Amnesia

• 1. Introduction

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  Amnesia, in the words of author Jonathan Lethem, is mostly a rumor once you leave fiction behind. Real, diagnosable amnesia, people getting knocked on the head and forgetting their names, is a rare condition, and usually a brief one, he writes in the introduction to his anthology The Vintage Book of Amnesia. Yet amnesia is very real: a deficit in memory caused by brain damage or brain disease, though it can also appear temporarily after the use of a sedative or hypnotic drug. The resulting memory loss can be partial or total, depending on how much damage occurred. Two broad types account for most cases: retrograde amnesia, the inability to recall information from before a particular date, sometimes reaching back decades, and anterograde amnesia, the inability to move new information from short-term into long-term memory. The two are not mutually exclusive and can strike the same person at once. What separates these two patterns inside the brain, and why has so much of what we know about memory come from a small number of patients who lost the ability to keep their own?

• 2. Inside The Damaged Brain

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  Case studies consistently point to damage in the medial temporal lobe as the common thread running through amnesia, with the CA1 region of the hippocampus singled out as especially important for memory. Damage to the diencephalon can produce amnesia as well. A more recent line of research found that mice with damaged memory carried lower levels of a protein called RbAp48 than healthy mice, pointing to a specific molecular deficiency behind some memory loss. Anterograde amnesia in particular traces to damage in the medial temporal lobe or the medial diencephalon, with causes ranging from long-term alcoholism and severe malnutrition to stroke, head trauma, encephalitis, surgery, and Wernicke-Korsakoff syndrome; because the loss stems from neurons that no longer exist, no drug can reverse it, though structured daily routines can still strengthen a patient's remaining procedural memory. A cluster of anterograde amnesia cases among opioid users in Boston, Massachusetts, has more recently been linked to fentanyl use. Retrograde amnesia instead traces to the hippocampus itself, the structure responsible for encoding new memory in the first place, and researchers believe long-term memories consolidate gradually, moving from the hippocampus into more permanent storage in the cortex over years, which is why patients with hippocampal damage often recall childhood normally while losing the handful of years just before their injury. Doctors generally sort the causes of amnesia into three broader categories. Head trauma covers any direct injury or action against the brain, including electroconvulsive therapy, which can trigger both retrograde and anterograde amnesia in the patient receiving it. Traumatic events are more subjective, defined by whatever the individual experiences as too distressing to hold onto, such as a person forgetting a fatal, graphic car accident involving loved ones, a pattern known as dissociative amnesia. Physical deficiencies, a smaller category, include conditions such as Alzheimer's disease, the neurological condition anti-NMDA receptor encephalitis, and vitamin B12 deficiency. Alcohol belongs in its own bracket: beyond causing blackouts, it can permanently damage the brain's capacity to form memories.

• 3. What The Amnesiac Still Knows

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  A patient known as LSJ lost her retrograde declarative memory after bilateral medial temporal lobe damage, yet she could still read music and apply the watercolor painting techniques from her professional career, in fact outperforming a healthy control group on those specific skills. Her case illustrates how declarative memory, which splits into semantic memory for plain facts and episodic memory for personal events, can fail in some domains while sparing others entirely. Semantic knowledge can survive surprisingly well elsewhere, too: a man known as H.M. could accurately draw a floor plan of the home he had lived in after his surgery, even though he had not set foot there in years. Episodic memory tells a different story, since the CA1 region of the hippocampus cannot properly connect to the cortex once it is damaged, leaving patients with lesions there unable to form new episodic memories; researchers have traced this same CA1 damage to at least one documented case of transient global amnesia. Non-declarative memory, by contrast, often survives largely intact. Patients including K.C. and H.M. retained perceptual priming, completing word fragment tasks correctly and faster after prior exposure to related words despite having no conscious memory of that exposure. fMRI studies show that acquiring this kind of procedural memory activates the basal ganglia, the premotor cortex, and the supplementary motor area, brain regions not normally tied to declarative memory formation at all. Whether pure motor skills count as fully non-declarative remains disputed, since some researchers argue they still depend partly on declarative knowledge.

• 4. Other Forms Of Amnesia

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  Transient global amnesia can be visualized directly: diffusion-weighted MRI sometimes reveals abnormalities in the hippocampus during an episode, though symptoms typically clear within a single day and researchers still debate whether the trigger is a brief drop in blood flow, a seizure, or an atypical migraine. Post-traumatic amnesia generally follows a head injury and can mix anterograde and retrograde features; even mild trauma, such as a car accident causing no more than whiplash, can erase the moments just before impact, and more severe cases can leave a person temporarily unable to recognize the people around them. Childhood amnesia, the common inability to recall one's own earliest years, was once attributed by Sigmund Freud to sexual repression; most modern research instead points to brain development, including the fact that most adults cannot remember anything from before age two or three. Repressed memory, formerly called psychogenic amnesia, describes an inability to recall stressful or traumatic events even though the memory itself remains stored, blocked by psychological defense mechanisms rather than erased outright; some patients later recover part or all of what they had lost. Dissociative fugue, in which a person forgets or grows confused about their own identity and sometimes travels hundreds of miles from home, is exceptionally rare in practice; in one study of five people with the condition, two had committed crimes during their fugue state despite having no prior criminal record. Posthypnotic amnesia occurs when suggestions made during hypnosis erase memory of events that happened during the session, an effect research has shown can be selective rather than total. Lacunar amnesia leaves a single gap, a lacuna, in memory for one specific event, typically traced to damage in the limbic system. Korsakoff's syndrome, caused by a vitamin B deficiency usually tied to long-term alcoholism, combines both anterograde and retrograde amnesia and is closely associated with confabulation, in which patients unknowingly fill memory gaps with invented details. Drug-induced amnesia is deliberate: doctors sometimes use a premedicant such as midazolam, flunitrazepam, propofol, or scopolamine to erase a patient's memory of a traumatic medical procedure performed without full anesthesia. Source amnesia, the inability to recall where or how a fact was learned while still retaining the fact itself, can leave people vulnerable to false memories.

• 5. Coping And Treatment

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  No medication exists to cure amnesia itself, but treating an underlying condition, such as low thyroid function, liver or kidney disease, stroke, depression, bipolar disorder, or blood clots in the brain, can sometimes improve memory. Wernicke-Korsakoff syndrome responds specifically to replacing thiamine, the vitamin it depletes, through foods such as whole grain cereals, legumes, nuts, lean pork, and yeast. Treating alcoholism and stopping illicit drug use can prevent further damage, though in most cases it will not recover memory already lost. Cognitive and occupational therapy instead work with what remains: therapists help patients build on the memory skills they still have, find new retrieval strategies, and organize information so it is easier to hold onto. Technology fills some of the remaining gaps. A personal digital device can hold reminders for appointments, medication times, and birthdays, while low-tech aids such as notebooks, wall calendars, pill organizers, and photographs of family, friends, and coworkers serve the same purpose. How far a person ultimately recovers, and how long the amnesia lasts, depends mostly on the type and severity of the underlying brain injury.

• 6. Ribot's Law And Henry Molaison

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  French psychologist Theodule-Armand Ribot was among the first scientists to systematically study amnesia, and the law that bears his name describes a time gradient in retrograde amnesia: patients lose their most recent memories first, personal memories second, and intellectual memories last. The most influential single case, though, belonged to a patient long known only as H.M., first reported by neurosurgeon William Beecher Scoville and psychologist Brenda Milner in a 1957 paper. Henry Molaison had developed severe epilepsy after a bicycle accident at age nine, and when drugs failed to control his seizures, Scoville performed a bilateral medial temporal lobe resection on him in 1953, removing large portions of both anterior medial temporal lobes. His seizures improved, but Molaison lost the ability to form new long-term memories; given a list of words, he would forget them within about a minute, along with the fact that he had ever been given a list at all, even though his digit span and short-term memory tested as completely normal. Asked to trace a shape while watching his hand only in a mirror, he could never recall having done the task before, yet his performance steadily improved with repetition, proof he was still learning unconsciously even as his conscious memory failed him. A follow-up study fourteen years after his surgery found Molaison still unable to recall anything that had happened since the operation, though he could discuss national and international news; asked about his own life, he had nothing to offer. When he died, Molaison donated his brain to science, and researchers were able to confirm that the damage responsible for his amnesia centered on the medial temporal lobe.

• 7. Three More Landmark Patients

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  Clive Wearing, a conductor and musician, lost his memory after contracting a herpes simplex virus infection that damaged his hippocampal regions; from that point on, he could not hold new information for more than a few moments, and he reported feeling as though he had just regained consciousness every single time his memory reset. Patient R.B. lived a normal life until age 52, three years after being diagnosed with angina and undergoing two heart surgeries; an ischemic episode during a heart bypass operation left him with a loss of new memory formation but almost no loss of memories from before the surgery, aside from a couple of years immediately preceding it. Only after his death did researchers examine R.B.'s brain and discover that his damage was restricted entirely to the CA1 region of the hippocampus, a finding that helped establish that single region's role in forming new memories. Patient G.D., a white man born in 1940 who had served in the Navy, developed chronic kidney failure and depended on hemodialysis for the rest of his life; in 1983 he underwent a parathyroidectomy and a left thyroid lobectomy, and cardiac complications from that surgery left him agitated and unable to recall what had happened to him even five days after leaving the hospital. Memory tests over the following years confirmed that G.D.'s impairment persisted for nine and a half years, until his death, after which his brain was donated, photographed, and preserved for further study.

• 8. Amnesia In Fiction

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  Author Jonathan Lethem traces literary amnesia back to Franz Kafka and Samuel Beckett, crediting the trope's spread through popular culture in large part to the influence of Sigmund Freud's ideas on genre films, especially film noir. The device is so common in movies that a recognizable stereotype has grown up around it, with an amnesiac character melodramatically asking, Where am I? Who am I? What am I?, or puzzling over their own name. Television sitcoms and soap operas have popularized another myth: that a second blow to the head, similar to the one that caused the amnesia, will cure it. In reality, a repeat concussion can cause cumulative cognitive damage and, in extremely rare cases, the deadly brain swelling known as second-impact syndrome. Fictional amnesia is also almost always retrograde, wiping out memories of the past while leaving the ability to form new ones intact; the film Memento stands out as one of the few well-known depictions of anterograde amnesia instead, following a protagonist who cannot create new long-term memories at all.