Video
Memory disorders
Y. Pritham Raj, MD, describes how to assess cognitive changes in your patient.
Conversion disorder as well as the dissociative disorders and substance-related disorders are notorious for causing confusion. In Ms. T’s case, pseudodementia stemming from her underlying bipolar disorder and anxiety figured prominently in the differential diagnosis, but she did not have any other overt psychopathology, personality disorder, or signs of malingering to further complicate her picture.
Notebook. I recommend that my patients keep a small notebook to record medical data ranging from blood pressure and glycemic measurements to details about sleep and dietary intake. Such data comprise the necessary metrics to properly assess target conditions and then track changes once treatment is initiated. This exercise not only yields much-needed detail about the patient’s condition for the clinician; the act of journaling also can be therapeutic for the writer through a process known as experimental disclosure, in which writing down one’s thoughts and observations has a positive impact on the writer’s physical health and psychology.16
Diagnosis. The first rule in medicine (perhaps the second, behind primum non nocere) is to determine what you are treating before beginning treatment (decernite quid tractemus, prius cura ministrandi, for Latin buffs). This means trying to fashion the best diagnostic label, even if it is merely a place-holder, while assessment of the confused state continues. DSM-5 has attempted to remove stigma from several neuropsychiatric disorders. On the cognition front, the new name for dementia is “neurocognitive disorder (NCD),” the umbrella term that focuses on the decline from a previous level of cognitive functioning. NCD has been divided into mild or major cognitive impairment headings either “with” or “without behavioral disturbance” subspecifiers.17
Aside from NCD, there are several other diagnoses in the differential for confusion. Delirium remains the most prominent and focuses on disturbances in attention and orientation that develops over a short period of time, with a change seen in an additional cognitive domain, such as memory, but not in the context of a severely reduced level of arousal such as coma. Subjective cognitive impairment (SCI) is when subjective complaints of cognitive impairment are hallmark compared with objective findings—with evidence suggesting that the presence of SCI could predict a 4.5 times higher rate of developing mild cognitive impairment (MCI) over 7 years.18 MCI was originally used to describe the early prodrome of AD, minus functional decline.
Treatment
After even a provisional diagnosis comes the final, all-important challenge: treating the neuropsychiatric symptoms (NPS) of the confused patient. NPS are nearly universal in NCD/delirium throughout the course of illness. There are no FDA-approved treatments for the NPS associated with these conditions. In terms of treating delirium, the best approach is to treat the underlying medical condition. For control of behavior, which can range from agitated to psychotic to hypoactive, nonpharmacotherapeutic interventions are paramount; they include making sure that the patient is at the appropriate level of care, which, for the confused outpatient, could mean hospitalization. Ensuring proper nutrition, hydration, sensory care (hearing aids, glasses, etc.), and stability in ambulation must be done before considering pharmacotherapy.
Antipsychotic use has been the mainstay of drug treatment of behavioral dyscontrol. Haloperidol has been the traditional go-to medication because there is no evidence that low-dose haloperidol (<3 mg/d) has any different efficacy compared with the atypical antipsychotics or has a greater frequency of adverse drug effects. However, high-dose haloperidol (>4.5 mg/d) was associated with a greater incidence of adverse effects, mainly parkinsonism, than atypical antipsychotics.19 Neither the typical nor atypical antipsychotics have shown mortality benefit—the real outcome measure of interest.
In terms of treating major (or minor) NCD, there are only 2 FDA-approved medication classes: cholinesterase inhibitors (donepezil, galantamine, rivastigmine, etc.) and memantine. However, these medication classes—even when combined together—have only shown marginal benefit in terms of improving cognition. Worse, even when given early in the course of illness they do not reduce the rate of NCD. For pseudodementia, selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors tend to form the mainstay of treating underlying depression or anxiety leading to cognitive changes. Preliminary data suggest that some SSRIs might improve cognition in terms of processing speed, verbal learning, and memory.20 More studies are needed before definitive conclusions can be drawn.
For the confused patient, a personalized therapeutic program, in which multiple interventions are considered at once (targeting all areas of the patient’s life) is gaining research traction. For example, a novel, comprehensive program involving multiple modalities designed to achieve metabolic enhancement for neurodegeneration (MEND) recently has shown robust benefit for patients with AD, MCI, and SCI.21 Using an individual approach to improve diet, activity, sleep, metabolic status including body mass index, and several other markers that affect neural plasticity, researchers demonstrated symptom improvement in 9 of 10 study patients.