Neuropsychological Staging of AD
A variety of cognitive and behavioral taxonomies are used to categorize AD's progression. One of the simplest ways to categorize the condition is to frame neuropsychological changes into three progressive stages: early, middle, and late. These stages describe a person's decreasing amount of cognitive reserve.
Cognitive reserve is the amount of remaining neurological integrity that is viable to produce neural activity. Such activity translates into cognitive ability. Cognitive reserve accumulates as neuronal connections are forged by lifelong learning, mentally stimulating and educational pursuits, interactive social supports, and health-promoting opportunities. Someone with a great deal of cognitive reserve may build a strong network of neuronal connections that take longer to be compromised by AD's pathological features, delaying the cognitive symptoms of this illness (Vance & Crowe, 2006).
As neurons become damaged due to the build-up of AD-associated amyloid plaques and neurofibrillary tangles, the physiological integrity of the brain becomes compromised (Yaari & Corey-Bloom, 2007). These disease processes translate into reduced cognitive efficiency and expressions of cognitive impairment of dementia at a certain threshold of damage. AD compromises the brain and reduces cognitive reserve, resulting in early, middle, and late disease stages with various cognitive abilities declining at different rates (Fig 1).
During the early stage of AD, adults begin to exhibit difficulty performing more complex instrumental activities of daily living (IADL) such as remembering to take medications, operating a vehicle, paying bills and negotiating finances, and executing other tasks requiring a high degree of cognitive ability. Although in most cases they are able to function socially and interact with others, adults may become frustrated with declines in their cognitive ability during this stage.
Cognitive declines occur in several areas, but most notably in attention and concentration, short-term memory, and declarative and episodic memory. Declines in declarative memory manifest as difficulty retrieving learned information (e.g., Who is the president of the United States?). Declines in episodic memory involve difficulties retrieving information about oneself (e.g., What did you have for breakfast yesterday?). These memory abilities often are referred to as explicit memory abilities and entail conscious recollection and information recall. These memory abilities are dependent on the connections between the prefrontal cortex and the hippocampus, which are more negatively affected by the disease process (Grady, Furey, Pietrini, Horwitz, & Rapoport, 2001). These prefrontal and hippocampal areas decline much sooner than and are compromised with disease progression more than other abilities such as procedural memory ability.
Procedural memory abilities, often referred to as implicit memory, involve more rote or unconscious recollections (e.g., riding a bike, using utensils, turning a doorknob). Procedural memory abilities are better spared from AD because these abilities are less dependent on the affected regions of the brain such as the basal ganglia and the cerebellum (Poldrack & Gabrieli, 1997). Figure 1 shows that as cognitive reserves decline, declarative and episodic memory deteriorates faster than procedural memory (De Vreese, Neri, Fioravanti, Belloi, & Zanetti, 2002; Gabrieli, 1998; Hirono et al., 1997).
Similar to procedural memory abilities, attachments and emotional processing also are highly resistant to AD's effects. Although emotional processing and subsequent expressions may at times be exaggerated or inappropriate, it is clear that emotional attachments remain strong during the course of AD. This fact clearly is reflected in the common problem of patients or care recipients who follow or "shadow" their caregivers (Mace & Rabins, 1991). Such shadowing is believed to be caused by two factors. First, there is the attachment to the caregiver, usually a spouse or adult child, who provides emotional and physical support for the confused care recipient. The second factor is the intense emotional reaction brought on by patients' inability to cognitively negotiate their environments (Hall & Buckwalter, 1987).
Developmental psychologists have observed that infants' first automatic, psychological goal is to form intense, emotional attachments to their caregivers (i.e., attachment theory). The development of such attachments is instinctual and necessary for survival. Attachment to caregivers helps to form a dyadic bond that provides infants with warmth, protection, and sustenance (Ainsworth, Blehar, Waters, & Wall, 1978; Bowlby, 1973; Hunter & Maunder, 2001). The limbic system, which is responsible for processing such emotions, may be spared from the ravages of AD more than other higher cortical functions such as declarative and episodic memory (Grady et al., 2001). Maintaining such attachments, even at an unconscious level, occurs whether the objects of attachment are family members or other forms of security.
As the damage caused by AD progresses, the middle stage of the disease is marked by increased confusion, increased short-term memory loss, and more progressive long-term memory loss. Declines in executive functioning and alterations in sensory perception, such as depth perception and odor identification, also are observed (Nebes, 1992; Nordin & Murphy, 1996; Peters et al., 2003). The hallmarks of this decline in conscious memory ability include increasing agitation and disruptive behavior and a greater need for assistance with activities of daily living (ADL), such as dressing and bathing. During this stage, however, procedural memory abilities remain intact along with emotional processing abilities. Patients still can perform basic, familiar tasks and experience emotional attachments to things that are familiar even though they are not able to process emotions consciously.
During the late stage of the disease, short-term and long-term memory declines are pronounced along with the loss of most, if not all, language abilities. Patients require assistance for all ADLs. Loss of self-recognition and additional perceptual and sensory losses also are observed. Even at this stage, rudimentary procedural memory is observed, such as the ability to open a door or twist a knob on a faucet. Gross motor abilities such as walking and grasping still may be present. Primitive attachments, albeit at more implicit levels, may remain. At the very end, even instinctual abilities, such as the ability to swallow, may be compromised (Clibbens, 1996).
In all forms of cognitive and emotional abilities observed with the progression of AD, the gradual loss of these abilities is likened to reverse ontogeny (i.e., backward development). Reisberg and colleagues (2002) remarked that the pattern of myelin loss accompanying AD reflects that of myelin acquisition found in normal development. Similarly, neurological infantile reflexes are the last to remain during the later stages of AD. This reverse ontogeny or retrogenic process is reflected in other neurological abilities.
When an infant is born, the development of attachments is the first goal. Procedural memory abilities form later as infants learn to physically negotiate their environments. Later, declarative and episodic memory abilities emerge and become stronger with maturation. Likewise, with the progression of AD, declarative and episodic memory abilities deteriorate first. More complex procedural memory abilities are lost later and are followed by more gross procedural memory ability loss. Finally, although emotional attachments remain well into the last stage of the disease, as noted by shadowing and emotional responses, these too are lost as the adult enters a vegetative state.
J Neurosci Nurs. 2008;40(2):96-102. © 2008 American Association of Neuroscience Nurses
Cite this: Procedural Memory and Emotional Attachment in Alzheimer Disease: Implications for Meaningful and Engaging Activities - Medscape - Apr 01, 2008.