Makindo Medical Notes

Transient Global Amnesia (TGA)

Introduction

• Transient Global Amnesia (TGA) is a short-lived, dramatic but ultimately benign episode of memory loss. The person suddenly can’t lay down new memories for a few hours, then goes back to normal.
• 📜 First properly described by Fisher & Adams in 1964.
• 🧠 The key picture: abrupt onset of anterograde amnesia and confusion about recent events, while the person still knows who they are, where they are, and their distant past.
• ❓ The exact cause is still debated – ideas include transient venous congestion, a migraine-like mechanism, brief hippocampal ischaemia, or stress-related vulnerability.
• ⚠️ It is easily mistaken for TIA or a seizure in the ED, but unlike those, the prognosis is excellent and most patients never have another episode.

📊 Epidemiology

• Incidence: roughly 5–10 cases per 100,000 people per year – so not common, but not ultra-rare either.
• 👵 Typically affects people in their 50s to 70s; it’s very unusual in young adults.
• 👨 There’s a slight male predominance in most series.
• 🔁 Recurrence happens in about 5–25% of patients, and if it does come back it’s usually just a single repeat episode many years later.

⚙️ Etiology & Pathophysiology

• 💧 One popular theory is transient venous congestion in the hippocampal region, leading to temporary dysfunction of memory circuits.
• ⚡ There are strong links with migraine in some patients, so a migrainous aura–type mechanism may play a role.
• 🩸 Some studies suggest brief hippocampal hypoperfusion, but not the sort of clear arterial occlusion you see in stroke.
• ⚡ Epileptic activity is thought to be unlikely in classic TGA – EEG is usually normal and there are no typical seizure features.
• ⏱️ Common triggers: sudden immersion in cold water, intense exertion, emotional shock, sexual activity, and sometimes medical or interventional procedures – i.e. anything that gives a big physiological or emotional jolt.

🩺 Clinical Presentation

• Sudden onset of anterograde amnesia with the classic repetitive questioning (“Where am I?”, “What’s happening?”) every few minutes.
• ✅ The person knows who they are and usually recognises family; older memories are mostly intact.
• ✅ They are awake, alert and able to follow commands; there is no loss of consciousness.
• ✅ There are no focal neurological deficits on examination (normal power, speech, visual fields, etc.).
• ⏳ The episode typically lasts 1–24 hours (most often 4–6 hours) and then fades, with memory gradually returning.
• ⏮️ A patch of retrograde amnesia (hours to days before the event) is common and may never fully come back.
• Patients usually feel very anxious or distressed during the episode – they’re aware that something is wrong, even if they can’t remember exactly what.

✅ Diagnostic Criteria (Practical Version)

• Witnessed episode of abrupt anterograde amnesia (family or staff can describe it).
• Clear inability to form new memories during the attack (repeats the same questions).
• No clouding of consciousness, no loss of personal identity, and the patient is otherwise “with it”.
• No focal neurological signs and no features suggesting a seizure (jerking, tongue bite, post-ictal confusion, etc.).
• Symptoms resolve completely within 24 hours.
• No recent significant head trauma to explain the amnesia.

🧾 Differential Diagnosis (Thinking Clinically)

• 🧩 Transient Ischaemic Attack (TIA): often has focal deficits (weakness, aphasia, hemianopia). Isolated amnesia without any other focal sign is unusual for a pure TIA.
• ⚡ Epileptic amnesia: events are usually shorter (minutes), may have automatisms, impaired awareness, post-ictal confusion, and an abnormal EEG.
• 🧠 Psychogenic/dissociative amnesia: often involves disturbed or lost identity, patchy autobiographical memory, and a strong psychological context.
• 🤕 Head injury: clear trauma history, possible LOC, headache, vomiting, or other concussion features.
• 🍷 Wernicke–Korsakoff: thiamine deficiency in heavy alcohol use – chronic confusion, ataxia, nystagmus, and confabulation rather than a single clean TGA episode.
• 💊 Drug-induced amnesia: classically benzodiazepines and other sedatives; the history often reveals recent medication or procedure.

🧪 Investigations (When the Picture Isn’t Textbook)

• 🧲 MRI with DWI: can show tiny punctate lesions in the hippocampus 24–48 hours after the event – supportive but not essential for diagnosis.
• 🖼️ CT head: usually normal; mainly used to rule out other acute pathology (e.g. bleed, large infarct) in the ED.
• 📉 EEG: typically normal in TGA; more useful if you’re genuinely worried about seizures.
• 🧪 Blood tests: check glucose, U&Es and other basics to rule out metabolic causes of confusion.
• 🫀 Cardiac / vascular work-up: ECG ± echo, carotid imaging if there are atypical features and TIA is still on the table.

💊 Management

• ✅ Reassurance is the main treatment. Explain that TGA looks frightening but is self-limiting and usually a one-off.
• 👀 Observe in a safe environment until the patient has clearly returned to baseline and you’re sure there is no stroke or seizure hiding underneath.
• 🚫 If the story and exam are classic, don’t automatically start anticoagulation or antiepileptic drugs – they don’t prevent TGA and add risk.
• 🧘 Explore and address obvious triggers (stress, sleep deprivation, acute emotional upset) and give simple advice on pacing and self-care.
• 🔁 Arrange follow-up, especially if the episode was atypical, prolonged, or if there is any diagnostic doubt.

📈 Prognosis

• 🌟 Prognosis is excellent – most people have a single episode and never see it again.
• 📉 Large cohort studies show no clear increase in stroke or epilepsy risk compared with the general population.
• 🧠 Cognitive function returns to normal, though there is often a “black hole” around the day of the event that never fully fills in.
• 🔁 Recurrence occurs in about 5–25% of patients, usually just once more over many years.
• 🚗 Driving (UK flavour): a single classic TGA episode doesn’t usually require DVLA notification; two or more documented episodes should prompt stopping driving and informing DVLA for individual assessment.

💡 Teaching Pearls

• 🗣️ In exams, the give-away phrase is “repetitive questioning in an otherwise well, alert patient” that lasts several hours.
• 🌊 Don’t forget common triggers like cold-water immersion, exertion, sexual activity or sudden emotional stress – examiners love that detail.
• ❌ Think pattern recognition:
  • TGA → hours of pure anterograde amnesia, no focal signs, full recovery.
  • TIA → focal deficit; isolated amnesia is unusual.
  • Seizure → brief, stereotyped, with post-ictal phase.
  • Psychogenic → identity disturbance and inconsistent exam.
• 👨‍⚕️ Your job at the bedside is to exclude dangerous mimics, then lean heavily into reassurance for the patient and family.

Conclusion

Transient Global Amnesia is a striking but ultimately self-limited amnestic syndrome: sudden onset, hours of repetitive questioning, then full recovery. If you recognise the pattern early, you can avoid over-treating it as stroke or epilepsy, minimise unnecessary investigations, and – most importantly – provide calm, confident reassurance to a very frightened patient and their relatives.

📚 References

• Hodges JR, Warlow CP. Syndromes of transient amnesia. J Neurol Neurosurg Psychiatry. 1990;53:834-843.
• Fisher CM, Adams RD. Transient global amnesia. Trans Am Neurol Assoc. 1964;89:143-147.
• Bartsch T, Deuschl G. TGA: functional anatomy and clinical implications. Lancet Neurol. 2010;9:205-214.
• Sattler JM, Rabinstein AA. Transient global amnesia. Mayo Clin Proc. 2019;94:662-672.