The human brain is a complex organ, and when its function is disrupted, the resulting symptoms can be varied and confusing. One common pattern of neurological and psychiatric symptoms is described as "waxing and waning," characterized by fluctuations in severity over relatively short periods. This article aims to explain the phenomenon of waxing and waning symptoms, particularly in the context of delirium, catatonia, Functional Neurological Disorder (FND), and dementia.
Delirium is a neuropsychiatric condition classically characterized by the acute onset of waxing and waning fluctuations in attention and level of arousal. It is a significant source of suffering and distress for patients and loved ones. Commonly encountered across treatment settings, it is especially prevalent among patients with serious illness, with studies demonstrating rates of delirium as high as 74% in inpatient palliative care units. The impact of delirium on a patient’s course is often significant.
Physicians describe delirium as a medical condition that causes a patient’s mental status to shift back and forth (sometimes explained as “waxing and waning”). Caregivers often think of it as when their family member seems “not themselves,” either in the hospital or after they come home. Sometimes a family member who is seriously ill seems upset, agitated, combative or even psychotic. They may see things that aren’t there or mumble in ways you can’t understand. They may try to climb out of bed or want to walk without assistance, despite being very weak. Other times a family member may seem sluggish, confused or very sleepy. They may not respond to you, or may fall asleep in the middle of a sentence. The term “sundowning” is often used in place of delirium, due to the fact that many of these changes take place in the evening and at night. Delirium is different from dementia, which is a slow progression of loss of memory and overall function.
Delirium is caused by another or multiple medical conditions and is not the primary diagnosis itself. Common causes in the general population include medications and toxin effects, metabolic derangements, central nervous system disorders, and infections. Something as simple as a bladder infection (sometimes called a urinary tract infection) or pneumonia can result in delirium. Other causes include certain medications, disturbances in electrolytes or other chemicals in the blood and failure of the kidneys or liver (both of which help remove waste and toxins from the body). In older people delirium can also be brought on by things such as severe constipation, heart attack, stroke or just simply being in the hospital or in an intensive care unit. Additionally, certain cancers may lead to a patient being more likely to experience conditions that cause delirium in the general medical population.
While predicting with total certainty which patients will develop delirium during an acute illness is challenging, several known factors increase a patient’s risk. Common risk factors in the general population include advanced age, presence of an underlying neurocognitive disorder (e.g., dementia), history of head injury, certain medical comorbidities (including cardiovascular or renal disease), visual and hearing impairment, and poor nutritional status. Among palliative care patients, a recent systematic review and meta-analysis of nine studies identified specific risk factors including older age, hypoxia, dehydration, cachexia, opioid use, anticholinergic burden, and poor Eastern Cooperative Oncology Group (ECOG) Performance Status.
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Multiple potential physiological mechanisms have been proposed including neurotransmitter dysfunction, disruptions in central nervous system network connectivity, neuroinflammation, neuronal aging, and oxidative stress, among others. Despite ongoing research in this area, there is no single accepted pathophysiological pathway or model that satisfyingly explains the development of delirium in all patients.
Patients typically initially present with a relatively acute onset of inattentiveness, with cognitive deficits including difficulty recalling information and losing orientation to their surroundings. Frequent accompanying symptoms include affective changes, perceptual disturbances, and disruption in the normal sleep/wake cycle. Based on the specific symptoms a patient presents with, clinicians usually categorize presentations of delirium as either hypoactive or hyperactive.
Delirium is diagnosed based on clinical presentation, focusing on the timing of symptom onset, associated symptoms, and thorough mental status and cognitive exams. Providers should assess for cognitive changes, including memory deficits, difficulty sustaining attention, or disorientation. Affective symptoms should also be evaluated including new onset of irritability or mood lability, or, conversely, restricted or flat affect. Perceptual disturbances including visual or auditory hallucinations, illusions, or sensory misperceptions are important to evaluate as well. Hallucinations are a common feature of delirium as are sensory misperceptions, in which patients misinterpret actual stimuli in their environment. For example, a patient might be reporting spiders or other insects on the ceiling of their hospital room.
The nature of delirium itself makes it difficult for patients to provide a history of recent events, so providers often rely on information provided by family or loved ones. Providers can inquire about unusual behaviors, forgetfulness, inattentiveness, recent physical symptoms, or medication changes. Gaining an understanding of the patient’s baseline cognitive functioning is especially helpful given the characteristic rapidity of delirium’s onset.
While delirium itself is diagnosed clinically, arriving at a diagnosis is often the first step, followed by a close exploration of potential triggers. The patient’s individual history will guide history gathering and additional work-up, including which lab studies or diagnostic tests to obtain. In general, a full physical review of systems is warranted. New onset of fevers, rigors, cough, diarrhea, or dysuria might suggest an ongoing infection. A close review of recent medication changes is also crucial. The addition of new deliriogenic medications, such as benzodiazepines, opioids, or anticholinergic agents should be noted.
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Special tests may be needed to find the cause of your loved one’s delirium so that the medical team can come up with a plan to try to fix the problem. Studies have shown, however, that even if the original cause of delirium is corrected, it may still take weeks or months for your family member to get back to “normal.” Unfortunately, in some cases, patients never fully recover.
Delirium can be very frightening to caregivers. In some cases a patient may not recognize their caregiver, may not respond or may even be hurtful. It is important to remember that delirium is a medical condition and your loved one can’t control these behaviors. You can help your loved one just by being with them. Your familiar face in a sea of doctors and nurses can be reassuring to a patient and help them remain calm. Surrounding your loved one with pictures or familiar objects may also help improve their mental status. In some hospitals, large clocks or calendars are placed in patients’ rooms to help enhance their sense of orientation.
Catatonia, a neuropsychiatric syndrome characterized by abnormal movements, behaviors, and withdrawal, is a condition that is most often seen in mood disorders but can also be seen in psychotic, medical, neurologic, and other disorders. Most studies on the incidence of catatonia find it to be between 5% - 20% in the acute inpatient psychiatric setting.
Most episodes of catatonia can be classified as excited, retarded, or malignant. Symptoms can wax, wane, or change during these episodes, and patients affected can have periods of withdrawal and periods of excitation. Studies have suggested a connected pathway between the cortex, basal ganglia, and thalamus underpins these different subtypes and results in catatonic symptoms.
The DSM-V gives 12 categories for symptoms that can lead to a diagnosis of catatonia. These symptoms include stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerisms, stereotypy, agitation not influenced by external stimuli, grimacing, echolalia, and echopraxia. At least three of these symptoms must be present for the diagnosis of catatonia. Some other criteria used in the Bush-Francis rating scale include automatic obedience, autonomic abnormalities, and the presence of a grasp reflex. These together present a wide variety of symptoms that can be present, and while there is a crossover between them and aspects of other illnesses, findings such as waxy flexibility, posturing, and automatic obedience can be more specific for catatonia.
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Catatonia is often thought to precipitate secondary to another underlying illness. Psychiatric disorders can present primarily with symptoms of catatonia. Mood disorders such as bipolar disorder and depression are the most common disorders in which catatonia manifests. A psychotic disorder such as schizophrenia can also be associated with catatonia, and historically schizophrenia recognition and diagnosis included symptoms of catatonia or was subtyped if catatonic symptoms were present.
When catatonic symptoms present, the cause is likely psychiatric, but many medical etiologies can lead to catatonia. Neurologic insults such as strokes, neoplasms, or other diseases such as Parkinson's can lead to catatonia. Autoimmune, paraneoplastic, infectious, metabolic, and certain drug exposures and poisonings can lead to the development of catatonia. The differential for the cause of catatonia is very broad, and a new case of catatonia without a significant psychiatric history should be a cause for further evaluation for an underlying insult.
In retrospective studies, rates of catatonia among all psychiatric patients range from 0.5% - 2.1%; although, some prospective studies have found the incidence to be as high as 17.1%. Among patients with mood disorders, rates have been higher, ranging from 13% - 27%.
The pathophysiology of catatonia is not fully understood, but as imaging studies have improved more structures and pathways have been implicated in the pathogenesis of this syndrome. Using FMRI imaging, dysfunction has been seen in the right medial orbitofrontal and lateral orbitofrontal prefrontal cortex. The right motor cortex has shown atypical lateralization after patients who were suffering from catatonia were given lorazepam. Dysfunction in GABA, glutamate, serotonin, and dopamine transmissions have been implicated in the initiation and progression of catatonia symptoms through clinical findings of catatonia as a result of agents that disrupt these pathways or agents that affect these pathways relieving the symptoms of catatonia.
The initial presentation for catatonia can vary greatly due to the different subtypes that this syndrome can present. A lot of causes for catatonia can also make a typical presentation difficult to describe. As most patients with catatonia have a psychiatric illness primarily causing catatonia, a progression of psychiatric illness will be the most likely history.
A patient will often present with worsening depression, mania, or psychosis antecedent to catatonia symptoms beginning. These symptoms can present as excited, withdrawn, or a mixture. A patient presenting with excited catatonia will often have odd mannerisms such as performing actions without purpose or at inappropriate times (e.g., saluting). They may be agitated, hold odd positions against gravity, or have stereotypic and repetitive movements such as picking at their clothes or making odd gestures repeatedly. Their speech may be repetitive or mimic the interviewer’s speech or actions. A patient with withdrawn catatonia will likely be stuporous, hold an odd position, have no response or opposition to outside stimuli, and have very little speech. These symptoms may be present at some times and not at others, may be present in a combination, and vary in intensity throughout the hospital course. If these symptoms begin because of a secondary medical illness that illness may also cause other psychiatric symptoms such as mania or psychosis.
The physical exam for a patient with suspected catatonia can help to diagnose and differentiate it between other conditions such as neuroleptic malignant syndrome. Passive movement of limbs and the type of resistance encountered can reveal what the underlying condition is. If the patient has waxy flexibility and catalepsy (holds a posture against gravity when passively moved into a posture,) catatonia is high on the differential. If there is lead-pipe rigidity, neuroleptic malignant syndrome should be suspected. Spastic rigidity would indicate potential serotonin syndrome. Cogwheel rigidity is more concerning for extrapyramidal symptoms from neuroleptics.
While the diagnosis of catatonia is a clinical diagnosis that does not require specific lab tests or imaging, certain testing can help determine the underlying etiology of the catatonia. An EEG in a patient with primary catatonia due to a psychiatric disorder will likely have diffuse slowing on EEG. As a post-ictal state can cause catatonia, an EEG may be helpful in detecting seizure activity driving the syndrome. While an MRI or CT scan cannot show catatonia, brain imaging could show abnormalities that are causing the catatonia. Imaging of the rest of the body may reveal neoplasms causing paraneoplastic encephalitis. Metabolic screens for illnesses such as diabetic ketoacidosis, glomerulonephritis, hepatic dysfunction, or other abnormalities may reveal a reversible cause. Inflammatory markers and autoantibodies may show autoimmune causes for catatonia. Vital signs should be monitored frequently as autonomic instability may indicate the onset of malignant catatonia - a catatonic syndrome characterized by fever, hypertension, tachycardia, and tachypnea which can progress to death if not rapidly treated. Overall in a patient with new-onset catatonia, psychiatric causes should be considered first, but somatic causes should not be ignored, especially if an underlying mental illness does not easily explain the clinical picture.
The initial treatment, once potential catatonia causing agents such as neuroleptics, steroids, stimulants, anticonvulsants, dopamine depleters, and others, are stopped, is to provide a lorazepam “challenge.” By giving a dose such as lorazepam 2 mg IV slowly, 60% - 80% of patients with catatonia will have some or significant improvement in catatonia symptoms within 15 min - 30 min. If the patient responds to this lorazepam challenge, lorazepam can be subsequently scheduled at interval doses, often three times a day (though different patients respond at different rates.) The dose of lorazepam can be titrated until catatonia symptoms resolve. Paradoxically catatonic patients do not become sedated on benzodiazepines. Once the dose is titrated for efficacy, patients will be alert and interactive. Throughout this titration, the patient’s underlying cause should also be treated. This lorazepam dose can be slowly tapered as tolerated. If this tapering occurs too quickly, catatonia symptoms may return. Some patients require tapering over months. When the dose makes the patient sedated instead of active, it can likely be reduced.
If the patient’s catatonic symptoms do not respond to benzodiazepines usually within 1 week, and the underlying cause either cannot be treated or treating it does not improve the symptoms, electroconvulsive therapy (ECT) can be used to reverse the symptoms. ECT is also recommended for malignant catatonia often used in combination with benzodiazepines.
Catatonia has historically responded well to the lorazepam challenge, thus, the prognosis is generally positive. Studies exhort response rates of up to 80% following the administration of lorazepam.
Functional Neurological Disorder (FND) is a problem with the functioning of the nervous system and how the brain and body send and receive signals. Physical and/or psychological risk factors can cause functional symptoms which include a variety of physical, sensory and cognitive symptoms that have yet to be explained by a recognised disease.
Functional Neurological Disorders are considered to be multifactorial, which means many different risk factors can contribute to the development of the disorder. The symptoms are real and can cause impairment in quality of life that is similar to and in some aspects worse than other neurological conditions. FND occupies a grey area between psychiatry and neurology that historically has failed to gain the interest of researchers and clinicians. The prevalence and potential reversibility of functional illness have peaked new research interests. FND is considered as a rare disease, However, the exact prevalence is unknown, and the mechanisms which cause FND continues to be poorly understood despite its prevalence within neurological clinics. Some researchers claim that functional symptoms are often seen in neurological services making it a common disorder. The most common misconception is that FND patients are in control of some or all of their symptoms. The patient does not consciously produce functional symptoms.
Functional Neurological Disorder symptoms are often described as appearing suddenly and progressing rapidly. Symptoms typically wax and wane, including complete remissions and sudden recurrences. It is common for other illness or physical injury to trigger functional symptoms or for patients to develop functional overlay with concurrent illnesses.
The diagnosis of FND should be approached in the same transparent and straightforward way a physician would do for other patient and diagnosis seen in their clinic. An FND diagnosis should be made from a detailed patient history and positive signs. The most important first step toward a successful treatment for Functional Neurological Disorder comes from clear and effective communication in a mutually respectable environment. The clinician’s ability to explain the diagnosis and educate the patient is of critical importance to the subsequent likelihood of successful treatment.
Despite the prevalence of Functional Neurological Disorder, the exact cause of FND is unknown. Many different predisposing factors likely make patients more susceptible to functional symptoms, and at the time of illness onset, these precipitating factors may likely trigger or exacerbate FND symptoms which then cultivate on-going functional symptoms. Perpetuating factors likely begin to create new neuropathways, which could eventually cause changes in the brain. In the most recent fMRI studies, patients with FND showed decreased functional connectivity in some parts of the brain compared to their healthy counterparts. While these findings do not identify the predisposing factors to functional symptoms, they suggest a decrease in function between voluntary motor pathways and self-agency. An impairment of self-agency or the sense that one is not in control of voluntary movement is a defining characteristic of FND. These findings play a critical role in how patient symptoms are understood. Given the physiological evidence that functional movements are voluntary in nature, medical professionals often mistake patients as feigning or malingering. The resting-state fMRI’s lend itself to support an organic abnormality of functional connectivity in the brains of FND patients.
Historically FND has traditionally been viewed as an entirely psychological disorder resulting in physical symptoms caused by suppressed trauma. Psychological disorders and stressful life events, both recent and in childhood, may be risk factors for developing the condition in some patients, but they rarely provide a full explanation for the cause of the condition and are absent in many patients. Patients do not have to be stressed, depressed or anxious to develop functional symptoms, nor had they had to have had an adverse childhood experience. Patients, physicians, and psychologists often fall into old paradigm traps searching relentlessly for underlying trauma that does not exist. It can be essential to address the possibility of psychological contributing factors for all patients.
The habitual change in terminology has resulted in a great deal of confusion, stigma, and frustration surrounding FND. While the individual labels have different meanings, they are all terms used for the same set of symptoms. Conversion Disorder is a term that is relatable to some patients who can clearly define a psychological trauma, which they are “converting” to their physical symptom.
Dementia is an umbrella term to describe brain impairment, a decline in cognitive abilities ranging from memory loss to difficulty with language, motor skills, and more. I often explain to patients and families that dementia simply means a waxing and waning of thinking ability. I use the example of an eight-cylinder car, and with dementia, patients often are driving with six or seven cylinders firing.
While all Alzheimer’s disease patients have dementia, not all dementia patients have Alzheimer’s Disease. Alzheimer’s disease is currently the most known and common form of dementia syndrome, accounting for 60-75% of cases. However, that is not all. The hallmark symptom of Alzheimer’s disease is memory loss, the most known and common form of dementia. Caused by an abnormal accumulation of amyloid proteins in the brain, these proteins form large clumps that stick together and form plaques in the brain over time. This form of dementia is often associated with behavior changes, which can be alarming for family members.
The most common symptoms of vascular dementia are a decline in critical thinking and the onset of confusion that interferes with daily life. This type of dementia develops due to impaired blood flow to the brain, particularly in areas responsible for cognitive reasoning. With this form of dementia, we often see a stepwise decline in cognitive ability.
In this form of dementia, patients experience changes in perception often associated with visual hallucinations, a decline in motor abilities, and more. In advanced cases, REM sleep disorder is present in which a patient may “act out” while dreaming.
Not exclusively affecting senior patients, this type of dementia affects the frontal and temporal lobes of the brain, resulting in abnormal behavioral changes such as socially inappropriate behavior, mood changes, and more. Early onset symptoms affect everything from mood to motor skills.
The following symptoms are generally associated with cognitive decline and impairment. Most of my patients ask, is dementia an inevitable part of aging? I tell them that while dementia most commonly affects adults 65+, dementia is not solely a senior person’s disorder.
Diagnostic testing in the form of MRI of the brain, EEG, vascular studies, laboratories for reversible causes of dementia, and neuropsychological testing can be very helpful.
It’s never too late to make a change. The earlier, the better!
Well, it may not be possible to reverse dementia, but we certainly can slow the progression with appropriate diet, nutrition, and lifestyle changes. The most important consideration is to make sure that the correct diagnosis has been established. This requires comprehensive assessment and neurologic evaluation.
Establish a family care network of support, obtain as much medical and social information as possible, and ensure that Grandma is in a safe, secure environment that can help her care for all her medical needs.
Individuals don’t die from dementia per se. However, complications of dementia, such as lack of appetite, social withdrawal, and poor self-care, can lead to medical conditions that can cause serious problems.
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