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The frontal lobe mediates executive function, judgment, and behavioral regulation. Its degeneration causes disinhibition and apathy rather than primary fear generation. While frontal impairment reduces control over limbic output, it does not originate the core anxiety/paranoia circuitry.

The parietal lobe integrates somatosensory and visuospatial processing. Parietal involvement in Alzheimer’s leads to neglect, constructional apraxia, and spatial disorientation. These deficits may secondarily increase distress, but they do not drive the emotional salience and conditioned fear responses underlying paranoia.

The hippocampus encodes declarative memory and contextual binding. Hippocampal atrophy causes anterograde amnesia and impaired context retrieval, which can exacerbate confusion. However, the primary generator of fear/anxiety and threat appraisal is the amygdala, not hippocampal memory circuits.

Secondary gains involve external benefits such as attention or avoidance of responsibility. Confabulation in Alzheimer’s is not purposeful or manipulative; it is an unconscious defense, making secondary gain an inaccurate explanation.

Perseveration is the involuntary repetition of words, phrases, or behaviors due to impaired cortical inhibition. It does not involve creating new false memories. The dinner cruise narrative is fabricated, not repeated, ruling out perseveration.

Perseveration does not serve to maintain self-esteem; instead, it reflects neurological dysfunction. The client’s statement demonstrates confabulation, which specifically functions to protect self-esteem and ego, not perseveration.

Sadness and anhedonia reflect mood symptoms (depression) rather than a specific language production deficit; aphasia concerns speech and language processing, not emotional experience.

Emaciation and wasting relate to nutritional or systemic deterioration, not specifically to language ability; they do not reflect impaired speech production or comprehension.

No longer able to speak” suggests mute behavior, which can be motor or severe, but aphasia describes disrupted language formulation rather than complete absence of speech output.

Loss of purposeful movement reflects motor system dysfunction involving basal ganglia, cerebellum, or motor cortex, not primarily due to cholinergic deficits in Alzheimer’s, which target cognitive circuits rather than motor execution.

Loss of sensory ability to recognize objects (agnosia) involves association cortex dysfunction, especially in parietal and occipital regions; while present in Alzheimer’s, it is not the deficit most directly tied to acetylcholine reduction.

Loss of language ability (aphasia) arises from degeneration in language networks, particularly left temporal–parietal areas; acetylcholine depletion contributes to overall cognitive decline, but memory loss is the dominant deficit linked to cholinergic loss.

Dismissing the concern as normal aging invalidates the client’s feelings and may discourage future disclosure of legitimate cognitive changes.

Self-disclosure by the nurse shifts focus away from the client, minimizing the client’s concerns a

Overly complex explanations without listening can confuse or overwhelm the client and negate the emotional component of their concern, preventing therapeutic dialogue.