology of TGA remains unidentified and different from TIA, even though vascular ischemia due to venous stasis, epilepsy and association with migraine has been implicated. (1,11) TGA presents as an isolated memory disorder whereas TIA is associated with other neurological signs. TGA patients cannot acquire new memories but can function normally and their personal identity is retained in contrast to TIA patients who have more global disorientation and confusion. There is no increased risk of TIA or CVA in patients who have had TGA and mortality is not affected compared to normal population. (12)

Conclusion

  • TGA is characterized by the sudden onset of significant anterograde amnesia, associated with variable degrees of retrograde amnesia, lasting no longer than 24 h and must not have any evidence of neurological signs or deficits, features of epilepsy, active epilepsy or recent head injury.

  • The challenge in ER arises when the patient is seen after the episode and there is difficulty in determining whether the problem was a transient confusional episode from seizure, severe hypoglycemia, alcohol or drug intoxication, hypnotic drugs, or a similar disorder rather than transient global amnesia. During an episode, signs of confusion such as inattentiveness and incoherence mark the disorder as different from transient global amnesia.

  • There are usually no long-term issues related to transient global amnesia. In majority of individuals, people experiencing TGA recover completely. When the episode is over, they can form new memories, but they won’t remember what happened during the episode.

  • Even though TGA is a clinical diagnosis, in the modern era, cerebral imaging is usually performed to reassure the patient and the physician that there has not been an infarction or other lesion as these studies are initially normal in patients with TGA. Diagnosis of TGA is by exclusion and management is observation, supportive care and reassurance to the patient.

References

  1. Ropper AH. (2023) Transient Global Amnesia. N Engl J Med. 388(7):635-640. doi: 1.1056/NEJMra2213867

  2. Arena JE, Rabinstein AA. (2015) Transient global amnesia. Mayo Clin Proc. Feb;90(2):264–72 https://doi.org/10.1016/j.mayocp.2014.12.001

  3. Spiegel DR, Smith J, Wade RR, Cherukuru N, Ursani A, Dobruskina Y, Crist T, Busch RF, Dhanani RM, Dreyer N. (2017) Transient global amnesia: current perspectives. Neuropsychiatr Dis Treat. Oct 24;13:2691-2703. doi: 10.2147/NDT.S130710.

  4. Fisher CM, Adams RD. (1958) Transient global amnesia. Trans Am Neurol Assoc. 1958;83:143–146. 

  5. Caplan LR (2022). Transient global amnesia: what’s in a name? J Neurol Sci 2022;441:120348-120348.

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

  7. Morris KA, Rabinstein AA, Young NP. Factors Associated With Risk of Recurrent Transient Global Amnesia. JAMA Neurol. 2020;77(12):1551–1558. doi:10.1001/jamaneurol.2020.2943

  8. Huber R, Aschoff AJ, Ludolph AC, Riepe MW (2002) Transient Global Amnesia. Evidence against vascular ischemic etiology from diffusion weighted imaging. .J Neurol 249(11):1520-4. doi: 10.1007/s00415-002-0881-3

  9. Singh RB, Ahmed AK, Vibhute P, Middlebrooks EH, Sandhu SJ (2023) Chronic hippocampal subfield damage in transient global amnesia revealed by 7T MRI: All is not reversible? Neuroradiol J. 18:19714009231177411. doi: 10.1177/19714009231177411

  10. Panuganti KK, Tadi P, Lui F. Transient Ischemic Attack. (2023) StatPearls Publishing; 2023 Jan: https://www.ncbi.nlm.nih.gov/books/NBK459143/

  11. M Zorzon 1, L Antonutti, G Masè, E Biasutti, B Vitrani, G Cazzato (1995) Transient global amnesia and transient ischemic attack. Natural history, vascular risk factors, and associated conditions Stroke 26(9):1536-42. doi: 10.1161/01.str.26.9.1536.

  12. Liampas I, Raptopoulou M, Siokas V, Tsouris Z, Brotis A, Aloizou AM, Dastamani M, Dardiotis E.(2021) The long-term prognosis of Transient Global Amnesia: a systematic review. Rev Neurosci.Feb 1;32(5):531-543. doi: 10.1515/revneuro-2020-0110.

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