Continuing Education Activity
Short-term memory, also referred to as short-term storage, or primary or active memory, indicates different systems of memory involved in the retention of pieces of information for up to 30 seconds. This type of memory is a scratchpad for temporarily recalling a limited amount of data from the sensory register and processing it through attention and recognition. The hippocampal network, including the parahippocampal gyrus, hippocampus, and neocortical areas, is not where memories are stored but has a crucial role in forming new memories and their subsequent reactivation. Different clinical conditions, including strokes, brain aneurysms, traumatic brain injuries, primitive or metastatic neoplasms, and infectious diseases, such as encephalitis, may impair various components of memory.
This activity describes the characteristics of short-term memory, the causes of short-term memory impairment, and the role of the interprofessional team in evaluating and treating patients with related conditions. Regardless of etiology, memories of recent events are most vulnerable, whereas older memories are more resilient and protected from damage. Participating clinicians are equipped with the necessary knowledge and tools to treat acutely and chronically ill patients within an interprofessional team.
Objectives:
Determine the pathophysiology of short-term memory impairment due to traumatic or non-traumatic etiologies.
Identify the clinical features of patients with short-term memory impairment.
Assess the therapeutic approaches for enhancing memory tasks in patients with short-term memory impairment.
Collaborate within interprofessional teams to improve outcomes for patients with short-term memory impairment.
Introduction
Short-term memory is also called short-term storage, primary memory, or active memory. The term indicates different systems of memory involved in retaining pieces of information, or memory chunks, for a relatively short time, typically up to 30 seconds. In contrast, long-term memory may hold indefinite information. However, the difference is not just the time variable but also their overall functionality. Nevertheless, the 2 systems are closely related.
Practically, short-term memory functions as a temporary scratchpad for recalling a limited amount of data, typically around 7 ± 2 items, in the verbal domain, based on George Miller's concept. This information originates from the sensory register and can be processed through attention and recognition. In contrast, information collected in long-term memory storage consists of memories for performing actions or skills, such as procedural memories (knowing how), and memories of facts, rules, concepts, and events, such as declarative memories (knowing that). Declarative memory includes semantic and episodic memory. The former concerns broad knowledge of facts, rules, concepts, and propositions (general knowledge), whereas the latter concerns personal and experienced events and the contexts in which they occurred (personal recollection).[1]
Although short-term memory is closely related to the concept of working memory, both are distinct entities. Short-term memory is a set of storage systems, whereas working memory indicates the cognitive operations and executive functions associated with the organization and manipulation of stored information. Nevertheless, the terms short-term memory and working memory are often used interchangeably. Short-term memory must also be distinguished from sensory memory, such as the acoustical echoic and iconic visual memories, which are shorter in duration, typically fractions of a second, and reflect the stimulus's original sensation or perception. In other words, sensory memory is specific to the stimulus modality of presentation. This raw sensory information undergoes processing and, upon processing to short-term, is expressed in a format different from that perceived initially.
The famous Atkinson and Shiffrin (or multi-store) model, proposed in the late 1960s, explains the functional correlations between different types of memory.[2] Many studies demonstrated the anatomical and functional distinctions between memory processes, neural correlates, and the functioning of short-term and long-term memory subsystems. In light of these findings, several memory models have been postulated.[3][4] Although some authors suggested a single memory system encompassing both short- and long-term storage after 50 years, the Atkinson and Shiffrin model remains a valid approach for explaining the memory dynamics.[5] In light of recent research, however, the model has several problems, mostly concerning the characteristics of short-term memory, the relationship between short-term and working memory, and the transition from short- to long-term memory.
Short-Term Memory
Short-term memory is a storage system that includes several subsystems with limited capacity. Rather than a limitation, this restriction is an evolutionary survival advantage, as paying attention to limited but essential information, excluding confounding factors, is important. A classic example in biology is prey, which must focus on the hostile environment to recognize a possible attack by the predator. Given the functional peculiarities of short-term memory, which involves the collection of sensory information, the subsystems are closely related to the modalities of sensory memory. Consequently, several sensory-associated subsystems have been postulated, including the visuospatial, phonological (auditory-verbal), tactile, and olfactory domains. These subsystems involve patterns and functional interconnections with the corresponding cortical and subcortical areas and centers.
The Concept of Working Memory
In 1974, Baddeley and Hitch developed an alternative model called working memory.[6] This model does not exclude the modal model but rather enriches the contents. The short-term store can be used to characterize the functioning of the working memory. Working memory refers to the entire theoretical framework of the structures and processes used for storing and temporarily manipulating information, of which short-term memory is only a component. In other words, short-term memory is a functional storage element, whereas working memory is a set of processes involving storage phases. Working memory is constantly used when we have to understand new information, solve a problem, or make an argument, and it is the cognitive strategy for achieving short-term goals. The importance of this type of operating system of memory is demonstrated by the evidence showing that working memory deficits are associated with several developmental disorders of learning, including attention-deficit hyperactivity disorder, dyslexia, and specific language impairment.[7]
A recent study on working and short-term memory in children with attention-deficit hyperactivity disorder suggested that these children had an inadequate hemodynamic response in a region of the brain that underlies phonological working memory. Functional near-infrared spectroscopy is a cost-effective, noninvasive neuroimaging technique that localizes and quantifies neural activation patterns related to executive functions.[8] Another study suggested that working memory impairment and attention lapsing are general features of psychotic disorders. Findings regarding capacity estimates from the Change Localization and Detection tasks related to functional capacity and outcome also implied that these methods may be useful in a clinical context.[9]
Short-Term and Long-Term Memory
Short-term and long-term memory can be distinguished based on storage capacity and duration. Short-term memory has limitations in the amount and duration of information maintained. In contrast, long-term memory features a seemingly unlimited capacity that can last years. The functional distinctions between memory storage systems and the exact mechanisms for how memories transfer from short-term to long-term memory remain controversial. Do short- and long-term memory represent 1 or more systems with specific subsystems? Although short-term memory probably represents a substructure of long-term memory, a form of long-term–activated storage, rather than looking for a physical division, verifying the mechanisms involved in transitioning from short-term to long-term memory seems appropriate. Although the classic multi-modal model proposed that the storage of short-term memories occurs automatically without manipulation, the matter seems more involved. The phenomenon concerns quantitative (number of memories) and qualitative (quality of memory) features.
Regarding quantitative data, although the number of Miller of 7 ± 2 items identifies the number of elements included among individual slots, grouping memory bits into larger chunks (chunking) can allow for greater storage capacity. The qualitative issue, or memory modulation within processing, is fascinating. Short-term memory elements undergo processing, providing a sort of editing involving each element's fragmentation (chunking) and re-elaboration. This phase of memory processing is called encoding and can condition subsequent processing, including storage and retrieval. The encoding process encompasses automatic (without conscious awareness) and effortful processing (through attention, practice, and thought) and allows us to retrieve information to make decisions and answer questions. Three pathways are followed during the encoding step—visual (information represented as a picture), acoustic (information represented as a sound), and semantic encoding (the meaning of the information). These processes interconnect, breaking down information into various components. During recovery, the pathway that has produced the coding facilitates the recovery of the other components through a chain reaction. A particular perfume, for instance, makes us recall a specific episode or image. The encoding process affects the recovery, but the recovery undergoes potential changes that can alter the initial content.
In neurofunctional terms, the difference is the occurrence in long-term memory of a series of events that must definitively fix the engram(s). This effect occurs through the establishment of neural networks and is expressed as a neurofunctional phenomenon, including long-term potentiation, which is an increase in the strength of the neural transmission deriving from the strengthening of synaptic connections. This process requires gene expression and the synthesis of new proteins and is related to long-lasting structural alterations in the synapses (synaptic consolidation) of the brain areas involved, such as the hippocampus in declarative memories.
The Role of the Hippocampal Network
Hippocampal neurogenesis regulates the maintenance of long-term potentiation.[10] However, the hippocampal network, including the parahippocampal gyrus, hippocampus, and neocortical areas, is not the storage site for memories but plays a crucial role in forming new memories and their subsequent reactivation. The hippocampus appears to have a limited capacity but acquires information quickly and automatically. Over time, the initially available information is permanent in other brain structures, particularly the cortex), independently from the activity of the hippocampus itself. The crucial mechanism of this transfer involves the reactivation (replay) of neural activity configurations.
In other words, the connected hippocampus and the medial temporal structures are crucial for holding an event as a whole as they distribute memory traces in an organized manner. The operating system can store, organize, process, and recover hardware files through different software. This hippocampal-guided reactivation (retrieval) leads to the creation of direct connections between the cortical traces and then to the formation of an integrated representation in the neocortex, including the visual association cortex for visual memory, the temporal cortex for auditory memory, and the left lateral temporal cortex for knowledge of word meanings. Moreover, the hippocampus has other specific tasks, such as spatial memory organization.
Recent reviews summarized the progress of hippocampal circuits and functions based on sharp-wave ripples. These ripples are crucial for consolidating spatial, episodic, and social memories in different hippocampal-cortical pathways. Dysregulation of sharp-wave ripples contributes to cognitive impairments in neurodegenerative and neurodevelopmental diseases.[11] Other brain areas are involved in memory processes; for example, learning motor skills has links to the activation of the cerebellar regions and brainstem nuclei. Learning perceptive activities, including improvements in processing perceptive stimuli essential in everyday life activities such as understanding spoken and written language, involves basal ganglia and sensory and associative cortices. In contrast, learning cognitive skills related to problem-solving involves the medial temporal lobes.
Etiology
Different clinical conditions, including strokes, brain aneurysms, traumatic brain injuries, primitive or metastatic neoplasms, and infectious diseases, may impair various components of short-term memory. However, the damage to short-term memory is seldom selective. For example, aneurysm rupture can lead to short-term and long-term memory loss. Apart from diseases that induce short-term memory alterations through direct neural damage, a wide range of medical conditions such as systemic infections; thyroid diseases; surgery, including neuroinflammation-mediated postoperative delirium and postoperative cognitive dysfunction; or psychiatric diseases, including depression; or psychological trauma can also impact short-term memory.[12] In this regard, evidence shows that violence during childhood impairs cognitive processes, including memory (psychogenic amnesia). Cancer treatments, including radiation and chemotherapy, can induce short-term damage through a complex neuroinflammation mechanism.[13][14]
Previous studies mentioned that sports-related concussions occur in approximately 21% of college athletes, with implications for long-term cognitive impairments in working memory.[15] Furthermore, a neuropsychological study on the effects of Boxing Upon Athletes' Memory suggested that 1 year of boxing training can impair the boxers' working memory, short-term memory, and long-term memory. In conclusion, boxers should strengthen their head protection during training to prevent frequent impacts to the head.[16] Neurodegenerative conditions are paramount causes of memory impairment. For instance, 1 of the first signs of dementia is short-term memory loss.
In particular, memory loss without interference in daily life or independent function is the main feature of mild cognitive impairment, which represents the stage between the expected cognitive decline of normal aging and the more severe decline observed in Alzheimer disease. A recent study showed that the difference between mild cognitive impairment and visual short-term memory from normal cognitive aging is evident only where the spatial configuration of stimuli is retained at original locations. Findings also revealed a reduced ability to inhibit irrelevant items and location priming (by repetition) deficits. However, visual short-term memory for simultaneous items declines significantly in normal aging but is not influenced differently by spatial or object configuration change.[17] Moreover, alterations in different memory domains have been shown in Parkinson disease, in those affected by Huntington disease, and in primary progressive aphasia.[18][19][20]
Recent reviews reported impairments of executive function in primary progressive aphasia. Executive functions pertain to a set of cognitive processes, specifically shifting, inhibition, and updating of working memory, and are involved in the cognitive control of behavior. Results revealed that the primary progressive aphasia variant and disease duration were significant moderators of performance, whereas task modality and years of education were not. The non-fluent or agrammatic primary progressive aphasia and the logopenic primary progressive aphasia variants were similarly affected, but the semantic variant was affected to a lesser extent.[21] Another study described the semantic variant of primary progressive aphasia as a progressive loss of semantic knowledge impairing the ability to name and recognize the meaning of words, which can be improved through learning therapy.[22]
Other conditions that impair memory tasks include alcohol and drug abuse, such as marijuana; heavy cigarette smoking; sleep deprivation; severe stress; and vitamin B12 deficiency. Prolonged alcohol intake can lead to Korsakoff syndrome, which is a complex amnestic disorder with neuropsychological sequelae caused by vitamin B1 (thiamine) deficiency. In addition to alcohol, other causes can lead to vitamin B1 deficiency (non-alcoholic Korsakoff syndrome) with related memory disorders, including dietary deficiencies, prolonged vomiting, and eating disorders. Korsakoff-like amnestic syndromes have also been observed after brain lesions involving the anteromedian thalamus and hippocampus.[23]
Recent reviews have emphasized the crucial role of the prefrontal cortex in mediating executive functions and organizing a person's thinking, decision, and behavior, particularly to stress. Stress activates the hypothalamic-pituitary-adrenal axis, releasing prefrontal neurotransmitters, with dopamine neurotransmission responding as a stress modulator. Different reviews showed that stressful events are associated with increased dopamine concentrations in the medial prefrontal cortex. This increase affects working memory by causing an inability to process information selectively and impairing cognitive function.[24]
Among other causes of memory impairment, a common adverse effect of electroconvulsive therapy is short-term memory alteration during treatment. Another notable concern is medication-induced memory loss. The list of drugs implicated includes benzodiazepines, antiepileptic drugs, opioids, and tricyclic antidepressants.[25][26][27] Limited evidence, primarily from observational data and case reports, is available regarding statin use and memory loss. Most of these drugs, such as benzodiazepines, impair memory processing and, in turn, can present an obstacle to the consolidation of information.[28][29]
Epidemiology
Epidemiological data are related to different conditions that induce memory impairment. For instance, concerning neurodegenerative diseases, about 15% to 20% of people aged 65 or older have mild cognitive impairment, with approximately one-third of them developing Alzheimer disease within 5 years of follow-up.[30] Furthermore, the prevalence of existing cases of Alzheimer disease is 5.8 million Americans, and estimates suggest that the annual number of new cases (incidence) of all types of dementia is expected to double by 2050.[31] Mild cognitive impairment is a syndrome of memory impairment with normal activities of daily living but may precede dementia for several years.
According to a recent study, around 5% to 15% of individuals with mild cognitive impairment progress to dementia annually. The prevalence of dementia in Blacks is almost twice compared to that of Whites.[32][33] In China, the population older than 60 is expected to increase approximately from 12% in 2010 to 33% of the overall population by 2050. Therefore, the increase in the aging population is projected to result in an Alzheimer disease prevalence of 27.7 million people in China by 2050.[34] Parkinson disease affects approximately 1% of the population older than 60, whereas the incidence of Huntington disease is 0.38 per 1,00,000 per year.[35][36] For non-neurodegenerative conditions, estimating epidemiological data is challenging as memory decline is not always in the clinical picture.
Pathophysiology
The Amnestic Syndrome
The amnestic syndrome is an impairment in the ability to form new memories. Regardless of its etiology, the memories of recent events are particularly vulnerable, whereas long-term memory is more resilient and protected from damage. This concept is not new; towards the end of the 19th century, the French psychologist Theodule-Armand Ribot (1839-1916) demonstrated that amnesia affects memories in reverse order of their development.[37] This idea underscores the importance of distinguishing between anterograde and retrograde amnesia. The former concerns the new memories, whereas the latter is well-established by neural networks. This distinction explains why some conditions involving drugs, such as benzodiazepines, can lead to a deficit, especially within short-term memory. In turn, amnestic disorders primarily affect anterograde memories. A recent study on short-term memory binding has identified amnestic mild cognitive impairment as the most typical preclinical stage of Alzheimer disease. Neuropsychological measures are relatively sensitive and specific diagnostic tools for amnestic mild cognitive impairment, although they do not replace the utility of biomarkers.[38]
Neural Correlates for Short-Term Memory
Research has shown that lesions in the prefrontal cortex of primates lead to short-term memory alterations. Depending on the affected brain area, specific modifications occur in different domains of short-term memory. The assumption is that these other components express different neuronal correlates. In this regard, neuroimaging studies reported significant information. For instance, the major neural correlates of the phonological short-term memory subtype are the inferior parietal lobule, frontal premotor regions, and insula in the dominant hemisphere.[39] Depending on the type of function, the cerebral areas appointed to the phonological aspects of verbal short-term memory are the inferior parietal cortex left for the phonological warehouse and the Broca area for articulatory revision. Neuroimaging studies have also shown that the neural correlates of spatial short-term memory involve the occipital extrastriate, posterior parietal, dorsolateral premotor, and prefrontal cortices.[40] However, functional magnetic resonance imaging studies have highlighted the importance of the dorsal frontal area, particularly the ocular fields within Brodmann area 8, for retaining oculomotor information and the intraparietal sulcus for retaining space positions.
The medial temporal lobes are crucial for coding and consolidating the type of memories accessible to consciousness. These regions do not permanently preserve memories and are not necessary for encoding or consolidating other types of memory. The demonstration arises from the emblematic case of patient H.M., who underwent a bilateral temporal lobe resection surgery due to severe posttraumatic epilepsy.[41] A serious picture of amnesia emerged in which the older memories, such as from childhood, had remained almost intact, but the patient showed difficulty recalling events from the 3 years before the operation, especially personal events (retrograde amnesia). Above all, he showed a severe incapacity to store new information (anterograde amnesia), although his short-term memory was not impaired. In other cases, however, patients showed deficits in working memory despite preserving long-term memory. For example, although patient K.M. had difficulty immediately recalling lists of 4 words, he was also faster and better compared to normal patients in learning long lists of words.[42] In this latter case, the damage had localized in the left temporoparietal region (perisylvian area).
Aside from damages to cortical areas, previous reviews on short-term memory, particularly working memory, compared modulations of transient receptor potential canonical channels and working memory through G-protein–coupled receptors and neuromodulators since the key component of working memory is persistent neural firing that is hypothesized to serve short-term (hundreds of milliseconds up to tens of seconds) maintenance of necessary information. The effects of G-protein–coupled receptors and neuromodulators, including acetylcholine, noradrenalin, serotonin, and dopamine, on working memory and transient receptor potential canonical channels were also reviewed. Based on comparisons, G-protein–coupled receptor and downstream signaling pathways that activate transient receptor potential canonical channels generally support working memory, while those that suppress transient receptor potential canonical channels impair memory.[43]
A recent study reported that the cholinergic system, particularly the pharmacological activation of the muscarinic receptor M1R, enhances N-methyl-D-aspartate receptor activity and induces short-term potentiation at the synapses called muscarinic long-term potentiation. Previous studies have also detected dysfunction of cholinergic transmission among patients with cognitive impairment and dementia. Systemic inflammation and neuroinflammation were found to alter synaptic transmission and long-term potentiation severely. The difference between acute and persistent systemic inflammation induced by lipopolysaccharide injections was explored in terms of their effect on the ability of hippocampal synapses to undergo muscarinic long-term potentiation. Findings showed that short exposure to lipopolysaccharide injections resulted in a transient deficit in muscarinic long-term potentiation expression, whereas a more prolonged exposure persistently impaired muscarinic long-term potentiation. These findings may involve cognitive dysfunctions following sepsis and neuroinflammatory processes.[44]
Relationship Between Short-Term and Long-Term Memory
As short-term and long-term memory are distinct with separate mechanisms, selective deterioration may not impair long-term memory tasks. However, difficulties in short-term memory performances can trigger a pathogenetic chain that involves other types of memory. The interconnections between short-term and long-term memory probably require more explanation.[45] Several clinical pieces of evidence prove a mechanical relationship between the 2 systems. For instance, deficits in verbal short-term memory are commonly recognized in children with reading difficulties and are associated with learning disorders featuring impairment in reading. Similarly, in the early stages, such as mild cognitive impairment, Alzheimer disease typically affects short-term memory but not long-term memory, which progressively alters as the disease progresses.
History and Physical
Short-term memory impairment involves forgetting information to which the patient has been recently exposed. An individual with signs of losing short-term memory asks the same questions repeatedly, forgets immediate location, forgets recent events, or forgets something they just saw or read. The loss of immediate memory is also termed fixation amnesia. The clinical features of short-term memory impairment are variable and depend on the underlying cause of the memory alteration. Within short-term memory, different memory domains, such as verbal or visuospatial components, and in different degrees, can be altered. In most cases, memory alterations are blurred and last as long as the pathology that caused them or resolved over weeks or months, for example, postoperative cognitive dysfunction.
In neurodegenerative diseases such as dementia, the decline of short-term memory is generally progressive, involving different domains and, in turn, other memory systems. On the other hand, memory loss in mild cognitive impairment can remain unaltered, worsen, or improve. In about 30% of cases of brain aneurysm, memory problems disappear over time, although recovery may take weeks. In most cases of psychogenic amnesia, memories can be recovered through psychological interventions (recovery of undeleted files); nevertheless, if amnesia persists for a long time, such as months or years, recovery is not possible (deleted files), and the patient projects into a new life (the fugue state).
Memory impairment can be part of complex clinical pictures. For example, alcohol-induced Korsakoff syndrome characteristically demonstrates memory impairment (anterograde, retrograde), confabulation (invented memories used to fill memory gaps and blackouts), and psychiatric symptoms. A recent study characterized Korsakoff syndrome as episodic memory impairment due to damage to the medial diencephalic structure. Research findings revealed that impairment in associative learning and transfer due to task complexity represents a distinct pattern from spared learning. However, impaired transfer was previously observed in patients with medial temporal lobe amnesia.[46] Another study linked Korsakoff syndrome with challenges in recalling specific autobiographical memories.[47] Neurological manifestations associated with thiamine deficiency (Wernicke encephalopathy) can accompany Korsakoff syndrome, and the combination is termed Wernicke-Korsakoff syndrome.
Evaluation
Different approaches are useful for evaluating short-term memory domains. For instance, the verbal component is assessed through simple tests based on the recall of words or digits. The simple span tasks approach, or short-term memory tasks, examines the storage of either verbal (phonological) or visuospatial information. Alternatively, more complex methods can be employed, such as those based on serial position effects in the immediate serial recall. Population-specific approaches are used, particularly in children. In this setting, short-term memory performance is investigated within the framework of working memory using tools such as the Automated Working Memory Assessment and the Working Memory Test Battery for Children.[48][49]
Recent reviews have highlighted the use of automated neuropsychological test batteries, such as the Cambridge Neuropsychological Test Automated Battery (CANTAB), for assessing working memory, which can aid in diagnosing mild cognitive impairment. CANTAB subtests, including spatial span, spatial working memory, and rapid visual information processing, can be used as suitable assessment tools for diagnosing mild cognitive impairment in clinical settings.[50] Although memory is investigated among cognitive performances by validated instruments such as the Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA), specific tools have been developed for assessing short-term memory impairment and providing information about the degree of memory impairment. The Short-Term Memory Recall Test and its simplified version can be useful for identifying memory impairment as a pre-dementia state. In contrast, the Temple Assessment of Language and Short-term Memory in Aphasia (TALSA) is a tool for investigating short-term impairment in post-stroke aphasia. Other tools can help evaluate memory alterations in different clinical conditions of progressive cognitive decline. For instance, the California Verbal Learning Test-3 (CVLT-3) is useful for distinguishing memory disorders of Alzheimer disease from those of Huntington disease.[51][52]
A recent study has outlined screening procedures for early Alzheimer disease to identify patients who fulfill clinical and biomarker criteria efficiently. These procedures include performance on the Free and Cued Selective Reminding Test (FCSRT) and Repeatable Battery for the Assessment of Neuropsychological Status (RBANS).[53] Further diagnostic examinations must focus on the cause of memory decline. Instrumental investigations, such as magnetic resonance imaging (MRI) or computed tomography (CT) scan, or laboratory examinations, such as vitamin B12, may be necessary. Previous radiologic studies have described the role of MRI in ruling out underlying causes of cognitive deterioration and revealing patterns of atrophy with a predictive value for certain types of dementias. Although these patterns are not specific or unique to each disease, they can help confirm diagnostic suspicion or identify certain processes.[54]
Treatment / Management
Several strategies have been proposed to enhance memory tasks, including behavioral and non-behavioral approaches. Behavioral approaches, or cognitive training, are mostly focused on the maintenance rehearsal, which facilitates memory processing through repetitive stimuli, and the elaborative rehearsal, which entails associating new information with stored knowledge and analyzing it. Several proposed behavioral strategies include the combination of Tai Chi movements and breathing. However, further research and controlled studies are required to confirm their real benefit. Concerning pharmacological approaches, although commonly prescribed, drugs approved to manage memory symptoms of Alzheimer disease, such as cholinesterase inhibitors, have not demonstrated significant benefits in slowing down or preventing the progression of mild cognitive impairment to Alzheimer disease.[55][56][57]
Apart from the complex strategies used in specific settings and when the deficit appears to be very clear, involving different domains and other types of memory, short-term memory training is accomplished using simple expedients. For example, rhymes can help children memorize numbers, months of the year, and other sequences. This strategy works by attaching a word, phrase, or image to an object. In practice, this is the same process that we put into practice when we choose a password. Similarly, memory games involving short exposure to objects, such as pictures of animals, can work to exercise memory.
Researchers have designed more complex training programs for specific contexts. These non-pharmacological approaches are crucial in cases of neurodegenerative conditions when no effective therapies are available and in those when the impairment is not severe and can still be slowed down or stopped. For example, in cases of mild cognitive impairment, for which no medications currently have approval from the United States Food and Drug Administration, computer-based memory training programs are adopted. Computer brain fitness training can also be combined with wellness education programs and physical exercise, such as yoga. According to a study, Kundalini yoga training has a more significant impact on stress-related hippocampal connectivity. In contrast, memory enhancement training improves hippocampal sensory integration, supporting better memory reliability in women with subjective memory decline and cardiovascular risk factors.[58] Another study focused on the effect of exercise interventions on subdomains of executive function in older adults with mild cognitive impairment and found that exercise significantly improved 3 subdomains of EF in mild cognitive impairment, particularly mind-body exercise. Moreover, exercise training of at least 4 weeks with a frequency of 3 to 4 times a week tends to have a significant impact.[59] Another study assessed the effects of long-term Wuqinxi exercise on working memory in older adults with mild cognitive impairment, and findings suggested that this exercise may be an effective intervention in delaying or preventing mild cognitive impairment progression to Alzheimer disease.[60]
On the other hand, web-based cognitive training, consisting of 30 internet sessions conducted 4 to 5 times a week, may be useful in modifying memory processing in Parkinson disease. Furthermore, the effect of virtual reality in a recent study showed improvement in executive function in older adults with mild cognitive impairment. A recent study on music therapy revealed that the assessment of music-related memory can be systematically categorized as assessing short-term or long-term memory and explicit or implicit memory. Comprehensive information about music-related memory is valuable for understanding dementia patients. This information is crucial for planning and applying musical experiences in music therapy.[61][62]
Another study focused on improving the naming ability of patients with a semantic variant of primary progressive aphasia through Errorless Learning Therapy. This effect may be due to the relative preservation of episodic memory, but the benefit is not maintained over time, probably due to the absence of consolidation.[22] Furthermore, the Train the Brain program is described in a study as a combined motor and cognitive intervention that markedly improves cognitive functions in patients with mild cognitive impairment. The beneficial impact on cognitive functions was preserved at the 14-month follow-up, with more significant effects in low-educated individuals compared to high-educated individuals and in women compared to men.[63]
Apart from cognitive training, non-behavioral strategies concern transcranial direct current stimulation in short-term memory impairment due to primary progressive aphasia. In contrast, current research is being conducted on the effects of nutraceuticals, such as thymoquinone or green tea, against Alzheimer disease–related short-term memory decline and tryptophan-tyrosine–related peptides, such as lactolin, to mitigate stress-induced memory alterations.[64][65][66] Although several studies have shown that Ginkgo biloba can improve the risk of short-term memory impairment, the scientific evidence is limited.[67]
A recent study examined the relationship between changes in brain activity associated with working memory and assessment scales of memory scores in amnestic mild cognitive impairment before and after moxibustion therapy. Findings showed that moxibustion treatment improved memory in patients with amnestic mild cognitive impairment and was associated with the activation of brain regions such as the insula, lingual gyrus, posterior cingulate gyrus, postcentral gyrus, superior temporal gyrus, and thalamus, which may be a significant process by which moxibustion enhances memory function.[68]
Differential Diagnosis
The differential diagnosis should include the following:
- Alzheimer disease is the most common type of dementia, characterized by the initial and most usual presenting symptom of episodic short-term memory loss along with relative sparing of long-term memory. Short-term memory impairment is followed by impairment in problem-solving, judgment, executive functioning, lack of motivation, and disorganization, resulting in multitasking and abstract thinking problems.
- Creutzfeldt-Jakob disease is a rapidly progressive, fatal neurodegenerative disorder. This condition presents with short-term memory loss, decreased concentration, and rapid progression of dementia, demonstrated by severe impairment in tasks with a predominantly visual component, including visual scanning, perceptual reasoning, and visual-spatial processing. Diagnosis is often confirmed by characteristic findings on brain MRI and the presence of real-time quaking-induced conversion of cerebrospinal fluid.
- Dementia with Lewy bodies is a neurodegenerative disease characterized by cognitive, behavioral, and motor symptoms. However, it presents a more challenging clinical management and a poorer prognosis compared to other forms of dementia.
- Frontotemporal dementia is the second most common presenile dementia, manifested as prominent behavioral, language, and cognitive impairment. This type of dementia has a vital genetic component contributing to the pathogenesis.
- Progressive supranuclear palsy is a progressive neurodegenerative tauopathy that presents with motor, behavioral, and cognitive dysfunction. This disease is atypical parkinsonism with prominent 4R-tau neuropathology, and the typical clinical manifestations include early postural instability or akinetic-rigid syndrome, unprovoked falls, cognitive decline, and prominent eye movement abnormalities that consist of saccadic slowing, followed by gaze limitation or vertical supranuclear gaze palsy.
- Semantic dementia is a lobar atrophy syndrome associated with the degeneration of anterior temporal regions that manifests as a predominant impairment of semantic memory. The appearance of possible additional cognitive or psycho-behavioral disorders can lead to a misdiagnosis in favor of frontotemporal dementia syndrome or Alzheimer disease.
- Traumatic brain injury is characterized by a wide range of cognitive deficits and behavioral changes due to diffuse axonal injury. These deficits include slowed information processing and impaired long-term memory, attention, working memory, executive function, social cognition, and self-awareness. Mental fatigue is also associated, which can be aggravated by the consequences of neuropsychological deficits. Personality and behavioral changes include impulsivity and apathy.
- Depression and other psychiatric illnesses can affect concentration and short-term memory.
- Vitamin deficiencies, such as B12 and B1, can adversely affect short-term memory.
- Medication use, such as narcotics, can also impair memory.
Prognosis
The prognosis for short-term memory loss varies greatly depending on the underlying etiology. For example, transient memory loss from the transposition of the great arteries typically reverses and improves without requiring extensive treatment. Memory loss from hypothyroidism, vitamin deficiencies, and depression is reversible once the underlying cause is treated. However, most short-term memory loss is a feature of degenerative diseases such as Alzheimer disease. Another common cause is stroke or traumatic brain injuries, which may be partially reversible depending on the amount of damage and brain reserve. However, these deficits are typically static but manifest more as the patient loses more brain reserve in aging.
Complications
Depending on its severity, short-term memory loss can lead to complications, significantly impacting the patient's social interactions. These complications may manifest as missing appointments, forgetting conversations, and a decline in communication with friends and family, resulting in withdrawal from the community without active support. In the latter stages, patients may struggle to complete complex tasks of daily living, such as grocery shopping and bill payments, requiring additional assistance. In severe cases of memory loss, patients can be a danger to themselves, such as forgetting to turn off the stove, getting lost in familiar places, and being unable to find their way home. When coupled with comorbid medical conditions, patients may forget to take medications or forget that they have already taken medications; hence, they may take multiple doses of their medications, leading to further complications. Activities of daily living are also compromised as the patient may forget to eat, bathe, or have difficulty dressing. Eventually, patients may become entirely dependent on others and may require relocation to a nursing home for adequate care.
Deterrence and Patient Education
In most cases of acute memory loss, such as stroke or traumatic brain injury, diagnosis is straightforward; however, treatment options are limited. However, diagnosis may be delayed in conditions such as vitamin deficiencies, depression, or hypothyroidism, as these patient presentations are gradual, and their level of functioning declines at the later stages of the disease. In such instances, patient education is necessary. Screening tests at the clinician's office for high-risk patients are also important.
Enhancing Healthcare Team Outcomes
In most cases, managing problems related to short-term memory alterations requires an interprofessional approach. The goal is to design a patient-centered treatment with the involvement of several health professionals. Many clinical conditions associated with memory disorders have complex clinical pictures requiring a care response to improve several outcomes, including cognition, functioning, mood, and quality of life. The team should include professionals who can—(1) perform a careful neuropsychological assessment; (2) collect information for the different diagnoses; (3) select the appropriate strategy (behavioral/non-behavioral); (4) manage communication for improving patient compliance and treatment adherence; (5) support patient and family; (6) implement appropriate psychological strategies, such as group cognitive-behavioral therapy; (7) conduct behavioral programs focused on wellness education, such as sleep hygiene; (8) manage pharmacological approaches; (9) design physical activity programs; and (10) evaluate outcomes.
A recent study indicates that applying neuropsychological measures of executive working memory for older adults with memory impairment may provide precise and tailored care, particularly for patients with mild cognitive impairment with poorer executive working memory and patients with mild dementia with relatively intact executive working memory.[77] Specialty-trained psychological nurses can greatly assist physicians in these cases. The patient histories and verification of medication compliance assess overall treatment effectiveness before clinicians investigate the patient's status or change of status. Although early short-term memory impairment does not fall into pharmaceutical therapy, as the decline continues and concerns about Alzheimer disease or Parkinson disease appear, the pharmacist plays a significant role, including agent and dose verification, medication reconciliation, and working directly with clinical staff to optimize therapy and minimize adverse effects. This interprofessional team approach is necessary for optimal patient results in managing short-term memory impairment.
A recent study focused on the perspectives of patients, care partners, and primary care clinicians on managing mild cognitive impairment and mild Alzheimer disease dementia. Findings revealed that primary care clinicians play a crucial role in the timely diagnosis and treatment of mild cognitive impairment and mild Alzheimer disease dementia, although they are typically not considered care coordinators. For most patients, the initial discussion with a primary care clinician occurred 15 months after symptom onset. The study highlighted the importance of educating patients, care partners, and primary care clinicians on mild cognitive impairment and Alzheimer disease risk factors, early symptom recognition, and early diagnosis and treatment.[78]
Short-Term Memory Impairment