INSOMNIA now elaborated by both cognitive and physiological models

INSOMNIAInsomniais measured as a symptom as well as a disorder due to which standard definitionis hard to explain. Recently ,there have been significant advancement  in organization, evaluation and treatment ofinsomnia to build more consensus on its definition and measurement.

(Summers, Crisostomo et al. 2006)Difficultyfalling, initiating or maintaining a sleep is termed as insomnia.Nonrestorative sleep that’s chronic or low quality sleep may be indicated asinsomnia.(Soldatos, Dikeos et al. 2000)Interruptedsleep characterized by difficulty initiating or staying a sleep is calledinsomnia.(Roth 2007)ETIOLOGY OF INSOMNIAInsomniais considered to be a disorder of hyper arousal that is experienced during the completeday.

This hyper arousal might display itself as a state of hyper vigilanceduring the day and difficulty in  initiating and keeping sleep at night.(Roth 2007)Thisarousal is now elaborated by both cognitive and physiological models ofinsomnia.Thecognitive model tells that fear, anxiety and contemplation about life stresses,disturbs sleep, producing acute episodes of insomnia, mainly in initiatingsleep and going back to sleep after an awakening.(Roth 2007)Followedby it, a person commences to experience sleep problems, worry and thoughtsabout life problems changes their direction and person starts worrying aboutsleep itself and about the daytime consequences of not getting enough sleep.

this negative feeling effect the intellectual activity of a person and it isincreased if sleep related problem is sensed or a sleep deficit is felt.(Roth 2007)Anothermodel of the evaluation of insomnia tells that physiological or neuro-physiologicalfactors are the main factors of hyper arousal. Physiological arousal has beenexamined through dimensions of the total body metabolic rate, heart ratevariability, neuro-endocrine measures, and functional Neuro-imaging.

Oxygenconsumption may be used to measure the whole body metabolic recentstudies patients who were suffering from insomnia were compared with peoplehaving healthy sleep cycle. It was observed that insomniac patients werehaving   metabolic rates (calculated at intervalsacross the 24-hour day) greater than the healthy controls. Heart ratevariability may provide a measure of arousal in that it is controlled by bothsympathetic and para-sympathetic nervous system activities.

It is found in  36-hour study that compared to healthy normalsleepers , average heart rates were increased and irregularity was decreased inall phases of sleep in insomnia patients.(Roth 2007)Theneuro-endocrine system may also plays a role in arousal as confirmed by chronicactivation of the stress response system. It is  revealed in many studies that in people having insomnia, free cortisol urinaryexcretion was higher in  Urine  free cortisol levels is positively linked withtotal time in which person remain awake, wake time after sleep onset and stage1 sleep percentage are effected by  catecholamines level in urine . When plasma level of cortisol and adrenocorticotropichormones (ACTH) have been measured in insomnia patients and healthy normalsleepers. although the evidence is somewhat diverse, it is found that primaryinsomniacs have higher levels of these compounds in their plasma, and the mostsignificant difference is seen in the evening and the first half of the night .urinaryand plasma measures of cortisol and ACTH suggest that the HPA (Hypothalamus,Pituitary, and adrenal) axis is linked with the chronic disease of insomnia.

(Roth 2007)Atlast, measurement of cerebral glucose metabolism through positron emissiontomography (PET) has been used (through it whole brain metabolism is measuredindirectly) in patients suffering from insomnia. When insomnia patient werecompared to the healthy persons it was seen that insomniac patient showedhigher metabolism of glucose in cerebral region during waking and non rapid eyemovement sleep. In addition to it, the patients suffering from insomnia establishedminor reductions in relative metabolism from waking to non-REM sleep in thewake-promoting regions of the brain. These result propose interacting neuralnetworks involved in the failure to fall asleep, which consist of a cognitivesystem ,general arousal system, and an emotion-regulating system.(Roth 2007)REGULATION OF SLEEPIthas been revealed in research over the past 30 years that two different butinterconnected processes control human sleep wake cycle, the circadian rhythmcontrol the sleep cycle in a way that after 24 hours person sleeps at the same time,and the homeostatic or recovery process, where when we sleep less the drive tosleep more increases.

When person does not sleep about 16 hours then he feelsenough desire to sleep. If these two drives, circadian rhythm and homeostatic processare in synchrony, and then sleeping will be initiated. on the other hand, thereis another factor which can overcome these two process , and this is the stateof physiological arousal, when someone is worry or  does physical or mental work near bed timethen state of physiological arousal is affected.(Wilson and Nutt 2014)DIAGNOSIS OF INSOMNIAInorder to help in diagnosis of short-or long-term insomnia, it is very importantto take a sleep history, having a conversation with bed partner, if any(pointers such as snoring or strange movements may point out other sleepdisorders), and make the patient to keep a sleep diary. And if patient bedtimeand rising time is  recorded withqualitative score for time to fall sleep , amount of  awakening  during the sleep and feeling of beingrefreshed  after the sleep in the morningis crucial for evaluating ,scheming and monitoring treatment, and  the adequate timing and time-span of sleepopportunity.(Wilson and Nutt 2014)Thepatient complains sometimes that they have deprived sleep, but their history showsthe problem is uncommon behaviors at night like heavy snoring, nightmares orsleepwalking and pauses in breathing.  Patientmay have circadian rhythm problem if sleeps adequately but  not on proper time .

if someone has sleephabit  irregular  say, between 4 am  and noon and when try to go to sleep beforethat timing because of important obligation like work and lectures  , so cannotdo it earlier than this time so patient is suffering from insomnia . It isnamed as delayed sleep phase syndrome and demands a different approach oftreatment. It is very important to find whether the sleep is related withanother disorder.(Wilson and Nutt 2014)MANAGEMENT OF INSOMNIAThepurpose of treatment of insomnia is to lessen suffering and to get efficientdaytime job. The patient guided treatment should be preferred, should consider theparticular pattern of problem, like beginning of sleep or continuing asleep,and evidence based treatment should be preferred. (Wilson and Nutt 2014)Aftera diagnosis has been completed, if it possible the cause which is speeding upthe problem should be taken care   and ameliorated. For example, if pain or depressionis cause of insomnia, then it should be efficiently treated. (Wilson and Nutt 2014)Itis seen that fear of insomnia is common so patient should need clarificationand encouragement.

Patient has to know that no serious harm will come to themin short period. If they think , they are sleeping less than they need , andthey are also worry about  theirperformance due to it  or they think theyare not fresh  because of lack of sleep ,these things are itself a common cause of insomnia.(Wilson and Nutt 2014)Ifpatients sleep habits are good and   theyactivating cause to solve their problem, then hypnotic drug is suitable forshort term solution. The time to fall sleep is decreased, awakening is reducedand sleeps efficiency and continuity is increased due hypnotic drug.Ifthe patient has a chronic problem, then CBTI (cognitive behavioral therapy forinsomnia) is a psychological intervention designed for insomnia is first linetreatment for chronic problem. This is collective educational, behavioral and mentaltherapies that lead to improvement of insomnia.

(Wilson and Nutt 2014)Therehave been many researches of CBTI, this therapy cannot be blinded that is why itis difficult to design a randomized controlled trial, and getting in touch withprofessionals is hard to match with the comparator group. There have been numerousrandomized (but not blinded) studies of physiological in comparison topharmacological treatment, and a new research meta-analysis  it is found that when the treatment is goingon , it produces improvement similar to sleeping tablets and importantbeneficial long-term effects is produced by it. It also tells studies thatshort term pharmacotherapy does not produced long term  effects .

(Wilson and Nutt 2014)Onthe basis of wide available evidence, nine reviews, the State of the ScienceStatement and the National Institute of Health (NHS) found out that a CBT therapywhich is set of cognitive and behavioral therapy is as good as prescription medicationsare for short-term treatment of chronic insomnia. In addition, it is seen thatbeneficial effect of CBT lasts beyond the termination of active treatment incontrast to medication. (Wilson and Nutt 2014)Onthe other hand, in |UK psychological therapy for insomnia is an issue that iswhy this therapy may not be available, with a rare skilled therapist, and insomniais not a main concern for psychologist in the NHS. However, there are patientswho are not capable or reluctant to involve in these treatments, and as aresult drug treatments need to be considered.(Wilson and Nutt 2014)DRUG TREATMENTS FOR INSOMNIAThereare few aspects that is to be considered when drug is being prescribed are safety,efficacy and duration of action. Some Other factors should be considered likeeither  drug is effective on patient ornot, adverse drug reaction and history of patients  substance abuse and dependence .

(Wilson and Nutt 2014)Hypnoticdrugs enhance the effects of the gamma-aminobutyric acid (GABA)neurotransmitter at the GABA-A receptor. The state of excitability is regulatedby GABA in all brain areas and the predominantly of neuronal activity isgoverned by the equilibrium between excitatory inputs and inhibitory GABAergicactivity. If the balance is heavier in favor of GABA then muscle relaxation, sedation,amnesia, and ataxia shows up and nervousness and anxiety are reduced. The slightestreduction of GABAergic activity excites restlessness, arousal, anxiety, insomniaand exaggerated activity.

(Wilson and Nutt 2014)Theeffectiveness of GABA is enhanced by benzodiazepines and also by the ‘Z’ drug;zolpidem, zopiclone and Zaleplon, it act at a site on GABA-A receptor hence permitGABAergic circuits to produce a great inhibitory effect. They have differenttiming of action comparing the  pharmacokinetic properties of each and thosewith a duration of action lasting longer than the night are accountable to causemorning sedation, and that is why  patient should be warned   aboutdriving.(Wilson and Nutt 2014) Three Zs’- zopiclone, zolpidem and zaleplonare the safest GABA-acting hypnotics currently available. These drugs havehalf-lives sufficiently short to be free of remaining hangover in mostpatients. The half-life of Zaleplon is so short, that if drug is taken at nightstill it will be eliminated by the morning. (Wilson and Nutt 2014)Theseall drugs will help in dealing with insomnia, but zolpidem and zaleplon are notas good as other drug (hypnotics) for maintain the sleep continuity at night. (Wilson and Nutt 2014)Thesedrugs have less undesirable effect than older drugs, but it should be kept in mindthat the effects of hypnotic agents are increased by simultaneous alcohol.Also, they are safest because all of the possible unsafe effects such as ataxiahappen during bedtime, but few people get up late at night like old people so itmay be problem for them.

(Wilson and Nutt 2014)Benzodiazepinesand Z drugs interact and enhance sedation when interact with other sedative drugand sometime it is risk to take it in combination. This is factual in case of alcoholand have revealed a problem with clozapine.(Wilson and Nutt 2014)Pharmacodynamicinteractions of benzodiazepines rely on their metabolic pathway. the largestpart of the drug  is metabolized in theliver through the enzyme CYP450 3A4,so any drug which effects these enzyme ,if  co administered with  benzodiazepines will change its concentration .(Wilson and Nutt 2014)worthmentioning interactions are with calcium-channel-blockers, it increases itsplasma level and carbamazepine  decreasesits concentration.(Wilson and Nutt 2014)olderdrugs are not indicated  such as chloralhydrate , clomethiazole and barbiturates due to their very less therapeuticration  (the ratio of the maximumtolerated dose to minimum effective dose) and its  abuse potential.(Wilson and Nutt 2014)it is seen that short acting benzodiazepines arevery successful  , temazepam one of itis  misused in UK   , so while prescribing it should be noticedthat patient is not having history of alcohol or drug abuse .(Wilson and Nutt 2014)