A colleague’s experience with insurance companies

“I’m sorry, but I’m unable to take on new patients at this time.”

I’ve said that line hundreds of times in the 15 years since I started my solo private practice in psychiatry. I feel terrible each time I say it. Someone on the other end of the phone is suffering and has taken the difficult step to call for help — probably multiple calls, given the longstanding shortage of psychiatrists — and yet I added to their hopelessness.

For most of my years in practice, I was in-network for some insurance; I’ve always felt strongly about helping a diverse group of patients, not just those who can afford to pay private practice rates. Like most doctors coming out of residency, I was taught that (a) working for a hospital yielded both the safest career path and the most diverse group of patients, and (b) taking insurance facilitated that diversity. Departmental administration conveyed that doing otherwise essentially meant selling your soul — you’d be consigning yourself to caring for “the worried well,” affluent suburbanites with the purported psychiatric equivalent of paper cuts. Implicitly, they were asking, “What about your societal commitment? Isn’t that why you got into medicine? Isn’t that what we’ve been working so hard to instill?”

I became increasingly skeptical of that message as residency progressed. Despite various duty-hour regulations and ostensible protections, the problematic working conditions combined with limited institutional support pushed me away from hospital-based clinical work. I enjoyed seeing patients, though, and didn’t want to flee to the relative safety of research or working in hospital administration. I decided to start a private practice and avoid the soul-selling trap by both taking insurance and providing very generous fee-scaling arrangements to patients for whom paying privately would be a financial burden. I kept overhead low by doing everything myself: the care (both therapy and medication management), the documentation, the billing, the calls, and the scheduling. My practice filled quickly, driven primarily by the tremendous mismatch between psychiatrist supply and demand. I soon had to start telling prospective patients that my practice was full.

At the same time, I found myself spending increasing amounts of time on the phone with insurance claims service representatives. At first, the issues involved paper claims that simply disappeared into the ether or were rejected because I had included too much or too little information. Filling out the forms became like defusing a bomb — be exceedingly careful about which wires to cut and which wires to leave alone, and maybe, just maybe, I’d receive payment a couple of months later. Slight deviations from the insurer’s opaque and ever-changing protocol would necessitate resubmitting the claim, even after waiting several weeks to hear back. Once the insurers permitted me to start filing online, the claims stopped disappearing, but the denials persisted, often for no apparent reason.

I increasingly allocated blocks of time every day to address claims problems, such that my administrative time started exceeding my clinical time. I logged each call in a spreadsheet so that when the reimbursement failed to materialize several weeks later, I could cite the relevant claims reference numbers to help the service reps locate my calls in their database, saving us precious minutes of time. I grew to know which service reps were helpful and unhelpful, and I’d hope before each call that I’d get lucky and reach one of the good ones. I considered hiring a billing service, but adding expenses and another layer of bureaucracy to address the first layer seemed counterproductive.

My breaking point came in 2022 with claims involving an older patient whom I’d treated for more than a decade. Despite a half-dozen calls over several months, at roughly 30 minutes per call (including the time spent navigating the lengthy automated menus and on hold), the insurer continued to deny the claims, stating that I should’ve submitted them to a different insurer. Each conversation ended with the service rep’s acknowledging the insurance company’s error, stating that the claims would be reprocessed, and asserting that I would know the outcome in a few weeks. Notably, the insurer’s portion of each of the five visits was a mere $30. I routinely debated just writing off the charges, or at least the insurer’s portion thereof. But if I were going to write it off, why take insurance. 

Meanwhile, throughout these months, I informed numerous prospective patients that I had no time available to see them. I did not tell them that I’d have more availability if I weren’t spending hours arguing with their insurance reps, trying to get paid $30 for work that everyone agreed I had performed.

Finally, I realized that from the insurer’s perspective, the numbers mattered more than the care: The insurer was getting paid from the premiums of my patient, and from the premiums of prospective patients, all while denying me payment for my work and preventing me from doing additional work. This is the business model — customers pay for the right to be deprived of the product they’re purchasing. I decided I would stop spending portions of my days fighting that model, and instead I’d follow most other solo practitioner psychiatrists who do not take insurance.

In late 2022, I notified the insurer of my intent to terminate our contract, and I prepared my patients for the transition. My first year post-insurance has gone reasonably well, albeit with some obvious challenges. I’ve kept nearly all of my patients, with some sacrifices on all of our parts. I have had to increase my already liberal fee-scaling, which reduces my income but allows me to continue to treat my longtime patients. Some of my patients — those who can afford it — have seen their out-of-pocket costs increase; many patients with out-of-network benefits are now submitting their own claims to get reimbursed for our appointments. So far, while the insurers have been somewhat slow to reimburse my patients, outright denials of claims have diminished. Most importantly, I’ve had more time to see patients. I’ve seen more new patients in the past six months than I did in the previous three years. While my practice revenues fell 10% (not counting inflation) in 2023, I am serving more patients in total. But asking clinicians to see more patients for less money is not a sustainable path to improving access to mental health care.

My experience runs counter to the prevailing psychiatric narrative that insurance = access. Commercial insurers primarily serve the interests of investors and/or highly paid executives, whether corporate or “nonprofit.” Their salaries indicate society values them more highly than clinicians in addressing the current mental health crisis, but these individuals’ interests are often misaligned with the public good. The insurance business model saps clinic revenues, so clinic administrators consequently push mental health clinicians to see more patients in less time. Dissatisfied clinicians then depart for out-of-network private practice, or shift into academia or administration, where they see far fewer patients, if any at all. If we care about solving the mental health access equation, we need to understand where the dollars flow.

is it any wonder of why it is so difficult to find an in network provider?

Bipolar disorder

75% of patients present to a clinician with depressive symptoms. 

Presenting symptoms include anhedonia, lack of energy, feeling tired, low mood. 

Symptoms of mania include reduced need for sleep, racing thoughts, talkative, and restless. 

Common features: anger, lack of attention, anxious, agitated. 

treatment for bipolar depression include quetiapine and cariprazine.

many medications to treat bipolar mania. 

Understanding ADHD

Understanding ADHD

Establishing a diagnosis of adult ADHD can be challenging. ADHD has a genetic link and adults may inquire if their children are diagnosed. In addition, many false positive cases of late-onset ADHD may be attributable to nonimpairing cognitive fluctuations.   care must be made to avoid overdiagnosing and inappropriately treating. As their are no reliable diagnosing tools, and clinicians rely on self reported questionnaires, the concerns regarding malingered symptoms are high.   College students may be particularly prone to overreport to obtain academic accommodations and or stimulant medication.  clinicians need to be astute to those students that report high on the various screening scales, yet managed to achieve.  there is also the need to differentiate poor attention form other disorders that present with concentration issues. these include anxiety disorders, PTSD, depression, bipolar disorder, or other cognitive disorders.   In addition a clinician also needs to screen for any underlying sleep disorder that may impair concentration or any other medical issue as well as a substance use disorder. Two studies of adult-onset ADHD concluded that 95% of cases were better explained by other cases. 

Concerns about overprescribing stimulants include risk of addition, and interactions with other medications.  Stimulants also increase the risk of anxiety, psychosis, irritability, insomnia, and trigger manic like behaviors. Stimulants can raise blood pressure and heart rate with potential  cardiovascular events like arrthymias and strokes.

There are only 2 stimulant medications available. this is either methylphenidate or amphetamine.  These 2 medications however are prescribed in various ways, from long acting to short immediate release.   There are prodrugs for each, which require an enzyme to release the active compound.  Other delivery symptoms include one based on osmotic release through the gut, different formulations with coated beads to delay release,  patch, oral disintegrating tabs, liquids, and a preparation that is taken the night before and released in the am. 

There are 2 non stimulant medications that work on norepinephrine reuptake blocking and two preparations that work on the alpha receptor. 

There are several medications also used off label which have shown some promise in improving concentration. These include bupropion, modafinil, and armodafinil. 

NO psychiatric patient with ADHD should be treated with medication alone. Behavioral tools in addition, are essential for optimum treatment. 

Insomnia and its treatment

Criteria for defining insomnia includes an average sleep latency of > 30 minutes, wakefulness after sleep onset > 30 minutes,. Sleep efficiency of < 85% and total sleep time < 6.5 hours.

Agents that treat insomnia:
  • Reduce brain activation, enhancing sleep drive, activation of GABA IN HYPOTHALAMIC SLEEP CENTER (VLPO) -VENTRAL LATERAL Preoptic Area
  •  Positive allosteric modulators of GABAa -benzodiazepines and Z. Drugs. 
  • Reduce arousal by blocking orexins (DORAS) blocking H1, Blocking serotonin (HT2 A antagonists) and blocking norepinephrine (alpha 1 antagonists) 
Benzodiazepine facilitate GABA neurotransmission in inhibitory sleep circuits arising from the hypothalamic VLPO. 
Benzodiazepines and Z drugs target GABAA receptors that have a gamma subunit. Postsynaptic, and mediate physic inhibitory neurotransmission. This also can lead to tolerance and dependence. 
DORAs 
Block the wake stabilizing effects of the orexins especially at orexins 2 receipts. Act on both orexins 1 and 2. 
They prevent the release of wake promoting neurotransmitters. 
Bought to lack dependence and withdrawal. 
Suvorexand and Lemborexant, drug names.
Lemborexant may wear off sooner in am. 
Trazodone
5HT2A/alpha 1/H1 antagonist 
Antidepressant. Works to reduce arousal 
5HT2A  specifically enhances slow-wave sleep/deep sleep.
Antihistamine as mechanism of action:
Doxepin at low doses almost pure H1 blocker
Benadryl
alpha 2 delta ligands: open channel, N and P/Q voltage-gated ion-channel inhibitors. Can enhance slow wave sleep, restorative sleep, and help with pain management.
Gabapentin 
Pregabalin (Lyrica) 
Behavioral treatments
Relaxation training, meditation, stimulus control therapy, CBT, and other forms of psychotherapy. 

Maternal Use of Specific Antidepressant Medications During Early Pregnancy and the Risk of Selected Birth Defects

Which antidepressants used by pregnant women are associated with specific birth defects and do associations between antidepressants and specific birth defects remain after partially accounting for the underlying condition?

In a case-control study of 30 ,630 mothers of infants with birth defects and 11, 478 control mothers, there were previous and new associations between individual selective serotonin reuptake inhibitors,  , and bupropion and specific birth defects. Many selective serotonin reuptake inhibitor and birth defect (particularly heart defect) associations attenuated after partially accounting for the underlying condition; most venlafaxine associations remained.

This study included 30 630 case mothers of infants with birth defects and 11 478 control mothers (aged 12–53 years). Early pregnancy antidepressant use was reported by 1562 case mothers (5.1%) and 467 control mothers (4.1%), for whom elevated aORs were observed for individual selective serotonin reuptake inhibitors (SSRIs) and selected congenital heart defects (CHD) (eg, fluoxetine and anomalous pulmonary venous return: aOR, 2.56; 95% CI, 1.10-5.93; this association was attenuated after partially accounting for underlying conditions: aOR, 1.89; 95% CI, 0.56-6.42). This pattern was observed for many SSRI-CHD combinations. Associations between SSRIs and non-CHD birth defects often persisted or strengthened after partially accounting for underlying conditions (eg, citalopram and diaphragmatic hernia: aOR, 5.11; 95% CI, 1.29-20.24). Venlafaxine had elevated associations with multiple defects that persisted after partially accounting for underlying conditions (eg, anencephaly and craniorachischisis: aOR, 9.14; 95% CI, 1.91-43.83).

Conclusions: Venlafaxine was associated with the highest number of defects, which needs confirmation given the limited literature on venlafaxine use during pregnancy and risk for birth defects. Our results suggest confounding by underlying conditions should be considered when assessing risk. Fully informed treatment decision-making requires balancing the risks and benefits of proposed interventions against those of untreated depression or anxiety.

Evidence based pharmacotherapy of major depressive disorder

Lifetime prevalence of MDD is 16.2% but most patients are not adequately treated. SSRIs demonstrate equal efficacy with older drugs but are better tolerated and accepted. 

NSRIs are slightly more efficacious 63% vs 59% for traditional SSRIS. 

The more severe the depressive symptoms, the more robust the response.

Review of several studies report a DECREASE in the rate of suicide and ideation with prescriptions of antidepressants.  The studies where depression was not the only diagnosis but included use of antidepressants for other clinical indications may show   higher rates. 

Studies show a true antidepressant reponse can occur within the first 1-2 weeks of treatment. 75% of patients respond by week 4. 

Factors predictive of risk of relapse: prior episode, more severely ill, and the  presence of residual symptoms.

TRD treatment strategies: switching to another medication.  25%,  Switching to a third medication 14%, and switching to another class demonstrate and additonal  13% improved. 

Augmentation strategies: add mirtazapine- (45%), bupropion (30%), buspirone, atypical antipsychotics, lithium, lamictal, T3, or SAMe. The most research has been with atypicals, lithium, and thyroid augmentation. 

Other possible treatments include :  Agomelatine- a melatonin receptor agonist and a 5-HT2c antagonist, and Glutamatergic agents. 

Glutamatergic agents: NMDA receptor antagonists – include memantine and ketamine. Riluzole-currently treats ALS and acts to increase  release of glutamate and block reuptake-with some additional promise in treating TRD. 

Pramipexole- pre-synaptic dopamine agonist. 

Modafinil-good for depression related fatigue and sleepiness. 

SSRI agents

Fluoxetine or Prozac- both a SERT blocker and 5HT2c blocker. also a weak blocker at the NET transporter. Inhibitor of CYP 2D6 and 3A$. Because of action on the 5HT@c receptor can be activating and has anti bulimic activity.

Sertraline or Zoloft – SERT inhibition and weak DAT inhibition. Also has some affinity for the sigma 1 receptor which may have both anxiolytic as well as antipsychotic properties. weak inhibition of CYP 2D6. calming antidepressant.

Fluvoxamine or Luvox – also acts on the sigma 1 receptor to a greater degree than sertraline . Inhibitor of CYP 1A2 and 3A4. Has indication for OCD and Social anxiety disorder.

Paroxetine or Paxil – weak NET inhibitor. mild anticholinergic activity. inhibits the enzyme nitric oxide synthetase therefore problem with sexual dysfunction. Inhibitor of 2D6 and also a substrate. Withdrawal when stooping abruptly. calming. helpful with IBS because of anticholinergic activity. 

Citalopram or Celexa- mild antihistaminic property. weak inhibition at CYP 2D6. the R enantiomer is the reason for this. 

Escitalopram or Lexapro- pure SERT inhibition. more potent and less sedating than celexa. 

Norepinephrine Facts to Know

Synthesized from the amino acid tyrosine

In the neuron tyrosine is acted upon by 3 key enzymes.

Tyrosine hydroxylase converts tyrosine into DOPA

DOPA decarboxylase coverts DOPA into dopamine

Dopamine beta hydroxylase converts dopamine to norepinephrine
Action is terminated both by enzymes : MAO located in mitochondria in the presynaptic neuron and COMT located outside the nerve terminal, and a transport pump that removes NE from the synapse and pumps back into the presynaptic neuron for future use. The pump is a site where many drugs work.

Norepinephrine receptor subtypes

NET pump

VMAt2 -packing into vesicles

Alpha 1

Alpha 2a

Alpha 2b

Alpha 2c

Beta 1

Beta 2

Beta 3
Only alpha 2 receptors are presynaptic autoreceptors. Act as a break stopping further NE release.

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Categories: Uncategorized
Norepinephrine facts to know
Synthesized from the amino acid tyrosine
In the neuron tyrosine is acted upon by 3 key enzymes.
Tyrosine hydroxylase converts tyrosine into DOPA

Sheri Spirt, M.D.
Ssdr18@aol.com
Please follow me on Twitter @DrSheriSpirt
www.drsherispirt.com
212 595-6901
16 East 96th Street Unit 1A New York, N.Y. 10128

CONFIDENTIALITY NOTICE: This communication, including attachments, is for the exclusive use of the person to whom it is addressed. The information contained in this transmission is confidential and may be privileged and/or contain confidential health information that is legally protected by state and federal law, including the Health Insurance Portability and Accountability Act of 1996 and related regulations. If you receive this message in error, please contact the sender by return e-mail, indicate that you are not the intended recipient, and confirm that you have deleted the original message. Use, disclosure, distribution or copying of documents transmitted to you in error is strictly prohibited. Please do not retransmit the content of this message.

Bipolar Spectrum Disorders

Bipolar 1/4 – designates an unstable form of unipolar depression that responds rapidly but is unsustained to antidepressants. They benefit to an addition of a moodstabilizer.

Bipolar 1/2- similiar to schizoaffective illness or coined schizobipolar.

Bipolar 1 1/2 – Hypomania without depression.

Bipolar II1/2 – cyclothymic patients that develop a major depressive episode.

Bipolar III – patients that develop a manic or hypomanic episode on an antidepressant.

Bipolar III 1/2 – Bipolar disorder with substance abuse.

Bipolar IV – association of depressive episodes with a pre-existing hyperthermia temperament. Hyperthermic patients are those with sunny outgoing personalities, and usually quite successful, that plunge into depression.

Bipolar V – depression with mixed hypomania.

Bipolar VI – bipolarity in the setting of dementia.

Dysphoria mania – mania with some depressive symptoms.

Tags:

Categories: UncategorizedBipolar Spectrum Disorders
Bipolar 1/4 – designates an unstable form of unipolar depression that responds rapidly but is unsustained to antidepressants. They benefit to an …
Sheri Spirt, M.D.
Ssdr18@aol.com
Please follow me on Twitter @DrSheriSpirt
www.drsherispirt.com
212 595-6901
16 East 96th Street Unit 1A New York, N.Y. 10128

CONFIDENTIALITY NOTICE: This communication, including attachments, is for the exclusive use of the person to whom it is addressed. The information contained in this transmission is confidential and may be privileged and/or contain confidential health information that is legally protected by state and federal law, including the Health Insurance Portability and Accountability Act of 1996 and related regulations. If you receive this message in error, please contact the sender by return e-mail, indicate that you are not the intended recipient, and confirm that you have deleted the original message. Use, disclosure, distribution or copying of documents transmitted to you in error is strictly prohibited. Please do not retransmit the content of this message.

Correlation of Hyperhomocysteinemia and Bipolar Depression

Depression may be associated with elevated homocysteine (HCY) levels. Procedures aiming at its decrease, i.e. supplementation with folic acid or vitamin B12, have antidepressant effect. Both depression and elevated HCY can increase cardiovascular risk. In this study, clinical and biochemical factors, including markers of endothelial function, in relation to hyperhomocysteinemia, in patients with bipolar depression during acute episode were studied. Method: One hundred and twelve patients (24 male, 88 female), aged 20-78 (mean 51 ± 14 years), with depressive episode in the course of bipolar mood disorder have been included. The assays were made of serum concentrations of HCY, vitamin B12, folic acid as well as markers of endothelial function such as E-selectin and intracellular adhesion molecule-1 (ICAM-1). Results: Hyperhomocysteinemia (>15 mM) was found in 50 patients (45%), significantly more frequently in male (67%) than in female subjects (39%). Female patients with hyperhomocysteinemia were significantly older than the remaining ones. A significant inverse correlation between HCY level and concentration of folic acid and vitamin B12 as well as with E-selectin and ICAM-1 was observed. Conclusion: The results point to a significant prevalence of hyperhomocysteinemia in bipolar depressed patients during an acute episode. They also corroborate the correlation between increased concentration of HCY and lower level of vitamin B12 and folic acid. An unexpected finding of negative correlation of HCY level with markers of endothelial functions in such patients is discussed in view of current concepts of the role of HCY in various conditions.