Memory misplaced

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Post written by Dr. Farida A. Malik , PGY3 Medical Resident, Monmouth Medical Center

Case Summary

This 69 year old lady had a remote history of breast cancer, hypertension and hypothyroidism.  She was brought to the Emergency Room by her husband because of abrupt onset confusion after waking up that morning. She was disoriented and was noted to ask the same questions over and over again. She had no difficulty walking, talking or dressing herself. She denied having headache or visual problems. There was no history of head trauma, seizures or any prior similar episodes.

When she was seen in the in the ER she knew her name and recognized her husband.  She was able to follow simple commands.  She had no recollection of events since morning or the day before. She repeatedly asked how she got to the hospital, despite being told several times that her husband brought her. Neurological examination otherwise was unremarkable.

CT scan of head, MRI of the brain and EEG were all normal.

She was diagnosed with TRANSIENT GLOBAL AMNESIA.

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The family was reassured about the benign nature of the condition and she was discharged home the next day still with memory lag.

Discussion

Transient global amnesia (TGA) is a clinical syndrome of reversible anterograde amnesia accompanied by repetitive questioning that occurs in middle-aged and elderly individuals.

The incidence of TGA is 5.2 to 10 per 100,000 per year overall, but 23.5 to 32 per 100,000 per year in adults aged 50 and over.

During a TGA episode recall of recent events simply vanishes. One may also draw a blank when asked to remember things that happened a day, a month or even a year ago.  Unlike “soap opera amnesia” (Jason Bourne) affected patients do remember who they are and recognize the people they know well.  But that doesn’t make their memory loss less any less disturbing.

Fortunately, episodes are usually short-lived, recover spontaneously, and are unlikely to recur.

The precise cause of TGA is unknown.  Atherosclerotic risk factors (eg. hypertension, diabetes, hypercholesterolemia) are not associated with TGA.
However there may be a link between TGA and history of migraines.

The primary site of neurologic functional disturbance is the medial temporal lobe and hippocampus.
The_hippocampus
The pathogenesis of this transient disruption is unknown. Current theories include arterial ischemia, venous congestion, and migraine, but no theory explains all of the clinical features.

The diagnosis is made by the following signs and symptoms:

  • Sudden onset of memory loss, verified by a witness
  • Retention of personal identity despite memory loss
  • Normal cognition, such as the ability to recognize and name familiar objects and follow simple directions
  • Absence of signs indicating damage to a particular area of the brain, such as limb paralysis, involuntary movement or impaired word recognition
  • Duration of no more than 24 hours
  • Gradual return of memory
  • No evidence of seizures during the period of amnesia
  • No history of active epilepsy or recent head injury

Some common triggers identified are:

  • Sudden immersion in cold or hot water
  • Strenuous physical activity
  • Sexual intercourse
  • Medical procedures, such as angiography or endoscopy
  • Mild head trauma
  • Acute emotional distress, as might be provoked by bad news, conflict or overwork

There are no confirmatory diagnostic tests. The initial evaluation and management of patients with TGA focuses on excluding other diagnoses and should include the following:

  • If the patient is symptomatic on presentation, the patient should be observed in the hospital until the amnesia resolves.
  • Diagnostic testing includes oxygenation status, serum electrolytes, glucose, and a toxicology screen.

The need for further testing varies depending on the circumstances, such as how typical the event is for TGA, the presence of vascular risk factors, and whether the ictus was observed. Patients with recurrent or brief episodes, or activity suggesting motor automatism should be evaluated with EEG for possible epilepsy. A neuroimaging study may be performed in all patients, preferably a brain MRI with DWI, to exclude acute ischemia, head trauma, and other causes.

Treatment is not required for TGA. The condition usually does not recur, and the patient does not need to be restricted from driving unless events are recurrent.

There is no increased risk of mortality, epilepsy, or stroke following TGA as compared with age-matched controls.

Amnesia, it’s not just for soap operas

When people of think of amnesia, they usually first think of the mysterious stranger in a soap opera, who shows up in town after an accident or traumatic experience, having forgotten their own identity, and the efforts that ensue to uncover the missing information.

Actually, in medical practice this type of “soap opera” amnesia is psychogenic, a so-called psychogenic fugue state, very different from the amnesia seen with organic neurologic disorders like head trauma or stroke.

The character Dory in the 2003 Pixar Movie Finding Nemo is a better representation of organic neurologic amnesia – she has anteriorgrade amnesia and cannot retain new information, but remembers her name and other details of her own identity.

Another good example of organic anteriograde amnesia is the media is Leonard in the 2000 movie Memento,

It is thought that new memories are formed by a structure of the brain known as the Papez ciruit or limbic system, which includes the hippocampus, (subiculum), fornix, mammillary bodies, anterior thalamic nucleus, cingulum, and entorhinal cortex.

MammillaryBodies1

Any lesion or process which interrupts this circuit will prevent the formation of new memories, leading to anteriograde amnesia.

Temporary Anteriograde amnesia can be caused by:

zzzzmedications, benzodiazepine anesthesia or “conscious sedation“,

zzzzhead trauma – post-traumatic amnesia or PTA,

zzzzand from Transient Global Amnesia (TGA).

TGA is a sudden onset of temporary anteriograde amnesia usually lasting lasting 4-12 hours.  It is often triggered by an emotional event or sexual intercourse.   During the episode, the affected patient is alert and lucid, cognizant of their own identity, but appears perplexed and may ask the same questions repeatedly.  The exact cause is unknown.  The recurrence rate is low.

More permanent anteriograde amnesia can be caused by:

zzzzinfarction of the hippocampi, as can be seen in the cardioembolic stroke syndrome “top of the basilar syndrome”,

zzzzbrain damage resulting from herpes encephalitis,

zzzzor from hemorrhage into the mamillary bodies – “Korsakoff’s psychosis”.

Korsakoff

Korsakoff’s psychosis is caused by thiamine deficiency, usually related to chronic alcoholism.  Affected patients have permanent anteriograde amnesia, and so they live in the past, and confabulate (make up details) to fill in the gaps in their memory.