Cognition FAQ
Cognitive decline and Brain Fog FAQ
Obviously it would take a long series of textbooks to begin to outline all of cognition, but this is where a Practical Neuropsychiatry approach differs. Patients coming to the neurologists’ office tend to fall into a few simple categories that can make identifying the cause/contributors to cognitive complaints relatively easy to narrow down. Most patients either ask for a neurology appointment because they are looking for relief or they are worried about Alzheimer’s. They often leave unsatisfied and feeling more confused because the Neurologist’s role is typically to rule out certain neurologic syndromes or comorbidities, consider degenerative diseases, and possibly to help a PCP to consider other medical causes. Unfortunately, neurologists no longer consistently focus on general internal medicine during or after training and this causes problems. In this FAQ, we hope to explain this process, its limitations, and ways to navigate this by answering common questions patients bring to the neurology clinic.
What’s the difference between Alzheimer’s and Dementia?
The best way to think about this is to say that Alzheimer’s is one of many possible causes/contributors to “dementia”. Generally a dementia diagnosis has a few primary features. Firstly, it must be a decline in at least 2 areas of cognition such as memory, executive functioning, language, planning, visuospatial reasoning, etc… Secondly, it has to be severe enough to cause some genuine loss of functioning, and not just deciding to stop doing things because others offer to help. Thirdly, it cannot be completely reversed even with treatment. Previously, it was taught that it must be progressive though many medical causes of dementia (like dementia from strokes) can be treated and worsening can be halted. Truly fulfilling criteria for dementia is very difficult because a thorough search for medical contributors is required, and aggressive treatment of those medical contributors must be undertaken. I will not, for example, diagnose someone with dementia when they have untreated depression or untreated sleep apnea (two very common reversible causes of cognitive decline) and many patients either lack interest in treating them or access to providers who might treat them. After identifying a patient as having a “dementia,” and likely medical contributors have been properly treated or ruled out, a good neurocognitive exam or formal Neuropsychological testing can identify if features are likely consistent with Alzheimer’s or another degenerative brain disorder like a Frontotemporal dementia, a Dementia with Lewy Bodies, a Multiple system Atrophy, or others. Biological markers for Alzheimer’s in the brain can be identified with a Lumbar Puncture or a very specific type of brain scan looking for Amyloid Plaques, though MRIs are not particularly useful in this endeavor.
Do I have Alzheimer’s?
This is a surprisingly complex question, and if you came to the appointment on your own and are very worried about Alzheimer’s the answer is likely no. Prior to the 1984 guideline paper, Alzheimer’s disease was an academic curiosity with genetic cases (like what Alzheimer himself identified in one patient) being very rare and occurring typically in a patient in their 40s. After those guidelines were published, millions of people were suddenly diagnosed with Alzheimer’s disease (often inappropriately) and a huge socio-cultural dynamic was formed around this poorly characterized illness. Currently, there are three completely separate diagnoses in the literature, the classic criteria (which persisted until DSM-5), the biological definition of Alzheimer’s (evidence of Amyloid and Tau protein changes in the brain regardless of clinical symptoms), and a very broad clinical diagnosis (supported by DSM-5 criteria) whereby nearly all older patients with cognitive decline are diagnosed as having “Alzheimer’s”. In short, the original criteria focused on “cortical symptoms” that most people don’t predominantly have, and lack of medical causes that most people predominantly do have. One of the main components of a “cortical symptom” involves loss of insight (a feature of a type of symptom called gnosis). Consequently, the more a patient is worried about their cognitive decline, the less likely it is primarily caused by Alzheimer’s. This gets more convoluted when considering the biological definition since 30% of healthy older individuals, without cognitive decline, can have evidence of amyloid and tau. Many in the neurology world would say those people without any symptoms already have “Alzheimer’s”. Fundamentally, though the academic world settled on a definition of Alzheimer’s in 1984, and continue to consider it an important diagnosis, there is more division now than ever before on who to diagnose with Alzheimers. However, fundamentally at the moment it isn’t particularly important because while there are many medications that can help symptoms in Clinical Alzheimer’s, there are no commonly available treatments for which a diagnosis of biological Alzheimer’s is specifically helpful.
But what about those new Alzheimer’s Infusion medications?
There are multiple new medications, given as intermittent infusions, designed to reduce amyloid in the brain. While there is an enormous amount of hope that they will have a role in the treatment of patients with cognitive decline in the future, the evidence so far has been quite underwhelming. They work by recruiting the immune system to help the body “clear out” alzheimer’s plaques in the hope that this would improve thinking and memory. Current evidence shows they clear amyloid quite well, but actual cognitive improvement or delay in progression are only minimally affected. Furthermore, even in the otherwise very healthy people in the research studies, between 30-50% of patients have brain inflammation which may or may not have serious complications. The current consensus is that they are not ready for use in the general population, outside of a research protocol. Expectations are that within the next few years larger research protocols will show which people are most appropriate for these treatments. Many in the field expect them to be helpful for patients in the very earliest stages of the disease, with no active medical contributors to cognitive decline, and with very specific genetic profiles. To find out if this would include you, Practical Neuropsychiatry can offer a consultation to discuss the data around these treatments and where active treatment can be obtained.
If my forgetfulness isn’t from Alzheimer’s, what is causing it?
The answer to this question is different for each individual. Most patients with cognitive complaints don’t describe mostly “cortical symptoms” but subcortical symptoms and there are a thousand possible contributors. Many primary care doctors will have a few lab tests they check for “possible dementia”. These may include Thyroid testing, Diabetes testing, Vitamin B12 testing, and looking for chronic infections like Hepatitis C, HIV, or Syphilis. This is often insufficient, though these are all very common contributors to cognitive decline. Unless there is a very obvious degenerative condition or severe medical condition, it is best not to think “what is the cause of cognitive decline?” but instead “what are the contributors to cognitive decline?”. Anchoring on an individual contributor typically leads to ignoring the other contributors. The quest for medical contributors is usually best done by someone who focuses on internal medicine as an individual’s risk is dependent upon the rest of their medical history and symptoms. Casting a net too widely can also be disastrous leading to harmful and invasive testing, especially when there are more common and easily treatable contributors that don’t require blood work or biopsies. The most common, easily identified, and treatable conditions tend to be in the field of psychiatry and psychology which is why it is good to have a psychopharmacologist and a therapist early after identifying cognitive complaints. Depression, anxiety, and insomnia syndromes all have cognitive slowing or forgetfulness as core features, especially in the middle aged and elderly. Poor nutrition, a sedentary lifestyle, sensory deprivation from hearing and vision loss, and cognitive/social isolation are also common contributors. Lastly, both prescribed medications and recreational substance use are very common contributors to cognitive slowing. In the majority of individuals, just working on these contributors can have a bigger impact on improving cognition and reducing cognitive decline than any medical treatment. In addition to working on any underlying anxiety and depression, psychotherapists are uniquely skilled at helping patients strategize habit changes around diet, exercise, sleep hygiene, social enrichment, and others.
My Doctor says the tests show I’m fine, but I have brain fog after a medical event.
Brain fog is a nebulous term, typically describing generalized forgetfulness, slowing of overall cognitive functioning, word finding difficulties, and cognitive fatigue. While it can develop slowly, many patients have sudden onset of brain fog after a medical event. Concussions are a common cause of brain fog, and since the pandemic began there has been a lot of literature on brain fog in “Long-Covid”. However, nearly any bio-psycho-social event can cause residual brain fog including emotional stress, depression, insomnia or poor sleep quality, nutritional deficiencies, brain or body inflammatory disorders, chronic infections, cardiovascular events like heart attacks or strokes, medication interactions, and even cortical dementias. Often formal cognitive testing is normal because symptoms fluctuate and may not be severe enough to show up on tests, which is frustrating to patients who feel it has upended their lives. Sometimes a previous cognitive strength was heavily relied on, and now that it is just “a little below average” that loss of a primary cognitive strength makes someone completely non-functional. Often the “cause” is a minor medical problem, but that was just the straw that broke the camel's back and many chronic contributors were already present. Because brain fog is so individual and subjective, impossible to prove or disprove, many doctors may seem to dismiss it, but monitoring it, looking for treatable medical contributors, and focusing on overall health improvements can help even if there is no way to reverse time and undo the concussion or the infection that kicked it off.
They said my parent’s confusion was because of a medical problem, but they fixed it and he/she isn’t better.
Generalized confusion during a medical event is typically Delirium or Toxic/Metabolic Encephalopathy. It was classically believed that when you fix the main medical contributors such as infections, metabolic disturbances, or organ dysfunction, the confusion should resolve quickly or at least within a month. Repeated studies have shown that recovery from delirium is typically much slower and not always complete. Only about half of people have reached their new baseline within 3 months after treatment, and their cognitive functioning is often not as good as before the medical event. We don’t fully understand delirium, but it is generally thought that the brain is fragile and its basic mechanisms to keep toxins out and energy in has faltered. Consequently, those chemicals get into the brain and cause dysfunction. Because good quality sleep is so important in “flushing out bad chemicals” from the brain, managing a person’s sleep quality can both prevent and speed recovery from delirium. The best way to improve sleep quality to prevent dementia includes establishing a sleep/wake cycle, reducing pain and emotional discomfort, keeping the brain active through socialization, and reducing psychoactive medications. These are impossible in the hospital, meaning that after treating the serious medical problems, getting out of the hospital either to rehab or home is very important in shortening delirium. I typically find examining a patient before the 3 month mark is not particularly useful as deficits are still expected to be improving, and primary care visits are most important as they will look at the medications a patient is on and make sure they are appropriate for the long term. However, when a family is frightened and doesn't understand what to expect, a Consult with a Practical Neuropsychiatrist can be very helpful in understanding what can be done to speed recovery.
My family member’s cognitive decline is very difficult to manage, how do I keep them safe and me sane?
There are many resources that caregivers should know about, even if the cause of cognitive decline hasn’t become fully clear. The Alzheimer’s Association has many resources including case managers, support groups, and educational seminars to help caregivers learn from each other about how to survive while caring for a declining family member. Applied behavioral analysis is a skill mostly utilized in working with children with autism and developmental delay, but similar treatments can be extraordinarily helpful in optimizing quality of life for dementia patients and their families. Many families insist they need to keep a parent at home, but in many cases families burn out too quickly and the home becomes a toxic environment for everyone including the patient. If it can be done, it maybe preferable, but many families find that they can give more and dementia patients are more comfortable, with trained caregivers at a nursing home and family staying in the role of family, visiting and loving. Finances and decision making power is also very complex, and a one time discussion with an elder law attorney can help families understand how to protect their parent’s finances as well as the difference between Health Care Proxy, Power of Attorney, Guardianship, and other formal delineations that can have a huge impact. Lastly, it is vital that everyone involved be on the same page regarding the patient’s wishes for end of life care. Whether to intubate or do chest compressions especially should be decided early, and there is definitely not a “right answer for everybody”. The biggest disasters occur when family start arguing in an ICU about a patient’s wishes.
Can medications help with dementia or alzheimer’s?
Obviously, identifying and treating medical contributors is the most important way to treat cognitive decline and there is no medication for dementia that can help if a patient is malnourished, severely depressed, or not sleeping. However, there are medications prescribed by primary care doctors, neurologists, and psychiatrists that can help with many of the symptoms of dementia, regardless of the medical contributors. Pro-cholinergic medications (donepezil, galantamine, rivastigmine) are the most common class of medications given and they can have a modest impact, especially on fluctuations. Daily fluctuations like sundowning in the afternoon in Alzheimer’s and similar but less predictable spells in parkinsonism related dementia (worsening of orientation, paranoia, hallucinations, and agitation) respond particularly well to pro-cholinergic medications, though in many cases removing anti-cholinergic treatment is more helpful. NMDA receptor medications (mainly memantine) can be very helpful with certain dementia symptoms, though the data on the specific benefits is unclear. Other classes of medications including stimulants, serotonin modulating antipsychotics, atypical and classic antidepressants, dopamine blocking antipsychotics, sleep aides, and others are often used in select patients for particular symptoms, but they should be used very carefully with frequent monitoring ideally by a geriatrician or a geriatric psychiatrist. I’ve found that starting all of these medications seem safe at first, but can have dire consequences without a clear discussion about what symptoms are supposed to be addressed and close monitoring while starting and escalating them. Even if ongoing treatment isn’t necessary, a brief Consult relationship with a Practical Neuropsychiatrist can be quite helpful in understanding options, possible benefits, and preparing to work with a PCP or general psychiatrist on optimizing medications.