A BRIEF REVIEW ON SLEEP PARALYSIS: MANAGEMENT AND TREATMENTHTML Full Text
A BRIEF REVIEW ON SLEEP PARALYSIS: MANAGEMENT AND TREATMENT
Debgopal Ganguly, Soumyadip Ghosh *, Madhumita Banerjee, Abid Alam and Rajesh Ghosh
School of Pharmacy, Calcutta Institute of Pharmaceutical Technology and AHS, Uluberia, Howrah, Bengal, India.
ABSTRACT: The brain alternates between wakefulness, nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep during sleep. Sleepwalking, sleep terrors, sleepwalking and sleep paralysis are common examples of the behavioral manifestations linked with parasomnias or partial arousals from sleep. Sleep Paralysis is a condition in which someone lying supine position, about drop off to sleep or just upon waking from sleep realize that she/ he unfit to speak or walk or cry out, this may lose many seconds or moments, occupationally longer. The sensation of being paralyzed can be accompanied by various vivid and powerful sensory sensations, such as mentation in visual, aural, and tactile modalities and a distinct sense of presence. People always feel that they've been hanging by someone or wrong, sometimes, cases report this type of problem. They feel that wrong is following, sitting behind them going to be attacked is the condition they feel, in this. Composition reviewed the causes of sleep palsy and what's sleep; many sleep diseases are bandied then. This review discusses details on the management and treatment of sleep paralysis, basic description of sleep paralysis and pathology, etiology, history, epidemiology, and pathogenesis involved in sleep paralysis.
Keywords: Sleep Paralysis, Rapid Eye Movement, Narcolepsy, Hallucination, Phytomedicine, Clinical pharmacology
INTRODUCTION: Sleep paralysis can be described as an unstable stage both physically and mentally during his/her sleep, in which a person is apprehensive but unable to do any normal movement. During this occasion, one may hallucinate which frequently results in fear 1, 2. Episodes generally last some moment. It may do on a single occasion or be intermittent. Sleep paralysis is a fairly new term to describe what hundreds of times numerous believed to be a visit by a vicious creature that attacked its victims as they slept 3.
History: The term sleep paralysis was found in a Dutch physician’s case history back in 1664, where it was appertained to as ‘Incubus or the Night-Mare (sic)’. After that 100 healthy people mysteriously died during their sleep in 1997; they belong to an Asia-specific region. The lethal rate is nearly 0.092% off, those who died suddenly in the nighttime 4, 5.
Etiology: The specific cause behind this case remains undiscovered; most studies have concluded this with sleep paralysis and nightmare. The mythological background of the nightmare is coming from Lilith. The reference of Lilith is found in the Sumerian King’s history of 2400 BC as a she-demon; she bore children from her nightly unions with men. In other derivatives, she was Adam’s first woman who became a demon that feed on women during parturition 6, 7.
In modern Middle Eastern motherliness wards, some women still wear phylacteries for protection. The clinical cause of these disturbances is sleep paralysis due to the infelicitous timing of REM (Rapid Eye Movement) sleep. During the ‘nightmare’ occasion, the sleeper becomes partially conscious in the REM cycle, leaving the existence in a state between dream and insomnia. Some people believed that their culture and tradition were primarily related to the nightmare 8, 9.
FIG. 1: STAGES INVOLVED IN SLEEP CYCLE (NON-RAPID EYE MOVEMENT AND RAPID EYE MOVEMENT SLEEP)
Physical State: The primary stage of nightmares and their strange cases of awakening and being unfit to move, the pressure on the chest, fear, visual daydream and perceiving some creature, or person in your immediate surroundings, or directly on your body, is known as sleep paralysis 10.
The phrase sleep paralysis was defined in medical science in 1928. Sleep paralysis can affect 1.7 percent of the population to a maximum of 40 percent. Most of the victims are scholars, above the age of 30 and appear with posttraumatic stress complaint, wakefulness and fear of attack 11, 12. A report shows 65 percent of sleep paralysis in a community of Cambodian deportees suffering from post-traumatic stress disorder.
Stress, abnormal sleep pattern, and depression are the key factors that can contribute to occurrences of sleep paralysis 13. A substantiation also talks about the common symptoms of sleep paralysis with schizophrenia and bipolar disorder. During the REM sleep cycle, the state when utmost dreaming occurs, the body is paralyzed to protect it from acting out those dreams. It's believed that during the nightmare occasion, the sleeper can witness both audile and visual hallucinations 14, 15.
Pathophysiology: To understand the pathophysiology behind sleep paralysis, we must read several articles. One of those articles includes parasomnia performed dysfunctional imbrication of the REM and multiple time waking during sleep 16. The studies of brain waves during sleep conclude that those who witness sleep paralysis have shorter REM sleep dormancy than normal people's NREM and REM sleep cycles and fragmentation of REM sleep. This study supports the observation that disturbance of regular resting patterns can precipitate an occasion of sleep paralysis 17, 18. Because fragmentation of REM sleep generally occurs when sleep patterns are disintegrated and have been seen in combination with sleep paralysis. Another major proposition about sleep paralysis is because of the neural function which regulates sleep if they are not properly working, then individuals may experience abnormalities during sleep 19. In this case, cholinergic sleep in neural populations is hyperactively actuated and the serotonergic sleep of neural populations is under-actuated. As a result, the cells able to transfer the signals that would allow for the complete thrill from the sleep state, the serotonergic neural populations, have difficulty prostrating the signals transferred by the cells that keep the brain in the sleep state. The vestibular nuclei are related to dreaming during the REM stage of sleep 20, 21.
Epidemiology: Several research on sleep paralysis talks about the genetic component that influences the character of fragmentation of REM sleep; hypnopompic and hypnagogic visions have an inheritable element in other parasomnias, which lends credence to the idea that sleep paralysis is also genetic 22. Twin studies have shown that if one twin of a monozygotic pair (identical halves) experiences sleep paralysis the other twin is veritably likely to witness it. The identification of an inheritable element means that there's some kind of dislocation of a function at the physiological position 23. Further studies must be conducted to determine whether there's a mistake in the signaling pathway for the thrill, as suggested by the first proposition presented, or whether melatonin regulation or the neural populations have been disintegrated 24.
Hallucinations: Different levels of hallucination may observe in the sleep paralysis, the belief that there's a meddler in the room, the presence of an incubus, and the sensation of floating. A neurological thesis is that in sleep paralysis the mechanisms which generally coordinate body movement and give information on body position come actuated because there's no factual movement, which induces a floating sensation 25, 26. The meddler and incubus visions largely relate to one another. They are relatively identified with the third daydream, vestibular-motor disorientation, also known as an out-of-body experience, which differs from the other two in not involving the trouble-actuated alert system 27.
Hyperactive-vigilance: A hyperactive-watchful state created in the midbrain may further contribute to visions; the sudden changes cause stress upon the brain, and when the victim wants to wake up, they may feel paralyzed and feel vulnerable to attack 28. This helplessness can disturb normal dreams, which could explain why similar fancies during sleep paralysis are so pictorial 29. The trouble-actuated alert system is a defensive medium that differentiates between dangerous situations and determines whether the fear response is applicable. The hyperactive-alert response can lead to the creation of endogenous stimulants that contribute to the perceived trouble. Some can feel the evil or create a panic that somebody is trying to choke them 30. A neurological explanation says that it is because of hyper activeness that may paralyze the brain and voluntary muscles. The feeling of suffocation may be felt by rapidly breathing, a high amount of carbon dioxide in the blood, and some blocks in the respiratory system, which is a symptom current in sleep apnea cases 31. The individual tries to breathe deeply and finds themselves unfit, creating a sensation of resistance. The trouble-actuated alert system interprets as an unearthly being sitting on their chest, hanging suffocation 32, 33. The sensation of these elevates the fear and the individuals struggle more in this sleep paralysis condition.
Mechanism of Action: Sleep paralysis affects those with narcolepsy, or it may run families because of the specific inheritable change. The condition can be started by sleep privation, cerebral stress, and anxiety, so the treatment of sleep paralysis recommended antidepressant and cognitive-behavioral therapy 34, 35.
Mechanism of Action: Yokukansan shows several effects on the neurotransmitter systems (e.g., glutamatergic, serotonergic, dopaminergic, cholinergic, GABAergic and adrenergic neurotransmission) in different brain regions, which affect the cerebral, emotional, cognitive, or memory functions 36. Yokukansan is tested for several psychiatric conditions like dementia, and it is effective, yokukansan could ameliorate the symptoms of behavioral and cerebral symptoms of madness (BPSD) in Alzheimer's disease, neuropsychiatric symptoms associated with Parkinson's conditions, including visions, anxiety, and apathy without severe adverse events or worsening of Parkinsonism. According to clinical studies, yokukansan may have multiple factors that effectively treat central nervous system dysfunctions 37.
As a medium of the ameliorative effect against central nervous system conditions. Yokukansan is widely used as a neuroprotective agent as it can nullify the excitotoxicity by glutamate and cytotoxicity by corticosterone. Research has found the anti-depressive and anti-nociceptive properties of yokukansan. Ananimal behavioral trial revealed that yokukansan showed anxiolytic effects against aversive stress inrats. Several studies have stated that yokukansan contains factors that act as agonists or antagonists against several receptors. The drug mainly acts upon the 5-HT1A receptor agonist. Therefore since 5-HT1A agonist has an antidepressant-suchlike effect, the antidepressant-like effect induced by yokukansan may be due to stimulation of the 5-HT1A receptor 37.
Also, habitual stress dropped the number of neural stem cells in the subventricular zone, and an antidepressant, such as a selective serotonin re-uptake inhibitor (SSRI), attenuated the corticosteroid. Furthermore, finding suggested that the 5-HT1A agonists that affected the cell cycle in the adult central nervous system may be related to anti-depressive mechanisms. Yokukansan has a cell-proliferative effect and the medium that underlies this effect by using B65 neuroblastoma cells induced from monoaminergic neurons 38. Yokukansan maintains neuronal survival and function by multiple salutary goods, include inganti-apoptosis, anti-oxidation, anti-endoplasmic reticulum stress, and neurogenesis 39. Yokukansan also acts on glial cells by easing the transport of glutamate into astrocytes; promoting the proliferation and isolation of oligodendrocytes, and enhancing the anti-inflammatory parcels of microglial cells. These glial effects are allowed to support neuronal functioning within the brain. The constituents involved in these effects can pass through the blood-brain barrier without dismembering the endothelial tight junctions 40, 41.
Interaction: Yokukansanco-administration with glycyrrhiza-, glycyrrhizin acid, or glycyrrhizinate-containing medications may lead to pseudo-aldosteronism hypokalemia and myopathy 41.
Contraindication: Contraindications of this herbal medicine haven't been found yet.
Adverse Effect: Nausea in some elderly patients; minor side effects are sedation, nausea, vomiting, diarrhea, and epigastric discomfort.
Use: Yokukansan is a Japan-origin drug, presently used to treat cerebral symptoms and decreased sleep cons quiescence. Reducing cerebral and behavioral symptoms in madness cases helps to maintain a standard life for those who suffer from psychiatric diseases like schizophrenia and framing personality complaints 42, 43.
Eschscholzia californica Alkaloids:
Mechanism of Action: Eschscholzia californica Cham (Papaveraceous) has been known to retain opiate, anxiolytic, and analgesic. The aqueous alcohol extract of Eschscholzia californica was estimated for benzodiazepine, neuroleptic, antidepressant, antihistaminic, and analgesic character; it also induces peripheral. The sedative effect of alkaloids detected in Eschscholzia californica was attributed to chloride-current modulation, which was extensively expressed in the brain substantially at the inhibitory interneuron’s 44. Electrophysiological analysis on recombinant α1 β2 GABAA receptor found that concentrations lower than 30havehas no effect on N-methyllaurotetanine. Still, (S)-reticuline is considered a positive allosteric modulator at the 𝛼3, 𝛼5, and 𝛼6 isoforms of GABAA receptors. Eschscholzia californica was assigned to chloride-current modulation by (S)-reticuline at the αβ2ϒ2 and α5 β2 ϒ 2 GABAA receptors 45.
Interaction: Opiate specifics (Benzodiazepines) drug with California poppy interaction might lead to drowsiness and sleepiness. Some of these opiate specifics drug include clonazepam (Klonopin), diazepam (Valium), lorazepam (Ativan), phenobarbital (Donnatal), zolpidem (Ambien) 46.
Contraindication: Avoid the use of California poppy use when pregnant or breast-feeding. California poppy has a major effect on CNS, there's some concern that it is more effective when combined with anesthesia and other specific drug used during and after surgery. Stop using California poppy at least 2 weeks before a listed surgery 47.
Adverse Effects: No such research found the adverse effects of an oral application. Noted that natural products aren't always safe and dosage can be important 46.
Use: Eschscholzia californica Alkaloid is used for Anxiety, Insomnia, Aches 47.
Synthetic Drugs: Selective serotonin re-uptake inhibitor is the main synthetic medication used in case of sleep paralysis; this class of drugs falls under antidepressants and is generally used for depression and anxiety disorders which may cause sleep paralysis 48.
Mechanism of Action: Duloxetine is a potent substance of neural 5-hydroxytryptamine and vasoconstrictive uptake and a less potent substance of monoamine neurotransmitter uptake. Duloxetine has minimal effect on dopaminergic, adrenergic, cholinergic, histaminergic, opioid, glutamate, and neurotransmitter receptors. Action on the external urinary musculus is mediated via duloxetine's CNS effects. Duloxetine is inflated 5-hydroxytryptamine and vasoconstrictive concentrations in Onuf's nucleus resulting in inflated activation of 5-HT2, 5-HT3, and α1 adrenergic receptors.5-HT2 and α1 are each GQ coupled. Their activation will increase the activity of the B-complex vitamin trisphosphate/ phospholipase C (IP3/PLC) pathway 49. This pathway results in the unleashing of intracellular calcium stores, which will increase the calcium concentrations, facilitating neural excitability. 5-HT3 functions as a ligand-gated sodium channel that permits sodium to flow into the nerve cell; once activated, it inflates the flow of sodium into the nerve cell, contributing to depolarization and activation of voltage-gated channels concerned in impulse generation. The combined action of those 3 receptors contributes to inflated excitability of the genitals nervus in response to salt 50. The mechanisms are concerned with duloxetine's edges in depression and anxiety. Dysfunctional 5-hydroxytryptamine and norepinephrine signaling will increase the concentration of neurotransmitters at the conjugation cleft, which mediates a therapeutic result 51.
Interaction: Drugs that may cause bleeding or bruising (e. g.: antiplatelet drugs like clopidogrel, NSAIDs like ibuprofen, "blood thinners" like warfarin). Other medications will remove duloxetine from your body, which can affect the duloxetine mechanism (Eliglustat, iobenguanei 123, dicarboxamide, phenelzine, procarbazine, selegiline, Tranylcypromine). Duloxetine has serious interactions with 86 different medications; CYP1A2 inhibitors or thioridazine should not be co-administered 52, 53.
Contraindication: Concomitant use of duloxetine with MAOIs meant to treat psychiatric disorders. Avoid Co-administration with serotonergic drug or wait for a minimum of fourteen days between termination of antidepressant drug and initiation of duloxetine; wait for a minimum of five days between termination of duloxetine and initiation of MAOI 54.
Linezolid and methylene blue are contraindicated to duloxetine, which inflated the serotonin syndrome; if the patients have already taken both drugs, then stop the duloxetine and keep the patient in observation for CNS toxicity; duloxetine could also be resumed twenty-four hours when the last linezolid dose or when a pair of weeks of observance, whichever comes 1st 55.
Adverse Effect: Duloxetine has minor adverse effects like Nausea, Dry mouth, Headache, Drowsiness, and Fatigue 56.
Use: Duloxetine is accustomed to treating depression and anxiety, it’s additionally accustomed to facilitating relieve nerve pain (peripheral neuropathy) in people with diabetes or medical conditions such as arthritis or chronic back pain. Duloxetineis used for mood swings; loss of appetite, and it reduces nervousness 57. Duloxetine falls under the class of serotonin-norepinephrine uptake inhibitor (SNRI). This drug maintains the serotonin and nor epinephrine concentration in the brain 58.
Mechanism of Action: Venlafaxine falls under the serotonin-norepinephrine re-uptake inhibitor (SNRI); however, it's conjointly been named a serotonin-norepinephrine-dopamine re-uptake inhibitor (SNDRI) 59. It works by obstructing re-uptake proteins for neurotransmitters affecting mood swings; therefore, many active neurotransmitters are available in the synapse. The neurotransmitters are affected by serotonin and norepinephrine; high doses of it also inhibit the re-uptake of dopamine. Since dopamine is inactivated by catecholamine re-uptake in the frontal cortex. For the most part, the cortical area lacks dopamine transporters; thus, venlafaxine can avail the neurotransmission of dopaminein this part of the brain 60. Venlafaxine remotely affects opioid receptors as well because the alpha2-adrenergic receptor was shown to extend the absolute threshold in mice. These advantages regarding pain were reversed with naloxone, an associate opioid antagonist, therefore supporting the associate opioid mechanism 61.
Interaction: Some drugs that cause bleeding or bruising (e.g.: antiplatelet drugs such as clopidogrel, NSAIDs such as ibuprofen, naproxen, anticoagulants like dabigatran, warfarin). Aspirin increases the chance of injury once both drugs are taken simultaneously 62. Take only, if necessary, take prevention (usually 81-162 milligrams a day), don’t stop unless your physician’s advice is to stop. This drug interacts with monoamine oxidase inhibitors, e.g., dicarboxamide, linezolid, methylene blue, moclobemide, phenelzine, procarbazine, rasagiline, safinamide, selegiline, tranylcypromine 63. Ought to conjointly should not take for 2 weeks before and a minimum of seven days after using this drug.
The risk of 5-hydroxytryptamine syndrome/toxicity will increase if you're conjointly taking different medications that increase serotonin 64. Examples-street drugs like MDMA / ecstasy, certain antidepressants (fluoxetine/paroxetine, different SNRIs such as duloxetine/milnacipran), tryptophan, and others, the chance of serotonin toxicity could be high if you begin or increase the dose for for of for these for For medications for 65.
Contraindication: Venlafaxine could contain inactive ingredients, which might cause hypersensitivity or different issues. Before use, consult with your doctor or pharmacist about your case history, particularly of injury issues, history of glaucoma (angle-closure type), high vital signs, heart problems (such as heart failure, previous heart attack), high cholesterol, kidney and liver disease, seizure disorder, thyroid level. This drug could cause drowsiness or blur your vision 66. Alcohol or marijuana (cannabis) will cause you a lot of dizziness or drowsy, don't drive or use machinery or do something that wants alertness or clear vision until you'll be able to do it safely. Avoid alcoholic beverages and consult with your doctor if you're taking marijuana (cannabis). Before any surgery, inform your surgeon about the prescription, nonprescription, and herbal products you used. Older adults should take prevention before this drug, especially dizziness when standing 67. Older adults may also develop a salt imbalance (hyponatremia), particularly if they're taking water pills (diuretics). Dizziness and salt imbalance will increase the chance of falling. Older adults may also be at a more significant risk of bleeding using this drug 68. Children may experience appetite and weight loss by using this drug. During pregnancy, use this drug only, if necessary; it can harm an unborn baby. A mother who takes this drug in the last trimester of pregnancy may develop withdrawal symptoms like feeding or breathing difficulties, seizures, muscle stiffness, or constant crying. Observe the babies and make the needful for proper treatment 69, 70.
Adverse Effect: Nausea, drowsiness, dizziness, dry mouth, constipation, loss of appetence, blurred vision, nervousness, hassle sleeping, unusual sweating, or yawning could occur. This medication could raise your blood pressure, decrease interest in sex, cause changes in sexual ability, muscle cramps/weakness, and shaking (tremor) 71-73.
Use: Venlafaxine is commonly used for symptoms like depression, anxiety, panic attacks, and social anxiety disorder (social phobia); it can elevate your energy and will facilitate restoring your interest in daily living 74. Venlafaxine is known as a serotonin-norepinephrine re-uptake inhibitor (SNRI). This drug maintains the concentration of serotonin and norepinephrine in the brain 75.
Mechanism of Action: Desvenlafaxine is a synthetic form of isolated active molecules of venlafaxine, and it falls under the class of serotonin-norepinephrine uptake inhibitor (SNRI). When metabolizers take venlafaxine 70% of the dose is metabolized into desvenlafaxine; therefore the effects of these two drugs aresimilar 76. It works by obstructing re-uptake proteins for neurotransmitters which affecting for mood swings, therefore, a lot of active neurotransmitters are available in the synapse. The neurotransmitters affected are serotonin (5-hydroxytryptamine) and norepinephrine (noradrenaline), inhibiting serotonin uptake 10 times more challenging than norepinephrine uptake 77.
Interaction: Desvenlafaxine and alfentanil, Tofranil, levorphanol each increase serotonin levels, which might cause serotonin syndrome 78, 79.
Contraindication: Phenelzine and desvenlafaxine each increase serotonin levels. Contraindicated, a minimum of fourteen days gap between discontinuance of MAOIs and initiation of treatment with a serotonergic drug should take 80. Desvenlafaxine with tedizolidcan induces a pharmacodynamics synergism. Desvenlafaxinemay increases the effects of alkaloids through adrenergic receptors; it includes high blood pressure and pulse rate 81. The alternate drug that supported the mechanism of action of iobenguane, reduces catecholamine uptake or depletes catecholamine stores and thus reduces iobenguane effectivity. Discontinue alternate drug a minimum of five half-lives before administration of iobenguane dose don't administer this medicine till a minimum of seven days after every ibogaines dose 82.
Adverse Effect: Adverse drug reactions (ADRs) occur over 50mg/day dosage; such as nausea, Dry mouth, sweating, Dizziness, Insomnia, Fatigue, Weight increase, liver performance check abnormal, blood prolactin increased, muscle-skeletal stiffness, Serotonin syndrome, Elevated blood pressure, abnormal bleeding 83.
Use: Desvenlafaxine is commonly used for symptoms like depression, anxiety, panic attacks, and social anxiety disorder (social phobia); it can elevate your energy and facilitate restoring your interest in daily living. Desvenlafaxine is known as a serotonin-norepinephrine re-uptake inhibitor (SNRI) 84. This drug maintains the concentration of serotonin and norepinephrine in the brain 85.
Mechanism of Action: Escitalopram will increase neurochemical serotonin's extrasynaptic levels by blocking the neurotransmitter's re-uptake into the presynaptic vegetative cell. SSRIs presently obtainable, escitalopram has the highest selectivity for the serotonin transporter (SERT) compared to the norepinephrine transporter (NET), creating the side-effect profile comparatively gentle compared to less-selective SSRIs 86. Escitalopram may be a substrate of multidrug resistance protein, and their inhibitors verapamil and quinidine may improve its blood-brain barrier penetrability 87, 88. A clinical study showed that in rats applying escitalopram with a P-glycoprotein substance, its antidepressant-like effects were increased 89.
Interaction: Some drugs that cause bleeding or bruising (e.g., antiplatelet drugs such as clopidogrel, NSAIDs such as ibuprofen, naproxen, anticoagulants like dabigatran, warfarin) 90. Aspirin increases the chance of injury once both drugs are taken simultaneously. Take only, if necessary, take prevention (usually 81-162 milligrams a day), and don’t stop unless your physician’s advice is to stop 91. This drug interacts with monoamine oxidase inhibitors e.g.: dicarboxamide, linezolid, methylene blue, moclobemide, phenelzine, procarbazine, rasagiline, safinamide, selegiline, tranylcypromine. Most MAO inhibitors ought conjointly should not take for 2 weeks before and a minimum of seven days after using this drug 21.
The risk of 5-hydroxytryptamine syndrome/toxicity will increase if you're conjointly taking different medicine that increases serotonin 92. Examples-street drugs like MDMA/ecstasy, certain antidepressants (fluoxetine/paroxetine, different SNRIs such as duloxetine /milnacipran), tryptophan, and others, the chance of serotonin toxicity could be high if you begin or increase the dose of for these for medications for 93. Escitalopram is incredibly similar to citalopram. don't use medications containing citalopram when using escitalopram 94.
Contraindication: Consult with your health professional about your family history of bipolar /manic-depressive disorder, personal case history of suicidal attempts, liver illness, seizures, internal organ ulcerations/bleeding (peptic ulcer disease) or hurt issues, low sodium in the blood (hyponatremia), case history of glaucoma (angle-closure type) before taking the drug. Escitalopram is also responsible for QT prolongation that causes irregular heartbeat, severe dizziness, and fainting. The chances of QT prolongation increase if you’re taking other drugs that can also affect QT prolongation. Before using escitalopram, tell your doctor or health professional of all the medicine you are taking and if you have any subsequent heart problems like heart failure, slow heartbeat, recent heart attack, QT prolongation in the EKG, fulminant viscus death 95.
This drug is additionally effective for drowsiness if taken with alcohol or marijuana (cannabis); don’t drive or do something that desires alertness till you'll have intercourse safely. Avoid alcoholic beverages. Visit your doctor if you're taking marijuana (cannabis) 96. The liquid type of this medication could contain sugaror sweetening. Caution is suggested if you have diabetes, an inborn error of metabolism (PKU), or other condition that needs you to improve before using this drug 24. Ask your doctor or health professional about the treatment of this medication safely. Older adults could also be additional sensitive effects of this drug, like QT prolongation (see above), loss of coordination, or hurt. They will even be additional probably to lose an excessive amount of salt (hyponatremia), particularly if they're conjointly taking "water pills" (diuretics) with this medication. Loss of coordination will increase the danger of falling. During pregnancy, this medication should be used only if required 97. A mother who takes this drug in the last trimester of pregnancy may develop withdrawal symptoms like feeding/breathing difficulties, seizures, muscle stiffness, or constant crying. Tell the doctor promptly if you notice any of those symptoms in your newborn. Significant symptoms like depression, anxiety, psychoneurotic disorder, and panic disorder may be vulnerable if untreated, don’t stop treatment without consulting your doctor 97. If you become pregnant or assume you will be pregnant, check with your doctor about the advantages and risks of mistreatment of this medication throughout your physiological state 98.
Adverse Effect: Escitalopram and SSRIs have a lower toxicity profile than older antidepressants. Despite this, they need to be related to vital adverse effects. The most commonly determined adverse effects reportable are; sleep disorder, sexual dysfunction (primarily weakened sexual desire, anorgasmia, and male ejaculatory delay), nausea, exaggerated sweating, fatigue, and sleepiness. Escitalopram will probably cause withdrawal symptoms like vertigo, nausea, lethargy, and vertigo if short-stopped 99. Escitalopram will cause SSRI-induced syndrome of inappropriate vasoconstrictor secretion (SSRI-induced SIADH), resulting in symptoms, particularly within the old population.
Looking at the severity of the symptom, symptoms will vary from eating disorders, nausea, vomiting, fatigue, and headache to additional severe conditions like 100 altered mental standing, seizures, and even coma. Serotonin syndrome results in an excess quantity of 5-hydroxytryptamine within the peripheral and central nervous systems 101. This medical condition will result in contractor excitation and involuntary stimulation. 5-hydroxytryptamine syndrome risk is high when patients take high-dose SSRIs or take more than one serotonergic drug, particularly if they work by completely different mechanisms (an SSRI plus a monoamine oxidase inhibitor) 102. Symptoms of the 5-hydroxytryptamine syndrome could embrace involuntary instability like arrhythmia, cardiovascular disease, dizziness, sweating, flushing, mydriasis, and exaggerated temperature (above thirty-eight degrees Celsius). It can even cause nausea, vomiting, diarrhea, and mental standing changes like agitation, delirium, hallucinations, somnolence, and coma. Contractor symptoms can even gift, together with unskillfulness, rigidity, clonus, hyperreflexia, tremors, and hypertonicity 103. Thereare reports of severe cases presenting with cardiogram changes and seizures. A 4 weeks gap before attempting another drug is suggested to avoid inflicting 5-hydroxytryptamine syndrome.
Use: Escitalopram is used to treat depression and anxiety. It works by serving to revive the balance of an explicit natural substance (serotonin) in the brain. Escitalopram belongs to a category of medication called selective serotonin uptake inhibitors (SSRI) it's going to improve your energy and feelings of well-being and reduce nervousness 104, 105.
Justification: Sleep dysfunction or sleep paralysis may be a feeling of being acutely aware but unable to maneuver 106. It occurs once a person passes between the stage of wakefulness and sleep. During this transition, you may be unable to maneuver or speak for some seconds or minutes; this is not so dangerous for us; this may management naturally with few changes in standard of living routine 107.
Causes for Sleep Paralysis:
- Poor mental state 108.
- Sleep on Back
- sleep disorder
- Narcolepsy (excessive and uncontrollable daytime sleepiness) 109.
How to Manage Sleep Paralysis:
- Getting enough sleep (6-8 hours).
- Avoiding alkaloids or alcohol nearer to bedtime.
- Avoid noise or light throughout sleeping.
- Pre-relaxation practices before bedtime 110.
- Avoid irregular standards of living.
- Improve your lifestyle and be happy 111.
- No immediate threat to physical health
- The only painful feeling throughout sleeping
- No health risks 112.
CONCLUSION: Through our project, we tend to analyze drugs that could be affected by sleep paralysis, which may be a condition marked by the shortcoming of maneuvering your body upon falling asleep or wakening. Whereas it typically is in the middle of horrifying hallucinations, sleep dysfunction doesn't cause damage. By treating any underlying conditions and raising your sleep health, you'll facilitate managing sleep dysfunction to guarantee a decent, fear-free night of sleep. There is no need to worry about nighttime demons or alien abductors. If you have occasional sleep disfunction, you'll take steps to manage this disorder. Begin by ensuring you get enough sleep. Do what you'll to alleviate stress in your life, particularly simply before bedtime. Attempt new sleeping positions if you sleep on your back, and make sure to ask your doctor if sleep dysfunction habitually prevents you from obtaining a decent night's sleep.
Consent for Publication: Not applicable.
ACKNOWLEDGEMENT: Thank you, Dr. Subhabrota Majumder, for supporting the work and revision of the manuscript and for designing the manuscript.
Author Contribution: Soumyadip Ghosh, Debgopal Ganguly, Madhumita Banerjee, Md Abid Alam and Rajesh Ghosh designed the work and revisions in the manuscript. Soumyadip Ghosh provided maximum effort in the correction, collected documents, makes proper format. Debgopal Ganguly did a proper literature survey and designed the manuscript. Madhumita Banerjee, Md. Abid Alam and Rajesh Ghosh did a proper review and data collection for writing this manuscript. All the authors design the final manuscript.
CONFLICTS OF INTEREST: Declared none.
- Conesa J: Geomagnetic, cross-cultural and occupational faces of sleep paralysis: An ecological perspective. Sleep and Hypnosis 2000; 2(3): 248-54.
- Gu W, Yang Z, Shangguan L, Sun W, Jin K and Liu Y: Editors. Intelligent sleep stage mining service with smartphones. Proceedings of the 2014 ACM international Joint Conference on pervasive and ubiquitous Computing 2014.
- Adler SR: Sleep paralysis: Rutgers University Press; 2011.
- Kompanje EJO. ‘The devil lay upon her and held her down’Hypnagogic hallucinations and sleep paralysis described by the Dutch physician Isbrand van Diemerbroeck (1609–1674) in 1664. Journal of Sleep Research 2008; 17(4): 464-7.
- Wing YK, Chiu H, Leung T and Ng J: Sleep paralysis in the elderly. Journal of Sleep Research 1999; 8(2): 151-5.
- Adler SR: Sudden Unexpected Nocturnal Death Syndrome among Hmong Immigrants: Examining the Role of the" Nightmare". Journal of American Folklore 1991; 54-71.
- Vatta M, Dumaine R, Varghese G, Richard TA, Shimizu W and Aihara N: Genetic and biophysical basis of sudden unexplained nocturnal death syndrome (SUNDS), a disease allelic to Brugada syndrome. Human Molecular Genetics 2002; 11(3): 337-45.
- Stefani A and Högl B: Nightmare disorder and isolated sleep paralysis. Neurotherapeutics 2021; 18(1): 100-6.
- Jalal B, Romanelli A and Hinton DE: Sleep paralysis in Italy: Frequency, hallucinatory experiences, and other features. Transcultural Psychiatry 2021; 58(3): 427-39.
- Wróbel-Knybel P, Karakuła-Juchnowicz H, Flis M, Rog J, Hinton DE and Boguta P: Prevalence and clinical picture of sleep paralysis in a Polish student sample. International J of Enviro Res and Public Health 2020; 17(10): 3529.
- Raduga M, Kuyava O and Sevcenko N: Is there a relation among REM sleep dissociated phenomena, like lucid dreaming, sleep paralysis, out-of-body experiences, and false awakening? Medical Hypotheses 2020; 144: 110169.
- Barnes JS: Stress and Distress in Recurrent Isolated Sleep Paralysis-The Effects of a Provider Training: Saint Louis University 2020.
- Kanayama M, Miyaoka T, Araki T, Hayashida M, Hashioka S and Horiguchi J: Salivary Alpha-Amylase Activity Levels in Catatonic Schizophrenia Decrease after Electroconvulsive Therapy. Case Reports in Psychiatry 2018; 2018.
- Libourel PA and Barrillot B: Is there REM sleep in reptiles? A key question, but still unanswered. Current Opinion in Physiology 2020; 15: 134-42.
- Yadav S and Yadav R: Behavioral Presentations of Parasomnias. Sleep and Neuropsychiatric Disorders Springer 2022; 303-16.
- Wróbel-Knybel P, Flis M, Dubiel R and Karakuła-Juchnowicz H: What do we know about sleep paralysis. Current Problems of Psychiatry 2018; 19(3): 174-84.
- Ryu S, Slopen N, Ogbenna BT and Lee S: Acculturation and sleep outcomes in Asian Americans and Pacific Islanders: Results from the National Epidemiologic Survey on Alcohol and Related Conditions-III. Sleep Health 2021; 7(6): 683-90.
- Young E, Xiong S, Finn L and Young T: Unique sleep disorders profile of a population-based sample of 747 Hmong immigrants in Wisconsin. Social Science & Medicine 2013; 79: 57-65.
- Bassetti CL, Adamantidis A, Burdakov D, Han F, Gay S and Kallweit U: Narcolepsy clinical spectrum, aetiopathophysiology, diagnosis and treatment. Nature Reviews Neurology 2019; 15(9): 519-39.
- Sharpless BA, McCarthy KS, Chambless DL, Milrod BL, Khalsa SR and Barber JP: Isolated sleep paralysis and fearful isolated sleep paralysis in outpatients with panic attacks b. Journal of Clinical Psychology 2010; 66(12): 1292-306.
- Sharpless BA and Grom JL; Isolated sleep paralysis: fear, prevention, and disruption. Behavioral Sleep Medicine 2016; 14(2): 134-9.
- Munezawa T, Kaneita Y, Osaki Y, Kanda H, Ohtsu T and Suzuki H: Nightmare and sleep paralysis among Japanese adolescents: a nationwide representative survey. Sleep Medicine 2011; 12(1): 56-64.
- Ohayon MM, Zulley J, Guilleminault C and Smirne S: Prevalence and pathologic associations of sleep paralysis in the general population. Neurology 1999; 52(6): 1194-.
- von Moltke LL, Greenblatt DJ, Giancarlo GM, Granda BW, Harmatz JS and Shader RI: Escitalopram (S-citalopram) and its metabolites in-vitro: cytochromes mediating biotransformation, inhibitory effects and comparison to R-citalopram. Drug Metabolism and Disposition 2001; 29(8): 1102-9.
- Asaad G and Shapiro B: Hallucinations: theoretical and clinical overview. The American Journal of Psychiatry 1986.
- O'Brien J, Taylor JP, Ballard C, Barker RA, Bradley C and Burns A: Visual hallucinations in neurological and ophthalmological disease: pathophysiology and management. Journal of Neurology Neurosurgery & Psychiatry 2020; 91(5): 512-9.
- Rudberg I, Reubsaet JLE, Hermann M, Refsum H and Molden E: Identification of a novel CYP2C19-mediated metabolic pathway of S-citalopram in-vitro. Drug Metabolism and Disposition 2009; 37(12): 2340-8.
- Nikisch G, Eap CB and Baumann P: Citalopram enantiomers in plasma and cerebrospinal fluid of ABCB1 genotyped depressive patients and clinical response: a pilot study. Pharmacological Research 2008; 58(5-6): 344-7.
- Van der Kolk BA and Van der Hart O: The intrusive past: The flexibility of memory and the engraving of trauma. American Imago 1991; 48(4): 425-54.
- Ikarashi Y, Iizuka S, Imamura S, Yamaguchi T, Sekiguchi K and Kanno H: Effects of yokukansan, a traditional Japanese medicine, on memory disturbance and behavioral and psychological symptoms of dementia in thiamine-deficient rats. Biological and Pharmaceutical Bulletin 2009; 32(10): 1701-9.
- Beausoleil N and Mellor D: Introducing breathlessness as a significant animal welfare issue. New Zealand Veterinary Journal 2015; 63(1): 44-51.
- Olunu E, Kimo R, Onigbinde EO, Akpanobong M-AU, Enang IE and Osanakpo M: Sleep paralysis, a medical condition with a diverse cultural interpretation. Inter J of Applied and Basic Medical Research 2018; 8(3): 137.
- Jalal B: How to make the ghosts in my bedroom disappear. Focused-attention meditation combined with muscle relaxation (MR therapy) a direct treatment intervention for sleep paralysis. Frontiers in Psychology 2016; 28.
- Paradis C, Friedman S, Hinton DE, McNally RJ, Solomon LZ and Lyons KA: The assessment of the phenomenology of sleep paralysis: the Unusual Sleep Experiences Questionnaire (USEQ). CNS neuroscience & therapeutics. 2009; 15(3): 220-6.
- Denis D, French CC and Gregory AM: A systematic review of variables associated with sleep paralysis. Sleep Medicine Reviews 2018; 38: 141-57.
- Matsumoto K, Zhao Q, Niu Y, Fujiwara H, Tanaka K and Sasaki-Hamada S: Kampo formulations, chotosan, and yokukansan, for dementia therapy: existing clinical and preclinical evidence. Journal of Pharmacological Sciences 2013; 122(4): 257-69.
- Ikarashi Y and Mizoguchi K: Neuropharmacological efficacy of the traditional Japanese Kampo medicine yokukansan and its active ingredients. Pharmacology & Therapeutics 2016; 166: 84-95.
- Furuya M, Miyaoka T, Tsumori T, Liaury K, Hashioka S and Wake R: Yokukansan promotes hippocampal neurogenesis associated with the suppression of activated microglia in Gunn rat. Journal of Neuroinflammation 2013; 10(1): 1-9.
- Mizoguchi K and Ikarashi Y: Cellular pharmacological effects of the traditional Japanese kampo medicine yokukansan on brain cells. Frontiers in Pharmacology 2017; 8: 655.
- Kaushik R, Morkovin E, Schneeberg J, Confettura AD, Kreutz MR and Senkov O: Traditional Japanese herbal medicine Yokukansan targets distinct but overlapping mechanisms in aged mice and in the 5xFAD mouse model of Alzheimer’s disease. Frontiers in Aging Neuroscience 2018; 411.
- Ebihara N, Ikemoto H, Adachi N, Okumo T, Kimura T and Yusa K: Analgesic Effect of Combined Therapy with the Japanese Herbal Medicine “Yokukansan” and Electroacupuncture in Rats with Acute Inflammatory Pain Medicine 2021; 8(6): 31.
- Matsuda Y, Kishi T, Shibayama H and Iwata N: Yokukansan in the treatment of behavioral and psychological symptoms of dementia: a systematic review and meta‐analysis of randomized controlled trials. Human Psychopharmacology: Clinical and Experimental 2013; 28(1): 80-6.
- Mizukami K, Asada T, Kinoshita T, Tanaka K, Sonohara K and Nakai R: A randomized cross-over study of a traditional Japanese medicine (kampo), yokukansan, in the treatment of the behavioural and psychological symptoms of dementia. The International Journal of Neuropsychopharmacology 2009; 12(2): 191-9.
- Hayashi Y, Ishida Y, Inoue T, Udagawa M, Takeuchi K and Yoshimuta H: Treatment of behavioral and psychological symptoms of Alzheimer-type dementia with Yokukansan in clinical practice. Progress in Neuro-Psychophar and Biological Psychiatry 2010; 34(3): 541-5.
- Fedurco M, Gregorová J, Šebrlová K, Kantorová J, Peš O and Baur R: Modulatory effects of Eschscholzia californica alkaloids on recombinant GABAA receptors. Biochemistry Research International 2015; 2015.
- Manda VK, Ibrahim MA, Dale OR, Kumarihamy M, Cutler SJ and Khan IA: Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloids. Planta Medica 2016; 82(06): 551-8.
- Californica E and Phytochemical A: Pharmaceutical Sciences.
- Mansoori P, Akhondzadeh S, Raisi F, Ghaeli P, Jamshidi A and Nasehi A: A randomized, double-blind, placebo-controlled study of safety of the adjunctive saffron on sexual dysfunction induced by a selective serotonin re-uptake inhibitor
- Jost W and Marsalek P: Duloxetine: mechanism of action at the lower urinary tract and Onuf’s nucleus. Clinical Autonomic Research 2004; 14(4): 220-7.
- Bauer M, Möller HJ and Schneider E: Duloxetine: a new selective and dual-acting antidepressant. Expert Opinion on Pharmacotherapy 2006; 7(4): 421-7.
- Jalal B, Moruzzi L, Zangrandi A, Filardi M, Franceschini C and Pizza F: Meditation-Relaxation (MR Therapy) for Sleep Paralysis: A Pilot Study in Patients With Narcolepsy. Frontiers in Neurology 2020; 922.
- Gertken J, Patel AT and Boon AJ; Electromyography and anticoagulation. PM & R 2013; 5(5): 3-7.
- Lynch SL, Boon AJ, Smith J, Harper CM and Tanaka EM: Complications of needle electromyography: hematoma risk and correlation with anticoagulation and antiplatelet therapy. Muscle & Nerve: Official Journal of the American Association of Electrodiagnostic Medicine 2008; 38(4): 1225-30.
- Branton MW, Hopkins TJ and Nemec EC: Duloxetine for the reduction of opioid use in elective orthopedic surgery: a systematic review and meta-analysis. International Journal of Clinical Pharmacy 2021; 43(2): 394-403.
- Team G: Clinical Problem and Management Issues 2011.
- Hunziker ME, Suehs BT, Bettinger TL and Crismon ML: Duloxetine hydrochloride: a new dual-acting medication for the treatment of major depressive disorder. Clinical Therapeutics 2005; 27(8): 1126-43.
- Hirschfeld RM, Mallinckrodt C, Lee TC and Detke MJ: Time course of depression‐symptom improvement during treatment with duloxetine. Depression and Anxiety 2005; 21(4): 170-7.
- Kirwin JL and Gören JL: Duloxetine: A dual serotonin‐norepinephrine re-uptake inhibitor for treatment of major depressive disorder. Pharmacotherapy. The Journal of Human Pharmacology and Drug Therapy 2005; 25(3): 396-410.
- Harvey AT, Rudolph RL and Preskorn SH: Evidence of the dual mechanisms of action of venlafaxine. Archives of General Psychiatry 2000; 57(5): 503-9.
- Horst WD and Preskorn SH: Mechanisms of action and clinical characteristics of three atypical antidepressants: venlafaxine, nefazodone, bupropion. Journal of Affective Disorders 1998; 51(3): 237-54.
- Papp M, Gruca P, Lason M, Niemczyk M and Willner P: The role of prefrontal cortex dopamine D2 and D3 receptors in the mechanism of action of venlafaxine and deep brain stimulation in animal models of treatment-responsive and treatment-resistant depression. Journal of Psychopharmacology 2019; 33(6): 748-56.
- Ereshefsky L: Drug-drug interactions involving antidepressants: focus on venlafaxine. Journal of Clinical Psychopharmacology 1996; 16(3): 37-50.
- Thase ME, Entsuah R, Cantillon M and Kornstein SG: Relative antidepressant efficacy of venlafaxine and SSRIs: sex-age interactions. J of Women's Health 2005; 14(7): 609-16.
- Owen JR and Nemeroff CB: New antidepressants and the cytochrome P450 system: focus on venlafaxine, nefazodone, and mirtazapine. Depression and Anxiety 1998; 7(1):24-32.
- Cheyne JA, Rueffer SD and Newby-Clark IR: Hypnagogic and hypnopompic hallucinations during sleep paralysis: neurological and cultural construction of the nightmare. Consciousness and Cognition 1999; 8(3): 319-37.
- Howell C, Wilson AD and Waring W: Cardiovascular toxicity due to venlafaxine poisoning in adults: a review of 235 consecutive cases. British Journal of Clinical Pharmacology 2007; 64(2): 192-7.
- Singh D and Saadabadi A: Venlafaxine. StatPearls [Internet]. 2021.
- Walker EM, Rodriguez AI, Kohn B, Ball RM, Pegg J and Pocock JR: Acupuncture versus venlafaxine for the management of vasomotor symptoms in patients with hormone receptor-positive breast cancer: a randomized controlled trial. J Clin Oncol 2010; 28(4): 634-40.
- Loprinzi CL, Kugler JW, Sloan JA, Mailliard JA, LaVasseur BI and Barton DL: Venlafaxine in management of hot flashes in survivors of breast cancer: a randomised controlled trial. The Lancet 2000; 356(9247): 2059-63.
- Sindrup SH, Bach FW, Madsen C, Gram L and Jensen T: Venlafaxine versus imipramine in painful polyneuropathy: a randomized, controlled trial. Neurology 2003; 60(8): 1284-9.
- Preskorm SH: Comparison of the tolerability of bupropion, fluoxetine, imipramine, nefazodone, paroxetine, sertraline, and venlafaxine. The Journal of Clinical Psychiatry 1995.
- Ghanizadeh A, D Freeman R and Berk M: Efficacy and adverse effects of venlafaxine in children and adolescents with ADHD: a systematic review of non-controlled and controlled trials. Reviews on Recent Clinical Trials 2013; 8(1): 2-8.
- Silvestro S: Hydroxyzine (Vistaril): dosage, uses, side effects. Drugs 2021.
- Bordeleau L, Pritchard KI, Loprinzi CL, Ennis M, Jugovic O and Warr D: Multicenter, randomized, cross-over clinical trial of venlafaxine versus gabapentin for the management of hot flashes in breast cancer survivors. Journal of Clinical Oncology 2010; 28(35): 5147-52.
- Dubey SK, Anand A and Saha RN: Stability indicating high performance thin layer chromatographic method for quantitation of venlafaxine in bulk and pharmaceutical dosage form. Drug Development & Therapeutics 2015; 6(1).
- Montejo AL, Becker J, Bueno G, Fernández-Ovejero R, Gallego MT and González N: Frequency of sexual dysfunction in patients treated with desvenlafaxine: a prospective naturalistic study. Journal of Clinical Medicine 2019; 8(5): 719.
- Johnson ED and Carroll DG: Venlafaxine and desvenlafaxine in the management of menopausal hot flashes. Pharmacy Practice 2011; 9(3): 117.
- Low Y, Setia S and Lima G: Drug d interactions involving antidepressants: focus on desvenlafaxine. Neuropsychiatric Disease and Treatment 2018; 14: 567.
- Kornstein SG, McIntyre RS, Thase ME and Boucher M: Desvenlafaxine for the treatment of major depressive disorder. Expert Opinion on Pharmacotherapy 2014; 15(10): 1449-63.
- Scott LJ: Desvenlafaxine extended-release tablets in major depressive disorder and menopause-associated hot flushes: a profile of its use. Drugs & Therapy Perspectives 2017; 33(10): 449-54.
- Pérez-Villegas EM, Negrete-Díaz JV, Porras-García M, Ruiz R, Carrión AM and Rodríguez-Moreno A: Mutation of the HERC 1 ubiquitin ligase impairs associative learning in the lateral amygdala. Molecular Neurobiology 2018; 55(2): 1157-68.
- Vollala VR, Upadhya S and Nayak S: Enhancement of basolateral amygdaloid neuronal dendritic arborization following Bacopa monniera extract treatment in adult rats. Clinics 2011; 66(4): 663-71.
- LeDoux J: The emotional brain, fear, and the amygdala. Cellular and Molecular Neurobiology 2003; 23(4): 727-38.
- Norman TR and Olver JS: Desvenlafaxine in the treatment of major depression: an updated overview. Expert opinion on Pharmacotherapy 2021; 22(9): 1087-97.
- Kotorii T, Kotorii T, Uchimura N, Hashizume Y, Shirakawa S and Satomura T: Questionnaire relating to sleep paralysis. Psychiatry and Clinical Neurosciences 2001; 55(3): 265-6.
- Braestrup C and Sanchez C: Escitalopram: a unique mechanism of action. International Journal of Psychiatry in Clinical Practice 2004; 8(1): 11-3.
- Zhong H, Haddjeri N and Sánchez C: Escitalopram, an antidepressant with an allosteric effect at the serotonin transporter a review of current understanding of its mechanism of action. Psychopharma 2012; 219(1): 1-13.
- Fabre V and Hamon M: Mechanisms of action of antidepressants: new data from escitalopram. L'encephale. 2003; 29(3): 259-65.
- Molholm S, Sehatpour P, Mehta AD, Shpaner M, Gomez-Ramirez M and Ortigue S: Audio-visual multisensory integration in superior parietal lobule revealed by human intracranial recordings. Journal of Neurophysiology 2006; 96(2): 721-9.
- Rao N: The clinical pharmacokinetics of escitalopram. Clinical Pharmacokinetics 2007; 46(4): 281-90.
- Gutierrez MM, Rosenberg J and Abramowitz W: An evaluation of the potential for pharmacokinetic interaction between escitalopram and the cytochrome P450 3A4 inhibitor ritonavir. Clinical Therapeutics 2003; 25(4): 1200-10.
- Denis D, French CC, Rowe R, Zavos HM, Nolan PM and Parsons MJ: A twin and molecular genetics study of sleep paralysis and associated factors. Journal of Sleep Research 2015; 24(4): 438-46.
- Jacobsen JP, Plenge P, Sachs BD, Pehrson AL, Cajina M and Du Y: The interaction of escitalopram and R-citalopram at the human serotonin transporter investigated in the mouse. Psychopharmacology 2014; 231(23): 4527-40.
- Sanchez C, Reines EH and Montgomery SA: A comparative review of escitalopram, paroxetine and sertraline: are they all alike. International Clinical Psychopharmacology 2014; 29(4): 185.
- Waugh J and Goa KL: Escitalopram. CNS Drugs 2003; 17(5): 343-62.
- Landy K and Estevez R: Escitalopram 2020.
- Hensley PL, Slonimski CK, Uhlenhuth E and Clayton PJ: Escitalopram: an open-label study of bereavement-related depression and grief. Journal of Affective Disorders 2009; 113(1-2):142-9.
- Otto MW, Simon NM, Powers M, Hinton D, Zalta AK and Pollack MH: Rates of isolated sleep paralysis in outpatients with anxiety disorders. Journal of Anxiety Disorders 2006; 20(5): 687-93.
- Becker AM, Holze F, Grandinetti T, Klaiber A, Toedtli VE and Kolaczynska KE: Acute effects of psilocybin after escitalopram or placebo pretreatment in a randomized, double‐blind, placebo‐controlled, crossover study in healthy subjects. Clinical Pharmacology & Therapeutics 2021.
- AlJhani SA: Escitalopram-induced epistaxis: A case report. Journal of Taibah University Medical Sciences 2021; 16(6): 938-42.
- Francescangeli J, Karamchandani K, Powell M and Bonavia A: The serotonin syndrome: from molecular mechanisms to clinical practice. International Journal of Molecular Sciences 2019; 20(9): 2288.
- Gordon S: Medical condition, demon or undead corpse? Sleep paralysis and the nightmare in medieval Europe. Social History of Medicine 2015; 28(3): 425-44.
- Phelps EA and LeDoux JE: Contributions of the amygdala to emotion processing: from animal models to human behavior. Neuron 2005; 48(2): 175-87.
- Lavretsky H, Alstein LL, Olmstead RE, Ercoli LM, Riparetti-Brown M and Cyr NS: Complementary use of tai chi chih augments escitalopram treatment of geriatric depression: a randomized controlled trial. The American Journal of Geriatric Psychiatry 2011; 19(10): 839-50.
- Klieger‐Grossmann C, Weitzner B, Panchaud A, Pistelli A, Einarson T and Koren G: Pregnancy outcomes following use of escitalopram: a prospective comparative cohort study. The Journal of Clinical Pharmacology 2012; 52(5): 766-70.
- Ness RC: The old hag phenomenon as sleep paralysis: A biocultural interpretation. Culture Medicine and Psychiatry 1978; 2(1): 15-39.
- Ghosh S, Ganguly D, Majumder S and Chowdhury A: A Review on Pharmacological and Therapeutical Insight of Satranidazole for Colon Targeting in the treatment of Colonic Diseases. Journal of Drug Delivery and Therapeutics 2022; 12(1): 186-91.
- D’Agostino A and Limosani I: Hypnagogic hallucinations and sleep paralysis. Springer 2016; 81-93.
- Rosenberg R, Hirshkowitz M, Rapoport DM and Kryger M: The role of home sleep testing for evaluation of patients with excessive daytime sleepiness: focus on obstructive sleep apnea and narcolepsy. Sleep Medicine 2019; 56: 80-9.
- De Jong JT: Cultural variation in the clinical presentation of sleep paralysis. Transcultural Psychiatry 2005; 42(1): 78-92.
- Jalal B: The neuropharmacology of sleep paralysis hallucinations: serotonin 2A activation and a novel therapeutic drug. Psychopharma 2018; 235(11): 3083-91.
- Denis D: Relationships between sleep paralysis and sleep quality: current insights. Nature and Science of Sleep 2018; 10: 355.
How to cite this article:
Ganguly D, Ghosh S, Banerjee M, Alam A and Ghosh R: A brief review on sleep paralysis: management and treatment. Int J Pharm Sci & Res 2023; 14(2): 661-73. doi: 10.13040/IJPSR.0975-8232.14(2).661-73.
All © 2023 are reserved by International Journal of Pharmaceutical Sciences and Research. This Journal licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License.
Debgopal Ganguly, Soumyadip Ghosh *, Madhumita Banerjee, Abid Alam and Rajesh Ghosh
School of Pharmacy, Calcutta Institute of Pharmaceutical Technology and AHS, Uluberia, Howrah, Bengal, India.
29 May 2022
31 July 2022
03 August 2022
01 February 2023