A BRIEF REVIEW ON SLEEP PARALYSIS: MANAGEMENT AND TREATMENT

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}.

Herbal Drugs:

Yokukansan:

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-HT_1A receptor agonist. Therefore since 5-HT_1A agonist has an antidepressant-suchlike effect, the antidepressant-like effect induced by yokukansan may be due to stimulation of the 5-HT_1A 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-HT_1A 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.

Duloxetine:

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 1^{st 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.

Venlafaxine:

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.

Desvenlafaxine:

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.

Escitalopram

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.

Threat Analysis:

• 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.

Funding: Nil

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.

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     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.

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