CASE A 63-year-old woman came to our emergency department with her fiancé following an abrupt onset of confusion that began 1 hour earlier. The patient had been working outside in the yard when she approached her fiancé, repeatedly asking where she was and what she was doing. She remained conscious of her identity, however, and exhibited no other neurologic symptoms, such as muscle weakness, gait imbalance, sensory loss, vision changes, slurred speech, or facial droop. The fiancé did not witness any loss of consciousness, head trauma, or seizure-like activity.
Before the event, the patient was feeling well, without any fever, headache, emesis, or vertigo. She denied using tobacco, alcohol, or illicit drugs. Her medical history was unremarkable, including an absence of diabetes, hypertension, and hyperlipidemia. The only significant finding in her family history was a stroke her mother experienced at an advanced age. During our interview, the patient remained confused about where she was and what was happening. She was aware of her confusion and distressed by it.
On examination, the patient was alert and oriented to self and year. She appeared appropriately anxious about her situation. She was afebrile and slightly hypertensive. Her other vital signs were normal. She could not recall events immediately preceding her arrival at the emergency department, but could recall events of the day before and earlier. There was no evidence of trauma. Head, neck, cardiovascular, lung, and abdominal exams were within normal limits.
Her neurologic exam revealed intact cranial nerves, symmetric face, 5/5 muscle strength in all extremities, intact sensation, and normal gait. Grossly, visual fields were intact. There was no Babinski sign, clonus, or pronator drift. She had 3/3 immediate recall of named objects, but 0/3 recall at 5 minutes. Results for complete blood count, basic metabolic panel, and urinalysis were within normal limits, including a blood glucose level of 77 mg/dL and a low-density lipoprotein level of 161 mg/dL. The result for cardiac enzymes was negative. Noncontrast computed tomography of the head revealed a remote pontine lacunar infarct.
WHAT IS THE MOST LIKELY EXPLANATION FOR HER CONDITION?
Transient global amnesia
We admitted the patient for further evaluation with a presumptive diagnosis of transient global amnesia (TGA).
With a chief complaint of amnesia, the differential diagnosis is broad (TABLE 1).1-3 In this case, a stroke was unlikely given the absence of neurologic deficits, specifically the lack of visual field defects. The elapsed time of her symptoms was too long for a transient ischemic attack or seizure. There was no supporting evidence for encephalitis, intracranial bleed, or hypoglycemia. While delirium could be considered, its characteristic features of inattention and a waxing and waning course were not present, nor was there any obvious underlying cause, such as infection or polypharmacy. The patient had no loss of self-identity that would suggest a psychogenic cause. The time course and the patient’s symptoms were congruent with the clinical criteria for TGA, and we confidently based our diagnosis on this.
TABLE 1
Rule out these disorders with acute anterograde amnesia1-3
| Transient ischemic attack |
| Delirium |
| Intoxication or alcohol/drug withdrawal |
| Concussion |
| Intracranial bleed |
| Complex partial seizures |
| Postictal state |
| Hypoglycemia |
| Encephalitis |
| Transient global amnesia |
| Psychogenic amnesia |
| Wernicke’s encephalopathy |
Type of memory loss as a clue to cause
Amnesia occurs when memory and learning in an alert person are impaired to a degree out of proportion to the person’s overall neurologic status. It may affect the formation of new memories (anterograde amnesia) or the recall of past memories (retrograde amnesia).
How memory works. Memory can be broken down into categories (TABLE 2).1 Explicit memory requires a conscious effort to recall. An example is episodic memory, in which memories are framed within a context, such as recalling what was served for dinner the night before. Its function is critical to creating new memories. Other forms of explicit memory are semantic memory—memorized facts that are independent of a context—and working memory, in which focused attention is used to manipulate information. Implicit memory operates subconsciously. The prime example is procedural memory, involving the ability to learn new skills and perform them without total concentration.
Memory function affected in TGA. In TGA, episodic memory—critical in the laying down of new memories—is most affected. Episodic memory relies heavily on the hippocampus to function correctly. When it dysfunctions, a person cannot consolidate and retain new information, thus resulting in anterograde amnesia.1
Retrograde amnesia generally requires dysfunction of the frontal lobe in addition to the temporal lobe.3 However, it may be present concurrently with anterograde amnesia when a lesion is isolated to the hippocampus; it is usually limited to more recent memories. That recent memories tend to be the more vulnerable is known as Ribot’s law. If retrograde amnesia is present, it usually resolves before anterograde amnesia.4