Category: Insomnia

Abstract

The issue of Fatal Familial Insomnia (FFI) is dangerously underrated in the contemporary world. More importantly, the patterns for diagnosing and addressing it have not been identified yet. Therefore, it is crucial to evaluate the existing options to come up with a unique strategy.

Krasnianski et al. (2014) suggest that the connection between the specifics of one’s genetic makeup and the progress of the disorder is evident. The study confirms that the issue may be predisposed by the characteristics of one’s gene pool. The research is fairly credible, yet it clearly requires a follow-up study to locate the tools for identifying the most efficient diagnosing tool and locating treatment options.

Background and Problem Statement

The issue of fatal familial insomnia (FFI) has been gaining increasingly large significance over the past few years. In their recent study, A proposal of new diagnostic pathway for fatal familial insomnia, Krasnianski et al. (2014) address the issue of diagnosing the disorder. Particularly, the researchers seek ways to identify the possibility for a problem to evolve and, therefore, address it at the earliest stages of its development, if not prevent it from occurring. However, studies show that the analysis of the genetic makeup of the patient, i.e., the study of their family history, may lead to an uninspiring small number of results (Krasnianski et al., 2014). Herein lies the problem that the study attempts to address.

Stating the Hypothesis

Trying to resolve the problem concerning the identification of the threat of fatal familial insomnia, the scholars suggest that a framework for determining the danger should be developed. In other words, the authors of the study propose that the study of the PRNP mutation resulting in the subsequent development of the framework for identifying the risks of developing the disorder in question will help solve the problem of FFI. The hypothesis states that the process of identifying the D178-M129 mutation causing FFI may be improved by developing an algorithm based on the observations of sleep disturbances in the target group.

Techniques, Results, and Hypothesis Support

To address the questions asked in the introductive part of the study and identify the veracity of the hypotheses stated at the beginning of the research, Krasnianski et al. (2014) adopted a quantitative approach. The required data on sleep disturbances and the patterns thereof was gathered by analyzing the existing patient records, including the results of the diagnostic tests, such as polysomnographies, blood samples, CSFs, etc. additional information was retrieved with the help of anamnestical tools, including conversations with patients, therapists, he relatives of the patients, the staff, etc. It should be borne in mind, though, that the tools for genetic testing were unavailable at the time, which called for the adoption of the sCJD diagnosing criteria was necessary for the study to take place. Specifically, MRI tests were included in the set of data to be processed so that conclusions regarding the FFI development could be made, which required the application of the aforementioned sCJD tools. In addition, EEGs were incorporated into the set of data to be analyzed in the course of the study. Among the rest of the tests, PET and SPECT, neuropathological and molecular studies, and biochemical CSF deserve to be listed. The data was organized and interpreted with the help of the statistical analysis (Spiegelhalder, Regen, Baglioni, Riemann, & Winkelman, 2013).

The results of the study point to the fact that the identification of the corresponding genetic makeup predetermining the disposition to the development of FFI-related issues may be unavailable: “In 13 patients, no M129V genotype was available, but the diagnosis had been confirmed by autopsy, and family history for (genetically proven) FFI was positive” (Krasnianski et al., 2014, p. 655). Therefore, relying entirely on the outcomes of the corresponding gene analyses may be viewed as insufficient to prove the threat of FFI or the absence thereof. Nevertheless, the outcomes of the research point to the fact that the M129V genotype defined the time lapse between the occurrences of the symptoms related to the FFI disorder.

As far as the results of the autopsy are concerned, an explicit connection between the thalamo-olivaric pathology and the manifestation of the FFI symptoms can be observed. In other words, the study showed a direct correlation between the phenomena above. Thus, it points graphically to the fact that the use of the corresponding genetic analysis known as the PET blot method (Wemheuer et al., 2013) is essential to the identification of the disorder and the location of the tools that may assist in the process. The approach in question is often juxtaposed with conventional immunohistochemical staining tools (Peng, Zhang, Dong, & Lu, 2015), yet the latter have proven to lack accuracy in locating the disorder and, therefore, should be discarded as the means of detecting the development of FFI. Similarly, the significance of diagnostic tests is not to be underrated when it comes to locating the possibility of the disorder development, the research outcomes show quite graphically that the adoption of the above techniques leads to a more accurate identification of the threat of FFI development in a patient. The use of the family history turned out to have a surprisingly low relevance in the specified situation. While the outcomes of the analysis showed that the factor above affected the development of the disorder in 10 cases out of 29 (approximately 34.5%), the percentage of cases displaying the connection is rather low.

The hypothesis, in its turn, can be considered proven. The study has revealed that there is, in fact, a pattern in the correlation between sleep disturbances and the neurological symptoms that patients display at the earliest stages of FFI development. Seeing that the sensitivity rates in the target group reached 90%, the outcomes of the research can be considered rather credible.

Results Significance and Possibilities for a Follow-Up Study

The importance of the results can hardly be overrated. As it has been stressed above, the rates of FFI have been getting increasingly high. Although the issue does not get as much interest as the health concerns related to diabetes, cancer, AIDS, etc., it remains one of the deadliest disorders and the greatest threats to the wellbeing of people all over the world. Moreover, the lack of control over the development of the disorder can be viewed as a rather disturbing characteristic of the current situation. Therefore, shedding some light on the issue of the disorder development and identifying the pathways for diagnosing FFI at the earliest stages of its development are crucial steps on the way to defeating the disease and providing patients with a cure. The outcomes of the study, however, call or a follow-up analysis identifying the elements of the framework to be adopted to the diagnosing process.

Reasons for Choosing the Article

Although the phenomenon of insomnia as been studied rather well over the past few years, the problem has always attracted me as the issue that could be addressed in a more efficient manner. With the problems such as diabetes types I and II, cancer, and AIDS, the issue of fatal familial insomnia has been glanced over in both media and contemporary research. I believe that though considered incurable nowadays, it can be treatable one day as long as researchers all over the world join their efforts and keep trying consistently to solve the problem.

Reference List

Krasnianski, A., Juan, P. S., Ponto, C., Bartl,M., Heinemann, U., Varges, D., Schulz-Schaeffer, W. J., Kretzschmar, H. A., & Zerr, I. (2014). A proposal of new diagnostic pathway for fatal familial insomnia. Journal of Neurology, Neurosurgery & Psychiatry, 85(8), 654–659.

Peng, B., Zhang, S., Dong, D., & Lu, Z. (2015). Clinical, histopathological and genetic studies in a case of fatal familial insomnia with review of the literature. International Journal of Clinical and Experimental Pathology, 8(9), 10171-10177.

Spiegelhalder, K., Regen, W., Baglioni, C., Riemann, D. J., & Winkelman, W. (2013). Neuroimaging studies in insomnia. Current Psychiatry Reports, 15(11), 405-411.

Wemheuer, W. M., Wrede, A., Gawinecka, J., Zerr, I., Schulz, W. J., & Schaeffer, E. (2013). Filtration of protein aggregates increases the accuracy for diagnosing prion diseases in brain biopsies. Journal of Neuropathology and Experimental Neurology, 72(8), 758-767.

Diphenhydramine

• Classification: first-generation nonselective antihistamine (Sicari & Zabbo, 2021).
• FDA-approved uses: dystonias, insomnia, pruritis, urticaria, vertigo, and motion sickness (Sicari & Zabbo, 2021), other allergy symptoms.
• Off-label uses: local anesthetic (Sicari & Zabbo, 2021).

Dystonias – involuntary muscle movements;

Pruritis – itchy skin;

Urticaria – rash;

Off label – for patients allergic to other drugs, oral mucositis treatment.

Federal and State Regulations

• Missouri regulations: no special regulation.
• Federal law: warning issued.
• Best practices regarding dispensing: with a doctor’s prescription (“Benadryl (diphenhydramine): Drug safety communication – Serious problems with high doses of the allergy medicine,” 2020).

State: there are no differing regulations specific to Missouri on this drug.

Federal: there has been a warning issued on the severe toxicity and side effects of the drug at high doses, as well as its misuse by young people.

How it works

• Suppresses cough.
• Local anesthesia.
• Causes drowsiness.
• Time until full action around 2 hours (Sicari & Zabbo, 2021).

Acts as a histamine 1 and muscarinic acetylcholine receptor antagonist (cough).

Also, an intracellular sodium channel blocker (local anesthesia).

Side effects

Most common side effects:

• Dry mouth, nose and throat;
• Drowsiness and dizziness;
• Nausea and vomiting;
• Loss of appetite;
• Constipation;
• Increased chest congestion;
• Headache;
• Muscle weakness;
• Excitement and nervousness.

Severe and rare side effects:

• Vision problems;
• Difficulty urinating or painful urination (“Diphenhydramine,” 2018).

Significant substance interactions

May interact with:

• Other antihistamines applied to the skin;
• Other drugs for sleep and anxiety, such as alprazolam, lorazepam, and zolpidem.

May increase drowsiness when taken in conjunction with:

• opioid pain or cough relivers;
• alcohol, cannabis;
• muscle relaxants

(“Sleep Aid Tablet – Uses, Side Effects, and More,” n.d.).

It is advised to ask the pharmacist about the particular substance interactions.

Informing patients

Tablet, capsule, liquid forms, as well as by intramuscular or intravenous injection

Starting dose:

• Adults:
  • 25-50mg at bedtime.

• Children:
  • 12 and older – 25-50mg at bedtime

(Sicari & Zabbo, 2021).

Expected costs comparison (using GoodRx)

Gerbes Pharmacy

• 30 capsules 25mg each: $2.23 with the GoodRx coupon;
• $7.00 retail;
• No insurance needed;
• Doctor’s prescription required.

Kroger Pharmacy

• 30 capsules 25mg each: $1.63 with the GoodRx coupon;
• $7.00 retail;
• No insurance needed;
• Doctor’s prescription required.

Other pharmacies

• Walgreens: $2.93 retail price;
• Target (CVS): $3.64 retail price;
• Walmart: $3.93 retail price.

Required labs

• May interfere with some laboratory tests, such as skin allergy.
• Consult with a doctor or the medical personnel.
• No labs are required prior or during the admission of the drug for insomnia (“Sleep Aid Tablet – Uses, Side Effects, and More,” n.d.).

Contraindications

• Documented hypersensitivity to diphenhydramine.
• Premature infants and neonates.
• Diphenhydramine has additive effects with alcohol and other CNS depressants (hypnotics, sedatives, tranquilizers).
• Monoamine oxidase A inhibitors prolong and intensify the anticholinergic effects of antihistamines (Sicari & Zabbo, 2021).

Pregnancy and Breastfeeding precautions

Not recommended for breastfeeding or pregnant women unless clearly needed (Sicari & Zabbo, 2021).

Age limitations

• Not prescribed for insomnia for children under 12.
• However, prescribed as allergy medicine for children as young as 2.
• Older adults and children might be more sensitive to side effects – children more likely to feel excited as a result (“Sleep Aid Tablet – Uses, Side Effects, and More,” n.d.).

Example of patient clinical profile

• Signs/symptoms: sleep disturbances.
• Diagnosis: insomnia.
• Age: 25.
• Gender: female.

Note: this is just one example, the drug might be prescribed to any adult (12+) with insomnia symptoms.

Example of patient clinical profile to avoid

• Signs/symptoms: sleep disturbances.
• Diagnosis: insomnia.
• Age: 5.
• Gender: male.

Note: this is just one example, the drug should not be prescribed as sleeping medication to any children under the age of 12.

References

Benadryl (diphenhydramine): Drug safety communication – Serious problems with high doses of the allergy medicine. (2020). FDA. Web.

DeCoy, H. (2018). Diphenhydramine Use in Insomnia. OhioPharmacists. Web.

Diphenhydramine. (2018). MedlinePlus. Web.

Sicari, V. & Zabbo, C. P. (2021). Diphenhydramine. StatPearls[Internet]. Web.

Sleep Aid Tablet – uses, side effects, and more. (2012). WebMD.

Benadryl is one of the most effective medicines that help people cope with insomnia and have a sound sleep every night. The tablet blocks several parts of the brain to make an individual forget about problems that do not allow them to live a normal life. The activity of the central nervous system decreases as specific neurons and potentials are affected (Milanaik et al., 2019). It is important to consult a specialist before taking the pills because the overdose effect might be irreparable. The normal dose is from 12,5 mg to 25 mg every 4 or 6 hours (Menon et al., 2021). Children can take the pills, but it is not suggested to those who are under 12 years old as the effect is still not approved.

The starting dose should be minimal to understand how the organism reacts. As the pill should be taken several times a day, the dose can be reviewed and increased during the day. Benadryl is not recommended for a pregnant or breastfeeding woman as the effect on the child is still unknown. Moreover, people cannot take pills when there is a personal intolerance to the drug. There also can be several side effects like dry mouth, loss of appetite, headache, stomachache, and nervousness.

Food and Drug Administration is responsible for the control of relationships between tablets and food. The FDA suggests that people do not take more than six tablets per day, leading to heart problems such as stroke (Knopf, 2020). Some consequences of the overdose might cause death. The active substance is effective, and at the same time, it does not worsen the level of health as it consists of natural components. To decrease the number of misunderstandings, doctors have to inform patients about the use of this medicine. For example, the tables might have different forms and be solid or liquid. Moreover, each package may contain a different number of milligrams, and people should be aware of this fact.

References

Knopf, A. (2020). FDA warns against doses of Benadryl. Alcoholism Drug Abuse weekly, 32(38), 6. Web.

Menon, A., Bachan, M. & Khan, Z. (2021). Non-Pulmonary Critical Care Case Reports, 203.

Milanaik, R., Fruitman, K. & Teperman, C. (2019). Parent reported frequency, efficacy, and side effects of over the counter medication use for improved sleep in 5 to 11 years old. Pediatrics, 144(96).

Insomnia is among the conditions, for which many individuals seek treatment due to the disturbing consequences and discomfort. The symptoms of insomnia include having trouble falling asleep or maintaining sleep. Such problems might have a detrimental impact on daytime functioning if they have been present for a minimum of three months, and are unrelated to another condition. In fact, those who suffer from insomnia have trouble concentrating, are more irritable and unstable emotionally, and are more likely to have accidents (Lancee et al., 2017). Long-term sleep disruption is linked to a number of physical and mental health issues, such as anxiety and depression. However, in order to deal with insomnia, most professionals recommend spending less waking time in bed before sleep.

The ability to fall asleep more quickly may be affected by spending waking hours in bed owing to the thinking that takes place. A person’s thoughts could become hyperactive when discussing difficult or delicate subjects (Lancee et al., 2017). The individual may remain aware as a result, which makes it more challenging to fall asleep. Persistent thinking is one possible recognized risk factor for insomnia. It is often described as “the process of thinking attentively, repetitively, or frequently about oneself and one’s world” and was first researched in the framework of depression and anxiety disorders (Lancee et al., 2017, p.54).

This focused attention leads to an exaggeration of the impact of daytime performance and sleeps on maintaining recurrent thoughts about sleeping, which in turn raises physiological arousal and leads to actual deterioration in sleep. Hence, repetitive thinking before bedtime causes arousal and anxiety, which in turn causes focused attention and enhanced monitoring of dangers connected to sleep.

Work Cited

Lancee, J., Eisma, M. C., van Zanten, K. B., & Topper, M. (2017). When thinking impairs sleep: Trait, daytime and nighttime repetitive thinking in insomnia. Behavioral Sleep Medicine, 15(1), 53-69. Web.

Introduction

Identifying Information

• Initials: P. E.
• Age: 26
• Gender: Female
• Insurance Status: Has PPO
• Ethnicity: Hispanic
• Her education comprises a 4-year college degree in English Language Arts.
• Information Received from P. E.

Presenting Problem

P.E. decided to address the specialist because of her insomnia and overall problems with sleep, and changes in her mood because of it. The given problem became a serious concern for a patient because of her inability to relieve stress and lack of rest. Moreover, she emphasizes the fear of going to bed because of the inability to fall asleep and the irritation associated with it. For this reason, the patient decided to go to the clinic. Following the P.E. words, she has already been suffering from insomnia for six months. At first, it was not a serious problem as she associated it with the high level of stress and the overall state of the body. However, it became worse as there were no signs of improvement. Currently, she is tired and cannot handle it by herself.

Usually, P.E. has only two or three hours of sleep with numerous wake-ups. She cannot fall asleep immediately when she goes to bed. Instead, she lies for long periods thinking of various unpleasant things and feeling growing anxiety. She might have one hour of rest, and then she starts thinking again. P.E. says that four hours of sleep is a great success for her, but such nights are rare. As a result, she is agitated and restless, with signs of anxiety and depression. Severe insomnia created the basis for the gradual deterioration of her mental health and inability to have the needed rest. She reports that close people admitted changes in her mood and behavior associated with the sleep disorder and the lack of sleep hours. For this reason, she views it as a reason to address a specialist and discuss the current state.

• Triggering Factor: Not identified.
• Protective Factor: Productive relationship with colleagues and friends.

Current Medication

P. E. does not use any medication for her insomnia and does not take any substances.

Past Psychiatry History

P. E. experienced a similar occurrence when she was 19 years old, although she received no formal diagnosis.

She has never sought the assistance of a professional, never seen a therapist or a psychiatrist, never been hospitalized for a mental health problem, and denied having suicidal ideas.

Social History

P. E. has a higher education: she earned a bachelor’s degree in English Language Arts.

After that, she was employed at several writing and advertisement agencies but regularly left them after several years of work for some reason.

Currently, P. E. is still employed but has a leave. She is considering resigning because of the problems mentioned above and the fact that P. E. plans to publish a book she has been working on for some years.

• P. E. believes the book would be a source of her financially independent living.
• P. E. has been in a relationship with a woman recently but at some moment considered it sinful and abruptly ended.
• P. E. has been living with her girlfriend recently. However, she has returned to her apartment after a breakup.

ROS:

• Constitutional: an average temperature, no shivers, cramps, or tremors.
• HEENT: No changes in vision and hearing, no difficulty swallowing.
• Pulmonary: No signs of shortness of breath and symptoms of cold in the pulmonary system.
• Cardiovascular: difficulty with breathing, headaches, fatigue, chest ache, and irregular heartbeat, which signifies that she has high blood pressure.
• Gastrointestinal: No gastrointestinal issues, namely, no abdominal pain or regurgitation.
• Genitourinary: No difficulty with urination.
• Neuromuscular: No muscle weakness or joint pain because of her work that urges her to sit at the table for a long time.
• Weight: 183 Height: 5’5” BMI: 30.4
• Vital Sign: 140/95 72 96.4 17 93 on R.A.

Mental Status Exam

• Appearance: Disheveled, obese
• Behavior: cooperative
• Speech: Clear
• Mood and Affect: Congruent
• Thought Perception: Logical
• Thought Content: No delusions or hallucinations
• Insight/Judgement: Intact
• Orientation: Alert and oriented x 3

Assessment

• Axis I- Bipolar disorder current episode mania
• Axis II- none
• Axis III- Asthma
• Axis IV- occupational problem
• Axis V- 50
• DSM-V Diagnosis

The working diagnosis of the patient is F31.1 Bipolar disorder with a current episode of mania without psychotic features (American Psychiatric Association, 2013). P. E. is diagnosed with bipolar illness due to mood swings between depression and, as it seems, mania. According to Marangoni (2018), “bipolar disorder has a lifetime prevalence of 2.1% in adults and 1.8% in children; at least two-thirds of the patients with bipolar disorder report onset before age 18” (p. 19). However, P. E.’s first occurrence of the disorder presented when she was 19 years old. The manic phase of borderline personality disorder manifests itself differently. Some people become sexually promiscuous, indulging in dangerous sexual practices, while others have no desire to sleep, spend excessively, have racing thoughts, and act grandiosely. P. E. seems to have racing thoughts, insomnia, and maybe sexually overwhelmed.

Following a manic episode, people generally have a depressive period in which they become the polar opposite of what they were before, with a lack of energy, drive, and sleeping excessively. According to Jann (2014), “A diagnosis of bipolar disorder is obvious when a patient presents with florid mania but is challenging when the initial presentation includes depressive symptoms; studies generally report that 50% or more of patients initially present with depression” (p. 491). These symptoms correspond to the description of P. E.’s experiences.

Many patients who come to the office with signs of suspected bipolar illness were previously treated with only antidepressants, but their symptoms did not improve. In the instance of P. E., her reluctance towards professional aid and disbelief in the presence of mental illness in her prevented her from going through any treatment. Bipolar illness diagnosis necessitates a thorough examination of prior experiences. The key contrast between the two forms of bipolar illness is the degree of manic symptoms. As such, full mania involves substantial functional impairment, can include psychotic symptoms, and frequently necessitates hospitalization. Hypomania, on the other hand, is not strong enough to cause significant impairment in social or occupational functioning or demand hospitalization (Jann, 2014). P. E. has all symptoms of hypomania and still needs treatment.

Treatment Plan

P. E.’s treatment plan includes several necessary steps described later in greater detail.

1. The first step is laboratory work, which includes CBC, CMP, TSH, lipid panel, and urine drug screen.
2. P. E. is prescribed to take 250 mg of Depakote BID as well as 5mg of Abilify Q.D.
3. After P. E. has followed the instructions (it is also recommended that someone monitor the process of taking medications), she should revisit the clinic for an assessment and instructions in two weeks.

Psychopharmacology

The use of psychopharmacology should be explained in greater depth. Mood stabilizers such as Depakote, Lamictal, and carbamazepine, as well as atypical antipsychotics, have been demonstrated to be useful in the treatment of borderline personality disorder. Depakote has been found in studies to be effective as a mood stabilizer. According to Janicak and Esposito (2015), “lithium and valproate appear to be comparably effective in treating pure manic episodes, while valproate may be more effective for mixed or rapid cycling presentations” (p. 31). Depakote is used as a mood stabilizer in the instance of P. E.

Depakote’s mechanism of action perfectly fits the case of the patient. It is known to entail blockage of “voltage-dependent sodium ion receptor channels and enhancement of gamma-aminobutyric acid activity by increasing its synthesis and release” (Janick & Esposito, 2015, p. 34). Depakote can induce thrombocytopenia and raise liver enzymes; consequently, labs should be done before starting the medicine. There have been concerns about P. E’s hypertension; the significance of close lab monitoring was brought to P. E. and her close friend, who accepted the task of taking care of the patient.

In addition to that, the discussion of Depakote should draw significant attention to the fact that this medication can lead to increased weight gain. Since P. E. has already had some weight issues, and her body-mass index demonstrates that she suffers from obesity, this aspect should be considered with caution. However, a closer analysis of the professional literature indicates that “bipolar disorder and its treatment increase the risk of comorbid medical conditions such as being overweight” (Grootens et al., 2018, p. 1489). This information indicates that every person receiving bipolar disorder treatment faces a risk of gaining weight, and this threat is more significant for people who have already had such health issues. That is why appropriate interventions are necessary to minimize the side effects of the medication. Suitable activities include regular laboratory tests, check-ups, and weight monitoring. Furthermore, P. E. was given the importance of following a healthy diet and involving in mild physical exercise on a regular basis.

Second-generation antipsychotics, such as Abilify, have been found to be successful in the treatment of bipolar illness, either as a monotherapy or in conjunction with a mood stabilizer. It is a great alternative for treating bipolar disease due to its multi neurotransmitter action on dopamine and serotonin. According to Jann (2014), “a vast body of evidence supports the use of atypical antipsychotics in the treatment of bipolar disorder… [and especially] acute mania” (p. 492). Atypical antipsychotics as a class have been shown to increase metabolic risk in individuals with bipolar illness, and monitoring ways to avoid, mitigate, or detect symptoms early so that appropriate actions may be implemented.

Strengths

There are several points that can contribute to the successful result of P. E.’s treatment.

• P. E. wants to participate in church activities due to her emerging religiousness. These programs can relieve the obsession of the patient with her “sins” since Christian meetings are supportive in their nature in the region where P. E. resides and plans to visit them.
• P. E. has several friends who care about her well-being and might have an impact on her opinion concerning treatment if she is reluctant towards it again. One of her friends agreed to look after while P. E.’s stays at home and monitor her taking the medications, as well as communicate with P. E. for psychological recovery.
• P. E.’s conservative parents, who might have caused her disbelief in the treatment and produced some utterances on religious matters, do not maintain any contact with the patient. Thus, they cannot intervene in the process of care or cause even more mania episodes by their possible misconduct.
• P. E. has a book to publish and can focus on this project.

Goals

• P. E. had discussed her goals by the end of the treatment when she eventually was convinced that it might be helpful.
• P. E. wants to publish her book, which she has already written, as soon as her mood is stable.
• P. E. desires to reconnect with her friends, some of whom she has been scared or confused by her behavior.
• P. E. intends to meet with her ex-girlfriend to discuss some routine matters about her new living and explain the reason for her actions.
• P. E. wants to be able to get enough sleep at nighttime so she can be functional during the day.

Expected Outcomes

There are expectations for the first two weeks of treatment.

• P. E. will sleep well all night and will be able to think clearly and perform normally.
• P. E. is expected to take her medicine exactly as directed.
• P. E. will take part in her extracurricular activities, namely church meetings.
• P. E. will have minor adverse effects from the drug.
• P. E. will continue to see the psychiatrist for medication maintenance.

Conclusion

Completing a psychiatric examination of this patient lends credence to the idea that culture and personality may influence how people perceive mental disease as well as their willingness to seek the necessary care. There are uncertainties about medication noncompliance in a patient like P. E., mainly because of her disbelief in medication and treatment, and there is a risk that she will wish to quit taking medicine once she improves. It is critical to be aware of patients’ surroundings, particular problems, and beliefs and to take them into account while discussing treatment options.

Introduction

This case study will assess and treat a 31-year-old male with insomnia. Since his fiancé’s unexpected death roughly six months ago, he has been experiencing worsening sleeplessness. He works as a forklift operator and claims that his sleepiness interferes with his ability to do his job properly and that he occasionally sleeps over the course of the day. To help him fall asleep, he has tried over-the-counter (OTC) drugs like diphenhydramine, but he does not like how they make him feel when he wakes up the next morning. He has a history of abusing opiates, that is, hydrocodone/acetaminophen, but he has not had a prescription for that in four years. The patient acknowledges that he has recently been drinking four beers a night to help him sleep.

According to the evaluation of his mental state, he is well-oriented to person, time, and place. He also maintains proper grooming, maintains eye contact, and exhibits sound judgment and understanding. According to him, he had no auditory or visual hallucinations nor any suicidal or homicidal thoughts. Nothing further was checked or tested for as a diagnosis of insomnia was made. It is crucial to bear in mind the patient’s history of substance abuse and present everyday drinking while prescribing them. There will be a step-by-step process for psychopharmacological treatments and the justification for each. The expected outcome for his therapy is for him to fall asleep and stay asleep the entire night, get a better night’s sleep, wake up feeling rested, and not need to drink to fall asleep. It is critical to consider the prescription therapy that will be most beneficial to him and have the fewest negative effects.

Decision One

As the mental health nurse, I would choose from my three options of drugs to start: Zolpidem 10 mg once daily at bedtime, Trazodone 50-100 mg once daily at bedtime, and Hydroxyzine 50 mg once daily at bedtime. The objective is to find a treatment that the patient tolerates and at least slightly improves his sleep cycle. I would decide to start the patient on 50–100 mg of trazodone. If he tolerates it, I would initiate him with a lesser dosage of 50 mg and suggest he increase it to 100 mg after two weeks. To reduce side effects like drowsiness, I would also instruct him to take it with or after meals. Trazodone is classified as a selective serotonin reuptake inhibitor (SSRI) and has a low side effect profile. Trazodone is originally prescribed for the treatment of depression; however, its use for treating sleeplessness has since surpassed that of depression (Yi et al., 2018). Still, there should be educated regarding combining alcohol and antidepressants.

I did not choose Zolpidem 10 mg for this reason—prolonged drug usage may result in physical and psychological dependence. The patient already has a history of drug dependency, making it more likely that he may also develop an addiction to this substance. Furthermore, Zolpidem is also available in a 5 mg dosage; a lower dose is advised when introducing a new medicine to a patient. Similar to benzodiazepines, Zolpidem acts on GABA receptor cells to produce its desired effects. Since GABA affects neurological functions and sleep, Zolpidem may have signs of central nervous system (CNS) depression (Edinoff et al., 2021). Alcohol is a known CNS depressant; combining it with alcohol can be extremely harmful.

Since Hydroxyzine 50 mg is an antihistamine, I decided against selecting it as the final choice. Antihistamines are often accompanied by anticholinergic adverse effects such as dry mouth, drowsiness, and blurred vision (Leung & Hon, 2019). Since it is a potent sedative, hydroxyzine might be harmful when used with alcohol. Additionally, the detrimental effects of hydroxyzine on anticholinergic systems have been documented. Trazodone 50–100 mg is the option from the list that can help this patient’s insomnia with the least number of side effects.

Decision Two

I currently have two options: I may either maintain the same course of treatment or inform him that sleepiness is a temporary adverse effect of trazodone. I may maintain the dosage the same and advise him on how to deal with daytime sleepiness and how long it might continue. On the other side, I could opt to decrease trazodone and only take 25 mg at night. The key objective at this point is to keep getting results from his sleep while also putting an end to his daytime sleepiness. Trazodone’s most frequent adverse effects are sleepiness, nausea, drowsiness, and dry mouth (Khouzam, 2017). Trazodone is typically well tolerated and may have a lower risk of sleeplessness, sexual adverse effects, and anxiety than certain other antidepressants. In terms of ethics, one should keep the patient on the drug that is helping rather than switching to one that could have more harmful side effects.

The patient’s concerns about feeling tired and drowsy were specific to this problem. Ethics dictate that the patient should not be given a prescription for a medication that may result in adverse effects. Trazodone dose reduction would be ineffective since there is no connection between drowsiness episodes and the quantity or length of the medicine that produces this side effect. In addition, the dose increased his sleep, which was our objective. The customer returns after two weeks and says his tiredness has lessened, especially during the day. Even though 50 mg of trazodone is the recommended dosage, he occasionally wakes up in the mornings still feeling sleepy—no other reported psychological symptoms. The signs of sleep disturbances include daytime sleepiness and difficulty falling asleep during the night (Mayo Clinic, 2020). Additionally, some people have a tendency to sleep when driving. Thus, the patient must receive health education and appropriate medications.

Decision Three

The psychiatry nurse should now choose whether to stop taking trazodone and start taking Sonata 10 mg at night with a four-week follow-up or stop taking trazodone and start taking Hydroxyzine 50 mg at bedtime with a four-week follow-up. The psychiatry nurse should determine whether to keep him on the present dosage and advise him he can divide the 50mg dose in half to aid with the next day’s drowsiness. The main goal is to reduce his morning drowsiness while preserving his sleep schedule through the night. My choice would be to lower the dosage in half and reevaluate him in four weeks. We want our patients to sleep better while still avoiding being exhausted the next day, which is why I settled on this option.

Sonata is a sedative for insomnia; however, I decided against its use. Sonata is categorized as a scheduled intravenous medication, which indicates that it has both medicinal use and the risk of abuse and dependency (Milhorn, 2017). There is no significant danger of overdose while using Sonata alone. Sonata and alcohol both increase the risk of overdose and severe respiratory depression. Since both drugs have a depressant effect on the CNS, they can reduce respiration and heart rate. Therefore, giving this drug to this patient would be unethical.

Hydroxyzine is an antihistamine and might have similar effects to diphenhydramine; hence, I decided against stopping trazodone and starting it. Since trazodone is helping, it is recommended to keep taking it, albeit at a lesser dosage. By the end of four weeks, it will be determined if the patient’s dosage was of benefit. If not, a decision would be made whether to put him on a different medicine that would be a better fit and put him on a drug that will not make him better would be unethical.

Conclusion

Conditions that are considered sleep disorders cause changes in how people sleep. Insomnia and other sleep disorders can impact general health, safety, and quality of life (Mayo Clinic, 2019). Lack of sleep can make it more difficult for one to drive safely and raise one’s chance of developing other health issues. Stress, an irregular sleep routine, eating late, drugs, caffeine, nicotine, medical illnesses, or mental health issues are just a few of the issues that can cause insomnia. To find the underlying reason, more research would be required.

The drug most frequently recommended to aid with sleep is trazodone, especially among those in alcohol addiction treatment. Trazodone is prescribed for depression but is often used off-label for insomnia. In the case study, after the death of his fiancé, the patient began to have sleeplessness. He also reports drinking daily and may still be experiencing some depression. He found that trazodone functioned best for him since it is safe to use with alcohol and has a serotonin-related impact that can aid his mood and sleep.

Educating this patient extensively about the medicine and its negative effects would still be necessary. If he does not cease alcohol consumption, it should be moderated. His primary concerns upon entering the facility were his daytime fatigue and sleeplessness. The therapy is ineffective if he can sleep at night but cannot function during the day, affecting his ability to work. It is only fair to focus on both of his issues.

References

Edinoff, A. N., Wu, N., Ghaffar, Y. T., Prejean, R., Gremillion, R., Cogburn, M., Chami, A. A., Kaye, A. M., & Kaye, A. D. (2021). Zolpidem: Efficacy and Side Effects for Insomnia. Health Psychology Research, 9(1). Web.

Khouzam, H. R. (2017). A review of trazodone use in psychiatric and medical conditions. Postgraduate Medicine, 129(1), 140-148.

Leung, A. K., & Hon, K. L. (2019). Motion sickness: An overview. Drugs in Context, 8, 1–11.

Mayo Clinic. (2019). Sleep disorders – Symptoms and causes.

Milhorn, H. T. (2017). Sedative-Hypnotic Dependence. Substance Use Disorders, 59–76.

Yi, X., Ni, S., Ghadami, M. R., Meng, H., Chen, M., Kuang, L., Zhang, Y., Zhang, L., & Zhou, X. (2018). Trazodone for the treatment of insomnia: A meta-analysis of randomized placebo-controlled trials. Sleep Medicine, 45, 25–32.

Insomnia is a prevalent mental disorder affecting a significant portion of the population. It manifests as a difficulty in sleeping and can become chronic after a certain period. Despite its prominence, the mechanisms behind insomnia’s causes are still not fully explored. The same applies to the disorder’s potential outcomes, the research into which is ongoing. However, some facts are well-established, which allows healthcare specialists to treat insomniac patients and predict/prevent the associated diseases. The essay will highlight what is known about insomnia’s epidemiology and its effects as far as a person’s health is concerned, although it also affects other aspects of one’s life.

Insomnia can have many precursors, some of which will lead to other conditions. For instance, the hypothalamic-pituitary-adrenal axis is said to cause the disorder if it experiences dysregulations (Javeheri & Redline, 2017). The consequences include the elevated activity of the sympathetic nervous system and hormonal imbalance (Javeheri & Redline, 2017). As a result, a person begins experiencing insomnia, which can manifest as a short sleep duration (Javeheri & Redline, 2017). The latter is directly associated with such cardiovascular conditions as hypertension, heart failure (HF), and coronary heart disease (Javeheri & Redline, 2017). They are mostly responsible for mortality cases in insomniac patients as the disorder itself is not lethal, but its consequences may endanger one’s life (Javeheri & Redline, 2017). On the other hand, HF is one of insomnia’s causes, which creates a cycle when one cardiovascular disease leads to insomnia, and it subsequently increases the incidence risk of similar outcomes (Javeheri & Redline, 2017). Thus, insomnia is a result of the dysregulated hypothalamic-pituitary-adrenal axis and, in turn, induces heart conditions with severe effects on one’s well-being, although a cardiovascular disease may also trigger insomnia.

Another prominent cause of insomnia is rooted in genetics, which has been established through family and twin studies. They indicate that the disorder is inheritable to a moderate degree, while the female population is more likely to be affected (Lind & Gehrman, 2016). Although examining twins contributed significantly to proving insomnia’s heritability, determining the exact genes responsible for its development remains challenging due to phenotype inconsistencies (Lind & Gehrman, 2016). Both serotonin and dopamine transporters are subject to genetic studies, and their association with insomnia continues to be supplied with more evidence (Lind & Gehrman, 2016). Their role is to cause hyperarousal through wake-promoting neurons, which prompts insomnia (Lind & Gehrman, 2016). The disorder’s inheritable nature is also evident due to its occurrence in children, who are less susceptible to other common stressors (Lind & Gehrman, 2016). Genetically, insomnia tends to be linked with similar mental conditions but may also result in such a physical health outcome as diabetes because a correlation exists between it and sleep duration (Lind & Gehrman, 2016). Overall, insomnia can be a genetic condition and entail type 2 diabetes, although the connection requires further studies.

Insomnia manifests as a response to trauma, which makes it related to other mental disorders. The traumatizing experience may occur in one’s childhood or adulthood: they differ in rapid eye movement fragmentation, with the former causing its increased form (Hertenstein et al., 2018). As a result, people develop certain conditions, varying from insomnia to depression, and their occurrence depends on many factors (Hertenstein et al., 2018). For instance, an insomniac person is unlikely to have post-traumatic stress disorder beforehand; moreover, such a trait as sleep reactivity makes one more susceptible to insomnia than other outcomes (Hertenstein et al., 2018). Whether the traumatic event happened as a result of the patient’s actions or beyond their control also matters: the former is more likely to provoke guilt and shame, which increases insomnia’s likelihood (Hertenstein et al., 2018). However, even if comorbidity does not develop initially, the latter will still serve as a foundation for other mental disorders (Hertenstein et al., 2018). Insomnia increases the risk of anxiety, depression, psychosis, and alcohol abuse, with the first two being particularly prominent outcomes (Hertenstein et al., 2018). Altogether, insomnia may be caused by trauma and induce other mental conditions.

Insomnia has multiple causes, and its health outcomes are also varied. One of the phenomena triggering it is the dysregulated hypothalamic-pituitary-adrenal axis, which affects the nervous system and hormones. As a consequence, insomnia develops and leads to cardiovascular conditions, which may significantly threaten a person’s well-being. Another cause is genetics, meaning that the disorder is inheritable by some of the population, affecting dopamine and serotonin transporters responsible for hyperarousal. In that case, insomnia may result in type 2 diabetes, which also has genetic correlations. Lastly, insomnia occurs as a trauma response, substituting other disorders, such as anxiety and PTSD, but it does not completely negate them. Furthermore, they tend to develop later due to sleep shortness, which is one of insomnia’s symptoms. Judging by the studied information, insomnia presents a vicious cycle, being both an outcome of another disorder or its main cause, insinuating that an afflicted person may struggle with treating the condition.

References

Hertenstein, E., Feige, B., Gmeiner, T., Kienzler, C., Spiegelhalder, K., Johann, A., Jansson-Fröjmark, M., Palagini, L., Rücker, G., Riemann, D., & Baglioni, C. (2018). Insomnia as a predictor of mental disorders: A systematic review and meta-analysis. Sleep Medicine Reviews, 43, 96-105.

Javaheri, S., & Redline, S. (2017). Insomnia and risk of cardiovascular disease. Chest, 152(2), 435-444.

Lind, M., & Gehrman, P. (2016). Genetic pathways to insomnia. Brain Sciences, 6(4), 64-81.