Try this mindfulness exercise whenever you’re feeling anxious or stressed
Try this mindfulness exercise whenever you’re feeling anxious or stressed
Ketamine is a drug/medication that was initially developed in 1962 as a structurally related alternative to phencyclidine (PCP). At that time, phencyclidine (PCP) was being used as a dissociative anesthetic for humans and animals, but its use was discontinued because of concerns about neurotoxicity.
Interestingly, ketamine and PCP demonstrated similar anesthetic properties, but ketamine was better tolerated and not neurotoxic at anesthetic doses. This resulted in ketamine’s approval as an anesthetic agent by the U.S. Food and Drug Administration (FDA) in 1970.
Ketamine is abused as a recreational drug and goes by many street names including Barry Farrell, Blind Squid, Cat Food, Cat Valium, Donkey; Green, Honey Oil, Jet, Keller, Kelly’s Day, Ket, Kit Kat, Kitty Flip, Purple, Special La Coke, Super Acid, Super C, Vitamin K, Wobble, Wonk, or simply the letter K.
Yes, ketamine has is a fast-acting antidepressant medication and some patients see improvements in mood within hours to days (rather than weeks or months for classic antidepressants). Ketamine appears to rapidly decrease thoughts of suicide as well. However, the effects are often short-lived. Ketamine by mouth, nasal spray, or intravenous infusion are viable options for those suffering with treatment-resistant depression.
Yes, ketamine has been shown to be effective for people with generalized anxiety, post-traumatic stress disorder (PTSD), and obsessive-compulsive disorder (OCD). A study published in the American Journal of Psychiatry found that repeated doses of ketamine can help reduce the symptoms of people who suffer from PTSD. Over a two-week period, patients received six infusions of ketamine.
Yes, studies have looked into ketamine’s effect on depressed people who have a family history of alcoholism. In research that appeared in the American Journal of Psychiatry, people with problem drinking were administered ketamine along with motivational enhancement therapy, compared with a control group, the ketamine plus therapy group drank less and did not relapse as much.
Ketamine has demonstrated efficacy for the following conditions:
Ketamine may be administered in oral form (as a troche/lozenge), through the nose (esketamine nasal spray), or by infusions (intravenously) in specialized clinics. A round of ketamine infusions typically comprises six (6) sessions spread over a two to three weeks and may cost several thousand dollars. Patients typically pay out-of-pocket for ketamine therapy except for the nasal spray, which has an FDA indication for treatment resistant depression. Some patients benefit from the oral form of ketamine, which is much less expensive but requires using a compounding pharmacy.
Ketamine itself is a mixture of two compounds, (R)-Ketamine and (S)-Ketamine. These are called stereoisomers. In stereochemistry, stereoisomerism, or spatial isomerism, is a form of isomerism in which molecules have the same molecular formula and sequence of bonded atoms but differ in the three-dimensional orientations of their atoms in space. By definition, molecules that are stereoisomers of each other represent the same structural isomer.
Ketamine itself is not FDA-approved to treat depression, but the stereoisomer S-ketamine, or esketamine, is. The drug is delivered by nasal spray and is designed to be administered alongside a traditional antidepressant. It was approved specifically for treatment-resistant depression, or depression that has failed to respond to other antidepressant medications.
Because esketamine, but not ketamine, is FDA-approved, it may be covered by insurance. But the drug must be administered under a doctor’s supervision, which limits its availability/accessibility.
Side effects of ketamine can include
Ketamine is toxic to the lining of the bladder and may cause inflammation of the bladder–called ulcerative cystitis.
Ketamine’s antidepressant effects are changing our understanding of the neurobiology of depression.
Ketamine affects multiple neurotransmitter systems—including the opioid system, monoaminergic (i.e., norepinephrine, serotonin, dopamine) systems, glutamatergic system, and the muscarinic (cholinergic) system to name a few—but the leading theories for how ketamine works as an antidepressant implicate the glutamatergic (glutamate) system.
Watch the video below before continuing.
As illustrated in the video, Ketamine’s primary mechanism of action is antagonism, or blockade, of N-methyl-d-aspartate (NMDA) receptors.
N-methyl-d-aspartate (NMDA) receptors are glutamate receptors (glutamate binds and activates NMDA receptors on neurons). NMDA receptors work together with AMPA receptors, another type of glutamate receptor, to initiate changes within neurons. These changes include increased survival, viability, and stronger connections with other neurons.
NMDA receptors are the primary targets for both ketamine and PCP. Interestingly, NMDA receptors are also targets for medications such as Memantine (Namenda), a medication for Alzheimer’s Dementia, and Dextromethorphan, the active ingredient in Robitussin. It isn’t surprising that both of these medications are now being investigated for depression.
Skolnick and colleagues (1996) first postulated a role for the glutamate system in depression when they noted that drugs that block NMDA receptors mimicked the effects of clinically effective antidepressants.
The leading hypothesis is that the initial effects at NMDA and AMPA receptors modulate cellular and molecular processes that are known to be important mediators in the formation of new and “stronger” neuronal connections–a concept termed neuroplasticity. This is the primary molecular mechanism for learning and memory.
Normally, glutamate stimulates both NMDA and AMPA receptors. Activation of BOTH these receptors “tells” the neuron to produce important proteins involved in cell growth and survival. Although both NMDA and AMPA receptors must be activated together for this to occur, it appears that AMPA receptors are most important. That is, when only NMDA receptors are activated and AMPA receptors are blocked, these changes don’t occur (see figure below).
Selectively blocking NMDA receptors with ketamine means there is more glutamate available to activate AMPA receptors. Increased activation of AMPA receptors hastens AMPA-mediated changes in the cell such as production of more AMPA receptors and production of growth factors to name a few. These changes ultimately strengthen the connection between neurons and produce more connections (see figure below). While this is a simplified explanation (it is much more complicated than this) it provides a basic understanding of how we think Ketamine works as an antidepressant.
In summary, ketamine’s downstream effects include upregulation of important growth factor proteins such as mammalian target of rapamycin (mTOR), eukaryotic elongation factor 2 (EEF-2), glycogen synthase kinase 3 (GSK-3), and brain-derived neurotrophic factor (BDNF) that increase neuronal cell growth, survival, and formation of new connections. It is important to mention that the precise mechanisms implicated in the antidepressant response to ketamine remains unknown and is likely multifactorial.
“Helping people talk themselves into changing”
Motivational interviewing is an evidenced-based technique to encourage people to find their own motivation for change. By identifying our fears and ambivalences about change, we can work to overcome the resistance to change bad habits. This is not a series of techniques to “trick” people into changing. Instead, it’s a skillful method for eliciting an inner motivation to make changes.
It is tempting to tell ourselves that we should change. But this is rarely effective. The “righting” reflex is our immediate tendency (or urge) to advise ourselves and others what they should or shouldn’t do. Although the advice comes from good intentions, it rarely works. The “Shoulds” and “Shouldn’ts” need to go.
It is important to understand why we want to change and what fears or ambivalences we have that are working against us.
Ask yourself, what are both the positives and negatives of changing this behavior? What do I fear will happen if I make this change? What does the current bad behavior provide, if anything, for me?
Many people who try to stop smoking find it difficult because they enjoy the stress-relieving qualities of smoking cigarettes. Exploring and better understanding our own ambivalences is a key part of helping us overcome the resistance.
Below are two approaches to starting a conversation with someone about their bad smoking habit. If someone was approaching you about a bad habit, which approach would you respond better to?
APPROACH ONE: “You should really stop smoking those cigarettes, they are so bad for you and can cause cancer and other horrible things!”
APPROACH TWO: “What do you enjoy about cigarettes? Is there anything you don’t really like about cigarettes?….Sounds like smoking really helps you in some ways but frustrates you in other ways. Have you ever considered quitting? If so, what prevents you from trying?”
People are more likely to change when they feel validated rather than criticized or judged. Active listening is a key principle of motivating ourselves and others. Active listening shows a level of understanding and empathy that can be very powerful in encouraging change. Be kind to yourself!
Empowering ourselves or others to change requires cultivating an optimistic and hopeful attitude. If pessimism and doubt cloud the picture, it is worth exploring and challenging these negative beliefs.
Motivation is/are the reason(s) one has for acting or behaving in a particular way. It is our willingness to do something. Motivation is multidimensional, dynamic, and has external and internal factors. It is the key to change. Motivation can be elicited and enhanced and is an important factor in our readiness to change.
There are two key dimensions of motivation:
Importance: the “why” of change
Confidence: the “how” of change
The importance of a change is about the “why” of change. Why is a change desirable? Why is it important that we change? The confidence we have about changing is the “how” of change. Our motivation increases when we understand the importance of change while also feeling confident that we CAN change.
Motivation to change a behavior or habit requires that we be ready, willing, and able to change. Our readiness is simply a matter of our priorities. Our willingness to change depends on the perceived significance of a change. And our ability to change depends on our confidence level. The “ABCs” of motivation and change are Acceptance that change is needed, Belief that change is better, and Confidence in one’s own ability to change.
A) Accept: One must accept that a behavior or habit is a problem and that a change is needed
B) Believe: One must believe that they will be better off if they change
C) Confidence: One must have confidence in one’s ability to change
Most of us will pass through a series of stages as we make a change.
(1) Precontemplation Stage: No way I can do this. Nope. Not happening! (Denial)
(2) Contemplation Stage: Okay, maybe I can do this. (Ambivalent)
(3) Determination/Preparation Stage: Let’s do this! (Motivated)
(4) Action Stage: I’m doing it!
(5) Maintenance Stage: I’m continuing it. I’m living it!
(6) Relapse/Recycle Stage: Ugh! Okay, I’m back to 1…
What makes you feel it might be time for a change?
Can you tell me more about that?
What have you noticed about your ____?
What concerns you most?
How would you like things to be different?
What will you lose if you give up drinking?
What have you tried before?
What do you want to do next?
“So you’ve started walking this past week!”
“You didn’t want to come today, but you did!”
“You are down to 5 cigarettes/day?! That’s great! You were smoking 8 cigarettes last week!”
Ordering, directing or commanding
Warning, cautioning or threatening
Giving advice, making suggestions or providing solutions or providing solutions
Persuading with logic, arguing, lecturing
Telling people what they should do Telling
Disagreeing, judging, criticizing or blaming
“Let me see if I understand thus far…”
What are some of the good things about X behavior?
People usually do X because they feel it helps in some way. How has it helped you?
What do you like about the effects of X?
What would you miss if you weren’t doing X?
Can you tell me about the down side?
What are some aspects you are not so happy about?
What are the things you wouldn’t miss?
If you continued as before, how do you see yourself in a couple of years from now if you don’t change?
On a scale of 1-10, how important is it to you to change X behavior?
Why did you give it a higher # and not a (lower #) ?”
What would have to happen to raise that score from # to #
Most medications for mental disorders require a gradual reduction in dosage over weeks to months. Unfortunately, there aren’t formal recommendations from drug manufacturers about how to do this. Most of the recommendations provided in this post are informed by both clinical experience and discussion among colleagues.
The withdrawal symptoms associated with stopping psychotropic medications can be unpleasant but are rarely dangerous. That being said, a few medications absolutely require a gradual reduction in dose over time to prevent potentially lethal withdrawal reactions. In general, but not always, medications with longer half-lives are less likely to cause severe withdrawal reactions.
Half-life is the time required for the total amount of drug in the body to be reduced by 50%.
For example, fluoxetine (Prozac) has an active metabolite (norfluoxetine) with a half-life of up to two weeks. This means that once you stop taking fluoxetine, it will take up to two weeks for the amount of norfluoxetine to be reduced by 50%. Because of its long half-life, fluoxetine is less likely to cause a withdrawal reaction.
In fact, fluoxetine is often prescribed to reduce withdrawal symptoms associated with tapering off other antidepressants that have shorter half-lives.
It is important to remember that each individual will have slightly different needs. The way medications are discontinued should be tailored to each individual. The recommendations provided below are for educational purposes only and should not be considered formal medical advice. Please consult your physician for personal health concerns including how to stop your medication.
Antidepressant withdrawal symptoms range in severity, but the mnemonic “FINISH” can help you identify them.
The selective serotonin reuptake inhibitors (SSRIs) generally require a daily dose reduction of about 25% every one to two weeks. Of the SSRIs, Paroxetine (Paxil) appears to be the most problematic likely due to its relatively short half-life and lack of active metabolites.
Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) such as venlafaxine (Effexor), duloxetine (Duloxetine), and tricyclic antidepressants (e.g., nortriptyline and amitriptyline) may produce more intense withdrawal symptoms if stopped abruptly. While many case reports suggest that both tricyclic antidepressants (TCAs) and SSRIs produce similar symptoms upon discontinuation, TCAs often have additional symptoms such as parkinsonism and balance/coordination issues.
Antidepressant discontinuation symptoms associated with Monoamine Oxidase Inhibitors (MAOIs) may have the most severe symptoms such as aggressiveness, agitation, catatonia, severe cognitive impairment, myoclonus and psychotic symptoms.
In most cases, symptoms develop within three days of stopping or reducing the dose of antidepressant.
Most traditional mood stabilizers, with the exception of lithium, are anti-seizure medications. Abruptly stopping an anti-seizure medication can not only put you at risk for developing withdrawal seizures but can also induce a manic or hypomanic state.
Withdrawal symptoms include seizures, myoclonic jerks (jerking movements), muscle twitching, severe anxiety, insomnia, agitation, and upset stomach (i.e., nausea, vomiting, diarrhea).
Lithium is worth extra mention as it must be tapered very slowly. Abruptly stopping lithium has been associated with inducing severe depressive or manic states as well as suicidal thoughts. It is very important NOT to stop lithium abruptly.
Benzodiazepines are also anti-seizure medications but are mainly used for anxiety and to aid with alcohol withdrawal symptoms. These medications are dangerous if stopped abruptly.
Withdrawal symptoms include seizures, myoclonic jerks (jerking movements), muscle twitching, tremors, severe anxiety, sweating, insomnia, tachycardia (fast heart rate), elevated blood pressure, agitation, sensory disturbances, hallucinations, confusion, and upset stomach (i.e., nausea, vomiting, diarrhea).
In general, benzodiazepines that are only taken “as needed” don’t require a taper. That is, if they aren’t taken daily. Daily benzodiazepine use will require a gradual taper. In general, the longer the time taking a benzodiazepine, the slower the taper will need to be.
Antipsychotic medications are a bit of a misnomer because they are prescribed for more than just psychosis. Antipsychotics are also prescribed for mania, hypomania, depression and anxiety. In general, the more anticholinergic the antipsychotic, the slower the taper needs to be. Quetiapine, Clozapine, and Olanzapine are highly anticholinergic and need to be tapered more slowly than the dopamine partial agonists (e.g., Aripiprazole, Brexpiprazole, and Cariprazine).
If switching to a different antipsychotic, the taper will depend on which medications are being switched.
DISCLAIMER: No formal recommendations have been provided drug manufacturers or organizations. The suggestions provided in this post are based on clinical experience and the references provided below. As stated previously, this post is for educational purposes only. Please always consult your physician for personalized medical advice.
(1) Resolution of internal conflict
(2) Improvement in the quality of one’s relationships
(3) Increased satisfaction with work
(4) More cohesive sense of self
Typical Structure of Therapy: Patient meets with the therapist 1–2 times/week for 45-50 minute sessions.
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Communicating effectively isn’t natural for many people. One of the most, if not the most, important contributors to a healthy relationship is effective communication. Whether it’s a loved one, a coworker, or your financial advisor, communicating effectively creates trust and respect between two people. Here we review different types of communication and provide a few tips for communicating your needs assertively and respectfully.
In passive communication, a person prioritizes the needs, wants, and feelings of others instead of their own. The person does not express their own needs or does not stand up for them. This can lead to being taken advantage of, even by well-meaning people who are unaware of the passive communicator’s needs and wants.
In aggressive communication, a person expresses that only their needs, wants, and feelings matter. The other person is bullied, and their needs are ignored.
In assertive communication, the needs of both parties are emphasized as equally important. During assertive communication, a person stands up for their own needs, wants, and feelings, but also listens to and respects the needs of others. Assertive communication is defined by confidence, and a willingness to compromise.
When a person feels that they are being blamed, it’s common that they respond with defensiveness. “I” statements are a simple way of speaking that will help you share your feelings in a productive and blame-less way. When using “I” statements, be sure to use a soft and even tone to describe how the other person’s actions affect you.
“I feel (EMOTION WORD) when _________”
“I feel concerned when you go so long without texting me back. I am afraid something bad happened to you.”
“I feel worried when you come home late. I find it hard to sleep.”
When bringing up a problem to someone else (like your partner, coworker, loved one, friend), the first three minutes are crucial. A soft startup sets a positive tone and helps resolve conflict. By starting a conversation calmly and respectfully, you and your partner are more likely to focus on the problem, rather than who’s to blame.
(1) Pill Rolling Tremor. Tremors occur due to rhythmic contractions of opposing muscle groups. In PD, the tremor typically occurs at a frequency of 3-5 muscle contraction cycles per second (Hz). The tremor occurs at rest, usually starts unilaterally in the hands and fingers, and diminishes during voluntary movement and sleep. As the disease progresses, the tremor becomes more prominent, bilateral, and eventually rigidity develops.
(2) Bradykinesia or hypokinesia (slowed movement). Patients with PD are slow in their movements, have difficulty with fine motor control, and experience problems writing and/or using their hands to play instruments or type on a computer keyboard. Spontaneous movements and associated movements are diminished. When we talk to others, we use facial gestures and hand movements to express our emotions; this requires spontaneous movement. When we walk, we swing our arms and move our legs in a specific way to keep our balance; this requires associated movements. When we feel thirsty while reading this lesson, we may reach for our cup of coffee (or water, or wine); this requires initiation of movement. All of these are affected in patient’s with PD which leads to the classic findings of “masked-like” facial expressions, minimal arm swing/shuffling gait, and delayed initiation of voluntary movement.
(3) Rigidity (Cogwheel Rigidity). When apposing muscle groups are contracting at the same time or are always in a contracted state, this leads to muscle rigidity. When you try to move the arms of an individual with PD, you will find it difficult. There is a passive resistance to movement similar to the negativism or waxy flexibility seen in catatonia.
(4) Posture problems. Standing or sitting up straight requires the axial/postural muscles. Patient’s with PD have difficulty maintaining appropriate posture and are seen stooped or hunched over.
(1) Cognitive deficits. About 30% of patients with PD may have an accompanying dementia or other forms of cognitive loss. The cognitive deficits seen in patients with PD are thought to be a result of damage to the cholinergic system (especially the nucleus basalis of Meynert) and buildup of insoluble protein aggregates within cortical and sub-cortical structures.
(2) Constipation. Likely related to cholinergic dysfunction.
(3) Olfactory deficits. Diminished sense of smell may occur before motor symptoms.
(4) Autonomic Dysfunction. Disrupted sympathetic innervation to the heart and other important organs may lead to bradycardia and hypotension, urinary retention, postural hypotension, sweating, and drooling.
(5) Rapid Eye Movement Sleep Behavior Disorder (RBD) and other sleep disturbances. During sleep, patients with PD may “act out” their dreams. REM sleep is normally characterized by muscle paralysis. RBD occurs when paralysis of muscles does not occur, and patients move around while dreaming. Insomnia and other sleep disturbances are common in patients with PD.
(6) Mood and personality changes. Depression, apathy, anxiety, irritability, agitation, and psychosis often occur in patients with PD–likely related to destruction of serotonergic projections from the raphe nucleus, noradrenergic projections from the locus coeruleus, cholinergic neurons, dopaminergic projections from the ventral tegmental area, and glutamatergic/GABAergic neurons.
The two main motor tracts that control skeletal muscles for movement originate in the motor cortex of the brain and are called the corticospinal tract (or pyramidal tract) and the corticobulbar tract. The corticospinal tract starts in the motor cortex and many, but not all, of the neuronal fibers cross over (or decussate) at the medullary pyramids to eventually synapse on lower motor neurons in the contralateral anterior horn of the spinal cord. Therefore, the right motor cortex primarily controls the left side of the body. Similarly, the corticobulbar tract originates in the motor cortex and many, but not all, of the neuronal fibers cross over and synapses on lower motor neurons in the brain stem. Therefore, the right motor cortex primarily controls movement of the muscles on the left side of the body.
The execution of motor movements involves more than just these two tracts. Information from the cortex and subcortical areas are integrated and processed and eventually transmitted to the motor cortex to execute movement. We call these motor “coordination/integration” pathways in the brain “extra pyramidal” because they occur outside of the traditional corticospinal/corticobulbar (pyramidal) motor tracts. The structures that make up the Extrapyramidal motor system include the Basal Ganglia, the Substantia Nigra (in the midbrain), and the subthalamic nucleus.
The structures that make up the Extrapyramidal motor system include the Basal Ganglia, the Substantia Nigra (in the midbrain), and the subthalamic nucleus. Basal Ganglia, as discussed in the Anatomy sections, include the caudate nucleus, the putamen nucleus, and the globus pallidus. The caudate nucleus and the putamen nucleus are called the “striatum” or “neostriatum” whereas the three nuclei together are referred to as the “corpus striatum.” The globus pallidus is divided into two parts, the internal and external parts. The substantia nigra (SN) is located in the midbrain and is named after the black pigmented neuronal cell bodies seen on anatomical sections. The SN is divided into two parts, the pars reticulata (SNr) and the pars compacta (SNc) Neuronal inputs to the striatum come from the motor cortex, substantia nigra pars compacta, the thalamus, and subcortical structures like the dorsal raphe nucleus. Information is processed in the striatum and eventually sent to the thalamic nuclei and back to the motor cortex. But from the striatum to the thalamic nuclei, neurons first synapse at the the globus pallidus internal (GPi) and substantia nigra pars reticulata (SNr). From the GPi/SNr, neuronal signals are sent to the thalamic nuclei. To make things more complicated, some of the neurons from the striatum don’t directly synapse on the GPi/SNr and instead take a detour at the globus pallidus external (GPe) and subthalamic nucleus (STN).
The extrapyramidal system and the motor nuclei of the thalamus form a loop that obtains information from the cortex and other areas of the brain, integrates and processes it, and relays it back to the motor cortex to modulate motor activity in the corticospinal and corticobulbar tracts. The diagrams can give you a headache but the simple concept is that stimulation of the direct pathway leads to activation of the motor cortex. On the other hand, stimulation of the indirect pathway decreases activation of the motor cortex (“indirect pathway inhibits”). This occurs through a series of glutamatergic and gabaergic connections. Please note that the diagrams are overly simplistic and do not show many of the other neurotransmitters involved (substance P, opioid peptides, neurokinin, etc).
Dopamine (DA) modulates this circuit. Stimulation of D1 receptors in the striatum by dopamine stimulates the direct pathway and increases motor cortex activity. Stimulation of D2 receptors in the striatum inhibits the indirect pathway. Therefore, the overall effect of dopamine is to increase activity at the motor cortex. Loss of dopamine input from the SNc (as seen in Parkinson’s Disease) or blockade of dopamine receptors via medications (like antipsychotics) will decrease activity in the motor cortex and cause slowed movements.
Acetylcholine (ACh) has the opposite effect of DA. Stimulation of M2 receptors in the indirect pathway stimulates the indirect pathway whereas stimulation of M1 receptors in the direct pathway inhibit the direct pathway. This leads to an overall net effect of decreased activity at the motor cortex. Note that ACh interneurons are activated by the glutamate neurons from the motor cortex but are normally under inhibitory control by DA from the nigrostriatal tract. This is why we give anticholinergic medications like benztropine (Cogentin) to help with extrapyramidal symptoms (EPS) and/or the slowed movements associated with Parkinson Disease.
Dopamine does not readily cross the blood brain barrier. However, its precursor, L-Dopa, does. The mainstay treatment for Parkinson’s disease is “dopamine replacement” with L-Dopa. Because L-Dopa is vulnerable to enzymatic degradation (via monoamine oxidases/MAOs, Catechol-O-Methyl transferases/COMTs, and aromatic amino acid decarboxylases/AADCs) within the intestine, L-Dopa is often administered with blockers of these enzymes (e.g. carbidopa) to ensure L-dopa reaches the brain. Despite the presence of inhibitors of these enzymes, therapeutic doses of L-Dopa still have some conversion to dopamine and norepinephrine in the periphery. This may explain the side effects seen with L-Dopa treatment.
Side effects of L-Dopa are thought to result from the conversion of L-Dopa to dopamine, norepinephrine, and/or epinephrine in the periphery. Dopamine in the medulla stimulates the chemoreceptor trigger zone to cause nausea/vomiting and dopamine alters gastrointestinal smooth muscle activity leading to gastrointestinal side effects. The conversion of L-Dopa to norepinephrine in the periphery can lead to sympathetic activation of the heart (tachycardia) and other cardiac arrhythmias. Neuropsychiatric symptoms such as depression, anxiety, agitation, aggression, impulsivity problems (gambling, spending) and psychosis (hallucinations and paranoia) can occur as side effects of L-Dopa treatment.
The COVID-19 pandemic has impacted the physical and mental health of many worldwide. Social isolation, work-life changes, and the socioeconomic effects of the pandemic have fundamentally changed the way many people live.
By now it is apparent that severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the virus responsible for COVID-19 disease, causes severe respiratory dysfunction (i.e., breathing problems) in a substantial number of individuals with acute infection. In addition to cardiopulmonary issues, there are a variety of acute and chronic neurological and neuropsychiatric sequelae that have been reported.
SARS-CoV-2 virus enters the nervous system through the olfactory (smell) and the circulatory (blood) routes. Active central nervous system (CNS) infection, environmental stress, financial stress, social isolation, loss of independence, and changes in family relational dynamics all contribute directly and indirectly to the neuropsychiatric sequalae of COVD-19 infection. It is important to note that individuals with pre-existing neuropsychiatric disorders are at higher risk for developing neuropsychiatric symptoms.
|Neuropsychiatric Symptoms of COVID-19|
|Neurological Sequelae of COVID-19|