Skip to main content icon/video/no-internet

Amnesia is a memory disorder characterized by a profound impairment in establishing new memories of people, places, and events and a deficit in retrieving information acquired prior to the onset of illness. It is important to note that amnesia is not an all-or-none condition—it is functionally diverse and its severity varies based on etiology and lesion extent. However, despite the heterogeneity observed across patients, some fundamental characteristics can be established. This entry presents an overview of the syndrome, including the different subtypes of amnesias and their behavioral and neurological characteristics.

Broadly speaking, amnesic patients are unable to consciously bring to mind information encountered after the onset of injury (anterograde amnesia), despite preserved general intelligence and other cognitive functions, such as language. In this sense, their cognitive deficit is selective (i.e., limited to memory). The memory impairment is often described as “global” because patients' inability to form new memories is ubiquitous across different types of material (e.g., verbal vs. visuospatial) and different modes of presentation (e.g., visual or auditory). Amnesic patients typically also have some difficulty recalling information acquired prior to the onset of injury (retrograde amnesia), but the temporal extent of retrograde memory loss is quite variable.

One of the most striking case reports of amnesia is that of patient H. M. As an experimental treatment for intractable epilepsy, H. M. underwent surgery that removed his medial temporal lobes (MTLs) bilaterally at the age of 27. Although the surgery was largely successful in relieving H. M.'s epileptic seizures, it left him with a profound amnesia, which H. M. described as “like waking from a dream … every day is alone in itself.” His anterograde memory loss was apparent both in his daily life and in laboratory testing. For instance, H. M. could not remember where he lived or what he ate for breakfast earlier that day. In laboratory testing, he failed to recall anything about a drawing that he copied merely minutes earlier. This pattern of forgetting was observed across different types of materials and presentation formats (e.g., spoken words, pictures, abstract patterns, spatial locations). H. M. also experienced retrograde memory loss that extended years prior to his surgery.

It is important to distinguish the memory loss experienced by amnesic individuals and that experienced by patients with more global cognitive decline (e.g., dementia). Whereas amnesics' cognitive impairments are memory-specific and fairly stable, dementia patients' cognitive decline tends to be global and progressive.

Etiologies and Neuroanatomical Correlates

Amnesia can result from a variety of causes, ranging from psychogenic (e.g., dissociative disorders) to organic. The focus here is on the organic, neurological conditions that are associated with amnesia. Although lesion location (and extent) as well as symptoms vary as a function of etiology, the pattern that emerges is that the MTL and the diencephalon (including the hypothalamus, thalamus, and epithalamus) are crucial to normal memory functions. Additional frontal lobe damage may lead to deficits in executive and strategic components of memory as well. The most common etiologies are highlighted in this section.

Herpes Simplex Encephalitis (HSE)

HSE is a viral infection that results in hemorrhagic lesions in the brain. In the acute phase, HSE patients are typically confused and disoriented, and they may also exhibit other cognitive impairments, including agnosia, aphasia, and amnesia. The course of illness is variable. In some patients, agnosia and aphasia resolve, and patients are left with a profound amnesia, in the absence of other cognitive deficits. Other patients continue to experience multiple cognitive problems, and yet others recover fully. HSE is associated with damage to the MTL, including the amygdala, hippocampus, and adjacent entorhinal, perirhinal, and parahippocampal cortices. In many cases, damage extends laterally to include the anterolateral and inferior temporal cortex; this damage may be linked to aphasic and agnosic symptoms in some patients. Lateral lesions have also been associated with extensive retrograde amnesia. When the lesion extends anteriorly, it may impact the ventromedial frontal cortex, including the insular cortex and basal forebrain. Laterality effects have also been observed, in which patients with damage focused in the left temporal region tend to have deficits primarily in verbal memory, and patients with damage focused in the right temporal region tend to have deficits primarily in visual/nonverbal memory.

...

  • Loading...
locked icon

Sign in to access this content

Get a 30 day FREE TRIAL

  • Watch videos from a variety of sources bringing classroom topics to life
  • Read modern, diverse business cases
  • Explore hundreds of books and reference titles

Sage Recommends

We found other relevant content for you on other Sage platforms.

Loading