Acute Memory Loss

Abrupt memory loss developing over minutes to days can be a striking clinical picture. Often the symptom is initially mistaken for a confusional state. While some causes of abrupt memory loss may indeed overlap with confusion, others—transient global amnesia being perhaps the best example—are characterized by preserved cognitive function in all domains except memory.

A.

Initial evaluation should determine if the symptoms are indeed isolated to memory, or if other neurologic symptoms or signs are present. Special attention should be paid to impairment in level of consciousness (even if mild), witnessed convulsive activity, ataxia, eye movement abnormalities, and visual field defects.
B.

If symptoms are isolated to memory loss, the nature of the memory impairment can provide important diagnostic clues. Temporal-limbic memory loss, often involving hippocampal function and its extended network, is marked by an inability to form new episodic memories (anterograde amnesia) and some degree of retrograde memory loss for episodes prior to the presenting event. Retrograde memory loss tends to have a temporal gradient in which memories formed closest to presentation are often more affected than remote ones. If an individual has an isolated retrograde memory loss but is able to form new memories, this generally reflects an underlying psychiatric condition. If there is loss of personal identity, one should consider a dissociative fugue state. Alternatively, if there is intact personal identity, psychogenic amnesia, including conversion disorder, is more likely.
C.

If there is alteration of consciousness or the presence of multiple seizures, consider infectious or autoimmune temporal-limbic encephalitis. In these cases, brain magnetic resonance imaging (MRI) with contrast should be performed looking for medial temporal and temporal pole signal abnormality. Herpes simplex virus (HSV) encephalitis is an important consideration, particularly if fever is present; when considered, acyclovir should be started as soon as possible. Lumbar puncture should be performed and cerebrospinal fluid tested with HSV polymerase chain reaction (PCR) with cell count, protein and glucose levels measured; autoimmune/paraneoplastic panels should be considered in the appropriate clinical context.
D.

The posterior circulation is the primary source of blood flow to the medial temporal lobe and thalamic regions in the memory network. If memory loss is hyperacute and associated with acute-onset focal neurologic findings such as double vision, visual field deficit, or hemisensory loss, posterior circulation stroke is likely. If present, brain MRI with diffusion weighted imaging will demonstrate infarction and confirm the diagnosis.
E.

Memory loss is common following prolonged or multiple seizures, particularly those emanating from the medial temporal lobe. If early recovery to baseline does not occur, electroencephalogram (EEG) monitoring should be pursued to evaluate for nonconvulsive status epilepticus.
F.

Relatively rapid memory loss in the setting of confusion or delirium, eye movement abnormalities, or ataxia should prompt consideration of Wernicke encephalopathy. A history of heavy alcohol use is common. Untreated, this can evolve into Korsakoff syndrome, which is associated with more isolated but often more profound amnesia. Immediate treatment with intravenous thiamine is required.
G.

The most common cause of isolated sustained anterograde memory loss is transient global amnesia (TGA), a benign though often frightening disorder for patients’ families. Memory loss generally lasts several hours, and there is no alteration of consciousness or other neurologic deficits. Due to their rapid rate of forgetting, patients repeatedly ask the same questions over and over, reflecting disorientation to place and time. TGA is often preceded by acute emotional events, strenuous physical activity, or pain. The underlying cause remains uncertain, with seizures, arterial or venous ischemia, and migrainous-type phenomena all proposed as explanations but with little supportive evidence. One should observe these patients to ensure the expected resolution of symptoms within 24 hours. If atypical features are present, brain MRI and EEG should be considered.
H.

Patients with recent cardiopulmonary instability, particularly in the intensive care unit setting, may have temporal-limbic memory loss due to the particular sensitivity of the hippocampus to hypoxia.