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What are the consequences of chronic lack of sleep? For example, insomniacs are known to sleep less than normal sleeping individuals.
I am wondering if there are any long term cognitive impairments from reducing sleep time to, say 4h instead of the normally recommended 8 hours in the long run, say for a year or so?
Wikipedia has some good information on this issue. Search for:
Effects of sleep deprivation on cognitive performance
In summary, 'yes', sleep deprivation can have a multitude of negative consequences on your cognitive abilities, like weakening your ability to handle complex cognitive tasks.
Factors the influence long-term effects of cocaine
Before getting to the long-term effects, it is important to highlight the fact that the effects a person experiences are often subject to individual variation. Two people could be using cocaine for the same amount of time, yet one may experience different effects than the other. Factors that account for differences include: exact duration of usage, frequency of usage, the format of cocaine, dosage, and other individual factors.
1. Time Span
The duration over which you’ve used cocaine may play a role in influencing the number and severity of long-term effects that you experience. If you’ve been using cocaine over an extremely long-term such as a decade, you’re more likely to experience unwanted effects than someone who has been using the drug for just a few years. That said, the frequency, format, and dosage also are important to consider.
2. Frequency of usage
How often have you used cocaine? Those that use the drug on a daily basis for a long-term are likely to end up with more severe long-term effects than someone who used the drug infrequently. Obviously the greater the frequency that you use the drug, the more likely you are going to end up with severe and prolonged long-term adverse effects.
Someone who uses the drug once a month isn’t likely going to suffer the same degree of impairment as someone who uses the drug four times a month. The more staggered the frequency, the less likely you will be to experience long-term effects.
3. Format + Administration
The type of cocaine that a person tends to use can play a role in the long-term effects that they experience. Snorting cocaine hydrochloride will not be as potent or addictive over the long-term as smoking freebase forms or “crack.” Those who use more potent formats of cocaine tend to end up with the most severe long-term problems.
- Cocaine hydrochloride: This is a white, powdery cocaine that is often insufflated (i.e. snorted) through the nose, but can be injected. This type of cocaine cannot be snorted simply because smoking will destroy its effect.
- Freebase cocaine: This is a type of cocaine that has been chemically altered. It is most commonly smoked and tends to make the user fee an instant “high.”
- Crack cocaine: This is a specific subtype of freebase cocaine that is in the format of “rocks” or “crystals.” Preferred method of administration is generally via smoking. This format involves the blending of baking soda and water or ammonia and water (or both). This removes the hydrochloride from the molecule, creating a more immediate “high.”
Smoking tends to reach the brain more quickly than snorting. When a person snorts cocaine, it needs to travel from the blood vessels in the nose to the heart, then needs to get pumped up to the lungs for oxygenation. Next the oxygenated blood makes its way back to the heart, and the heart pumps it out to the brain resulting in the “high.”
When the cocaine is smoked, it travels a direct path from the lungs to the heart and then brain, leading to a seemingly immediate high. People like immediate gratification and/or elevation in dopamine because it gives them a rapid pleasure response. Hence the reason that smoking various forms of cocaine is more likely to lead to abuse, addiction, and ultimately more unwanted long-term effects.
4. Amount (Dosage)
The amount of cocaine that you administer each time you use it plays a role in determining how severe the long-term effects will be. If you frequently abuse the substance and are smoking large quantities, you’re going to likely end up with more long-term problems than someone who only snorted a small amount. Since people tend to develop quick tolerance to cocaine, it is possible to end up using high doses to achieve a “high.” Unfortunately the higher the dose used on a consistent basis, the greater the severity of long-term effects.
5. Individual variation
It is also important to acknowledge that individual variation plays a role in determining what a person will experience after long-term cocaine usage. Various factors that likely contribute to long-term effects include: age at which cocaine was used, diet, genetics, whether the person also used other drugs, stress level, exercise habits, sleep patterns, etc.
A younger person who abuses cocaine may find that it affects the development of their brain, particularly the prefrontal cortex over a long-term. Genetics may also dictate the degree to which you experience impairment after long-term cocaine usage. Some people may have favorable genetics and may not experience much of any health problems from their usage.
For Healthcare Professionals
Applies to baclofen: compounding powder, intrathecal solution, oral liquid, oral suspension, oral tablet
Common (1% to 10%): Cardiac output decreased, hypotension, hypertension, diminished cardiovascular functions, peripheral edema
Rare (less than 0.1%): Arrhythmias, palpitations, chest pain
Uncommon (0.1% to 1%): Alopecia, diaphoresis
Frequency not reported: Rash, sweating, contact dermatitis, skin ulcer [Ref]
Common (1% to 10%): Ovarian cysts are palpable in 4% of women treated with for up to one year [Ref]
Very common (10% or more): Nausea (especially at start of therapy) (up to 11%)
Common (1% to 10%): Dry mouth, GI disorder/disturbance, constipation, diarrhea, retching, vomiting, increased salivation
Uncommon (0.1% to 1%): Dysphagia, dehydration, ileus, decreased taste sensation
Rare (less than 0.1%): Colicky abdominal pain, anorexia
Frequency not reported: GI hemorrhage [Ref]
Very common (10% or more): Urinary retention (up to 12%)
Frequency not reported: Dysuria, abnormal ejaculation, oliguria, vaginitis [Ref]
Frequency not reported: Leukocytosis, petechial rash [Ref]
Rare (less than 0.1%): Disorders of hepatic function (e.g., increased AST) [Ref]
Uncommon (0.1% to 1%): Septicemia [Ref]
Common (1% to 10%): Decreased appetite
Frequency not reported: Blood glucose increased [Ref]
Very common (10% or more): Hypotonia (up to 52%), lower extremity weakness (up to 15%), disturbances of gait and balance
Common (1% to 10%): Muscular weakness, myalgia, upper extremity weakness, back pain, muscular hypertonia [Ref]
Very common (10% or more): Somnolence (up to 28%), drowsiness (up to 18%), headache (up to 16%), seizures (especially on discontinuation of therapy) (up to 15%), sedation, dizziness (up to 12%)
Common (1% to 10%): Fatigue, ataxia, tremor, lightheadedness, lassitude, exhaustion, numbness/itching/tingling, slurred speech, lethargy, hypertonia, paresthesia
Rare (less than 0.1%): Dysarthria, dysgeusia, syncope, dyskinesia, coma, potentially life-threatening withdrawal symptoms (as a result of sudden interruption of drug delivery) [Ref]
Common (1% to 10%): Tinnitus, pain, asthenia
Uncommon (0.1% to 1%): Accidental injury, weight loss
Very rare (less than 0.01%): Hypothermia
Frequency not reported: Drug withdrawal syndrome
Uncommon (0.1% to 1%): Subdural hemorrhage, accidental injury, weight loss [Ref]
Common (1% to 10%): Nystagmus, visual impairment, accommodation disorder, blurred vision, double vision, amblyopia [Ref]
Common (1% to 10%): Confusional state, hallucination, depression, insomnia, euphoric mood, nightmare, personality changes
Uncommon (0.1% to 1%): Memory loss/impairment, suicidal ideation, attempted suicide
Rare (less than 0.1%): Excitement [Ref]
Very rare (less than 0.01%): Kidney calculus [Ref]
Common (1% to 10%): Respiratory depression, hypoventilation, dyspnea, bradypnea, feeling of pressure in the chest [Ref]
1. Cerner Multum, Inc. "UK Summary of Product Characteristics." O 0
2. "Product Information. Lioresal (baclofen)." Medtronic Inc, Minneapolis, MN.
3. Pharmaceutical Society of Australia "APPGuide online. Australian prescription products guide online. Available from: URL: http://www.appco.com.au/appguide/default.asp." ():
4. "Product Information. Lioresal Intrathecal (baclofen)." Medtronic Inc, Minneapolis, MN.
Anesthesia causes Personality Changesand even Dementia
Some people tell of relatives who were "never the same since the last operation". Yet other people tell of personal experiences of reduced ability to concentrate, reduced attention span, and of memory problems after undergoing an operation. These changes are sometimes severe enough to alter the personality of the affected person, or to interfere with their ability to perform normal activities. These changes may even be so severe that some elderly people actually become demented after undergoing an operation. Such postoperative alterations in mental function have been described, discussed, and studied since 1955 (see discussion in Hole 1982). Unfortunately, many of the complaints suffered by those reporting mental changes after undergoing an operation under anesthesia are frustratingly difficult to measure objectively (Fassolt 1986).
All these changes in mental function occurring after an operation actually affect the process of cognition, which is why they are bundled under the term POCD (PostOperative Cognitive Disorder). Cognition is defined as the mental process of knowing, including aspects such as awareness, perception, reasoning, and judgment. Typical complaints of those people reporting POCD are:
- Easily tired.
- Inability to concentrate. For example, they cannot concentrate sufficiently to read a book or newspaper.
- Memory dysfunction. For example, they have a reduced ability to remember things recently said or done.
- Reduced ability to perform arithmetic. For example, they make mistakes with normal money transactions while shopping.
An enormous amount of effort has been invested in studying this problem. The final view of this research is that POCD is a real problem affecting a significant proportion of people after undergoing an operation. Several studies excluding persons with initial stages of dementia, alcoholism, and those who underwent heart operations, reveal the following approximate figures for percentages of people experiencing POCD (Hanning 2005, Monk 2008).
1 week after
3 months after
up to 36.6% up to 5.7% 40-59 years
4.8-30.4% 5.1-7.8% 60+ years
4.2-41.4% 6.1-12.7% 60+ years
These are fascinating statistics. They mean that undergoing an operation can affect the mental function in quite significant numbers of people, revealing POCD to be an unrecognized but significant form of postoperative morbidity.
The real world and selective blindness
Nearly all physicians, together with nearly all non-medical people, as well as the popular press, attribute these changes in mental function to the effects of anesthesia. Many of these people even believe that anesthetic drugs remain in the body for many months exerting a deleterious effect upon mental function. This is the real world of people who themselves have experienced POCD, or who have relatives who manifested POCD.
Most people believe anesthesia is the cause of POCD, yet seem to forget that administration of anesthesia is never done without a purpose. This is a curious form of socio-culturally induced selective blindness. No one undergoes anesthesia without undergoing an operation. Anesthesia is always administered to make surgical procedures, or an operation, possible. So POCD is always a consequence of the combined effect of anesthesia plus surgery upon mental function. In fact the effects of surgery upon the functioning of the body can be quite profound. For example, major surgery has an effect upon body function comparable that due to being hit by a truck, only the wounds are tidier. Recovery from such major injury also has a long-lasting effect upon mental and body function. There are also several other factors determining whether a person develops POCD. In fact, studies reveal reasonably consistent information about who is most likely to develop changed mental function after anesthesia and operation. These are listed below.
- POCD is just as likely to occur after operations under loco-regional anesthesia as under general anesthesia (Hanning 2005, Neubauer 2005).
- More likely after major operations than minor operations (Hanning 2005, Neubauer 2005, Monk 2008).
- More likely after heart operations than other types of surgery ( van Dijk 2002).
- More likely in aged than in younger patients (Neubauer 2005, Monk 2008).
- More likely in older patients with high alcohol intake / abuse (Hudetz 2007).
- People with higher preoperative ASA-scores, (see page Is General Anesthesia Dangerous?), are more likely to develop POCD (Monk 2008).
- People with lower educational level are more likely to develop POCD than those with a higher educational level (Newman 2007, Monk 2008).
- People with prior history of a stroke, even though there is complete functional recovery, are more likely to develop POCD (Monk 2008).
- More likely in the elderly with pre-existing declining mental functions, termed MCI (Mild Cognitive Impairment) (Silverstein 2007). MCI is a transitional zone between normal mental function and evident Alzheimer's disease or other forms of dementia. It is insidious, and seldom recognized, except in retrospect after affected persons are evidently demented.
- Delirium and severe worsening of mental function is very likely in those with clinically evident Alzheimer's disease or other forms of dementia, as well as those with a history of delirium after previous operations (Meagher 2001).
Causes of POCD
The great variety of factors predisposing to POCD, or altered mental function after anesthesia and surgery, means that there is not one single cause or mechanism inducing this unfortunate condition. Accordingly, POCD is not explained by the simple one-liner: "Anesthetic drugs linger for a long time in the body and cause POCD." In reality, what does happen is that the effects of anesthesia and surgery on the body interact with the body through a variety of different mechanisms within the body to induce a final chain of events expressed as the cognitive dysfunction manifested by those with POCD. So what are some of the possible causes of altered mental functioning after anesthesia and surgery?
- Residual effects of trace concentrations of anesthetic, sedative, and painkilling drugs.
- Hyperventilation induced prefrontal dysfunction. (This will be discussed on another page of this website).
- Metabolic effects of surgery.
- Pre-existing abnormal mental function.
- Post traumatic stress disorder (PTSD).
So let us examine each of these causes, or predisposing factors
Residual effects of anesthesia, and painkillers
Many different types of drugs are used for medicinal purposes. To be effective the concentration of any drug must be above a certain level, otherwise that drug will not exert an effect. The body eliminates drugs by metabolism to inactive or other active forms, as well as excreting unchanged as well as metabolized drug in feces, or in urine, and sometimes even in exhaled air. The fact that a drug no longer exerts an effect upon the body does not mean that drug has been eliminated from the body - it simply means that the concentration of that drug within the body is too low to exert the effect for which that drug is used. Residual low concentrations of any drug may still exert effects upon the body as well as mental processes.
Drugs used to provide general anesthesia are no different. It takes several days before all anesthetic drugs administered to make an operation possible are eliminated from the body. These trace concentrations may exert an effect upon mental processes such as alertness, concentration, and memory, for several hours or days upon a person who has undergone an operation under general anesthesia. This is also one of the reasons why anesthesiologists always forbid people to drive an automobile or any other machinery, or to perform responsible intellectually demanding work for 24 hours after an operation performed under general anesthesia.
Anesthesia causes no pain, but operations are painful. Accordingly, people continue to use painkilling drugs after an operation to relieve the pain caused by the operation. The use of painkilling drugs may continue for days to weeks after an operation. Many drugs used to relieve pain also affect mental processes such as alertness, concentration, and memory. Opiates (morphine-like drugs) are good examples of drugs exerting just such effects upon mental processes.
Residual concentrations of general anesthetic drugs as well as the effects of painkillers explain many of the features attributed to POCD occurring during the first few days after surgery.
Metabolic effects of surgery
A surgical procedure is a form of injury, and the larger the injury, the larger and longer lasting the effects of operation upon the body. I discussed this earlier in this piece, comparing the metabolic effects of major surgery to being hit by a truck, only with tidier wounds. Everyone understands that recovery from such an accident with a truck will take a long time. Major surgery is the same. It also causes major injury to the body, even though the intention is to cure or manage a disease. Major metabolic changes lasting weeks and months occur in the body during recovery from major surgery (Hill 1993).
All these changes in body metabolism explain why people recovering from major surgery are easily tired, cannot concentrate, have memory deficits, and are not as alert as a healthy person for up to several months after undergoing major surgery (Rasmussen 1999).
Pre-existing abnormal mental function
POCD, or any other form of abnormal mental function developing after surgery is more likely in the aged than the young (Neubauer 2005, Monk 2008), in those with a high alcohol intake (Hudetz 2007), in those with lower IQ (Newman 2007), in those with prior history of a stroke (Monk 2008), those with pre-existing declining mental functions MCI (Mild Cognitive Impairment) (Silverstein 2007), as well as in those with clinically evident Alzheimer's disease or other forms of dementia (Meagher 2001). These facts mean it is likely these groups of patients have a diminished neuronal reserve, (also termed "cognitive reserve"). So when this cognitive reserve malfunctions due to the effects of drugs and the metabolic effects of surgery, they develop very evident subjective and externally evident signs of altered mental function such as: delirium, evident dementia, reduced alertness, inability to concentrate, and poor memory function.
Posttraumatic stress disorder (PTSD)
PTSD is a disorder that sometimes develops after undergoing one or more traumatic events that threatened or caused physical harm to themselves or loved ones. Usually PTSD develops after undergoing or witnessing violence, disasters, and accidents. The following manifestations and disabilities are typical of PTSD (Marshall 2001, PTSD-criteria).
- Impaired ability to work.
- Somatic complaints.
- Inability to concentrate, memory lapses.
- Lower quality of life.
- Suicidal thoughts and tendencies.
- Medical illness is more frequent.
- Negative body image.
- Impaired intimacy.
- Increased burden to spouse or partner.
- Social dysfunction.
Psychological studies of, patients having undergone operations reveals a reasonably high incidence of PTSD after having undergone anesthesia and operation. For example the percentage of patients developing PTSD after anesthesia and surgery for various conditions are: about 23% after breast cancer surgery (Shelby 2008), about 25% after peritonitis secondary to abdominal operations (Levenson 2007), 20.7% after hospitalization for civilian injuries (Zatzick 2008), 56.3% after experiencing awareness during an operation performed under general anesthesia (Osterman-2001). These are very high percentages. Anesthesia and surgery may actually cause more dysfunction than most clinicians seem to think. The development of PTSD after anesthesia and surgery is a real possibility. Accordingly, PTSD should always be considered in the differential diagnosis when a patient, or their relatives, tell of altered mental function after anesthesia and surgery.
Management of POCD or other mental changes after surgery
People reporting changed mental function after undergoing an operation should be taken seriously. The discussion above reveals this to be a real and serious problem, and one which potentially has an enormous impact upon the personal functioning of the individuals concerned, as well as a significant impact upon their surroundings and the societies in which they live. Management should be serious and efficient. Why efficient? That sounds cold and unpleasant. Actually, efficiency is of utmost importance. Delay and incorrect management reduces the chance of successful management, as well as increasing the distress of the individuals concerned and their families. Rapid placement of people into correct treatment regimes improves the chances of successful management, and means the incurable are placed in appropriate support programs.
Here are some personal thoughts regarding general management of POCD and postoperative altered mental function according to when they occur, and how long they last.
- Up to 1 week postoperative: Consider the cause to be the residual effects of anesthetic drugs, the effects of painkillers, and the metabolic effects of surgery. Manage patients symptomatically.
- Longer than 1 week postoperative: Consider the metabolic consequences of major surgery, other comorbidity, and the effects of medication. If these do not explain the existence of the observed postoperative changes in mental function, consider referral for neurological and / or psychiatric advice. Manage clinical manifestations symptomatically, and according to local protocols.
- Longer than 1-3 months postoperative: Consider the metabolic consequences of major surgery, other comorbidity, and the effects of medication. After one month, most recovery from the metabolic effects of surgery should have occurred, and any medication for pain or sedation should have long been stopped. After this time period, one should also start thinking about whether the effects of anesthesia plus operation have revealed a person with pre-existing abnormal mental function due to the initial phases of some neurological disorder, or a dementing process. The most efficient and rapid method of diagnosis of these conditions are CT-scan and MRI-scan of the brain. These will reveal the presence of most neurological and dementing disorders. If this is evident on the scans, then these unfortunate people can be placed in the appropriate neurological management and support programs. This is a sad occasion for those affected, but there is often little that can be done for many of these people. However, it does mean that they are placed in appropriate care programs, and their families know what has happened. The other group of patients with prolonged changes in mental function are those who develop PTSD. People with PTSD will have normal scans, and should be referred for appropriate neuropsychiatric assessment and management.
This discussion is short, and only touches on this fascinating, but very troublesome problem. Nonetheless, it does provide a starting point for understanding some of the possible causes of postoperative changes in mental function, by revealing these changes to be products of complex interactions between the minds and bodies of individuals with the effects of anesthesia and surgery. Moreover, it provides a way of explaining the causes of this problem to patients and their relatives.
Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance
Roca J, Fuentes LJ, Marotta A, López-Ramón M-F, Castro C, Lupiáñez J, et al. The effects of sleep deprivation on the attentional functions and vigilance. Acta Psychol (Amst). 2012140(2):164–76.
Boivin DB, Czeisler CA, Dijk DJ, Duffy JF, Folkard S, Minors DS, et al. Complex interaction of the sleep-wake cycle and circadian phase modulates mood in healthy subjects. Arch Gen Psychiatry. 199754(2):145–52.
Surridge-David M, MacLean A, Coulter ME, Knowles JB. Mood change following an acute delay of sleep. Psychiatry Res. 198722(2):149–58.
Kawano H, Motoyama T, Yasue H, Hirai N, Waly HM, Kugiyama K, et al. Endothelial function fluctuates with diurnal variation in the frequency of ischemic episodes in patients with variant angina. J Am Coll Cardiol. 200240(2):266–70.
Gottlieb DJ, Redline S, Nieto FJ, Baldwin CM, Newman AB, Resnick HE, et al. Association of usual sleep duration with hypertension: the Sleep Heart Health Study. Sleep. 200629(8):1009–14.
Bonsignore MR, Smirne S, Marrone O, Insalaco G, Salvaggio A, Bonsignore G. Myocardial ischemia during sleep. Sleep Med Rev. 19993(3):241–55.
Spiegel K, Tasali E, Penev P, Van Cauter E. Brief communication: sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med. 2004141(11):846–50.
Taheri S, Lin L, Austin D, Young T, Mignot E. Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Med. 20041(3):e62.
Redwine L, Hauger RL, Gillin JC, Irwin M. Effects of sleep and sleep deprivation on interleukin-6, growth hormone, cortisol, and melatonin levels in humans. J Clin Endocrinol Metab. 200085(10):3597–603.
Heiser P, Dickhaus B, Schreiber W, Clement HW, Hasse C, Hennig J, et al. White blood cells and cortisol after sleep deprivation and recovery sleep in humans. Eur Arch Psychiatry Clin Neurosci. 2000250(1):16–23.
Dinges DF, Douglas SD, Hamarman S, Zaugg L, Kapoor S. Sleep deprivation and human immune function. Adv Neuroimmunol. 19955(2):97–110.
Zhao H, Yin J-Y, Yang W-S, Qin Q, Li T-T, Shi Y, et al. Sleep duration and cancer risk: a systematic review and meta-analysis of prospective studies. Asian Pac J Cancer Prev APJCP. 201314(12):7509–15.
Kubo T, Ozasa K, Mikami K, Wakai K, Fujino Y, Watanabe Y, et al. Prospective cohort study of the risk of prostate cancer among rotating-shift workers: findings from the Japan collaborative cohort study. Am J Epidemiol. 2006164(6):549–55.
Davis S, Mirick DK. Circadian disruption, shift work and the risk of cancer: a summary of the evidence and studies in Seattle. Cancer Causes Control CCC. 200617(4):539–45.
Schernhammer ES, Laden F, Speizer FE, Willett WC, Hunter DJ, Kawachi I, et al. Night-shift work and risk of colorectal cancer in the nurses’ health study. J Natl Cancer Inst. 200395(11):825–8.
Jennum P, Riha RL. Epidemiology of sleep apnoea/hypopnoea syndrome and sleep-disordered breathing. Eur Respir J. 200933(4):907–14.
Bixler EO, Vgontzas AN, Lin H-M, Calhoun SL, Vela-Bueno A, Kales A. Excessive daytime sleepiness in a general population sample: the role of sleep apnea, age, obesity, diabetes, and depression. J ClinEndocrinolMetab. 200590(8):4510–5.
Durán J, Esnaola S, Rubio R, Iztueta A. Obstructive sleep apnea-hypopnea and related clinical features in a population-based sample of subjects aged 30 to 70 yr. Am J RespirCrit Care Med. 2001163(3 Pt 1):685–9.
Seneviratne U, Puvanendran K. Excessive daytime sleepiness in obstructive sleep apnea: prevalence, severity, and predictors. Sleep Med. 20045(4):339–43.
Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013177(9):1006–14. This study highlights the rising prevalence of sleep disordered breathing in the generalpopulation.
United States Department of Health and Human Services.National Center for Health Statistics. National Hospital Discharge Survey, 2004: Version 1 [Internet]. 2006 May [cited 2015 Sep 4]. Available from: http://www.icpsr.umich.edu/NACDA/studies/04442/version/1
Spurr K, Morrison DL, Graven MA, Webber A, Gilbert RW. Analysis of hospital discharge data to characterize obstructive sleep apnea and its management in adult patients hospitalized in Canada: 2006 to 2007. Can RespirJ CanThorac Soc. 201017(5):213–8.
Nowbar S, Burkart KM, Gonzales R, Fedorowicz A, Gozansky WS, Gaudio JC, et al. Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome. Am J Med. 2004116(1):1–7.
Berg G, Delaive K, Manfreda J, Walld R, Kryger MH. The use of health-care resources in obesity-hypoventilation syndrome. Chest. 2001120(2):377–83.
Sanders MH, Newman AB, Haggerty CL, Redline S, Lebowitz M, Samet J, et al. Sleep and sleep-disordered breathing in adults with predominantly mild obstructive airway disease. Am J RespirCrit Care Med. 2003167(1):7–14.
Bednarek M, Plywaczewski R, Jonczak L, Zielinski J. There is no relationship between chronic obstructive pulmonary disease and obstructive sleep apnea syndrome: a population study. RespirInt Rev Thorac Dis. 200572(2):142–9.
López-Acevedo MN, Torres-Palacios A, Elena Ocasio-Tascón M, Campos-Santiago Z, Rodríguez-Cintrón W. Overlap syndrome: an indication for sleep studies? A pilot study. Sleep Breath Schlaf Atm. 200913(4):409–13.
Turcani P, Skrickova J, Pavlik T, Janousova E, Orban M. The prevalence of obstructive sleep apnea in patients hospitalized for COPD exacerbation. Czechoslov: Biomed Pap Med FacUnivPalacky Olomouc 2014.
Goring K, Collop N. Sleep disordered breathing in hospitalized patients. J Clin Sleep Med JCSM Off Publ Am Acad Sleep Med. 20084(2):105–10.
Ely EW, Shintani A, Truman B, Speroff T, Gordon SM, Harrell FE, et al. Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit. JAMA. 2004291(14):1753–62.
Elliott R, McKinley S, Cistulli P, Fien M. Characterisation of sleep in intensive care using 24-hour polysomnography: an observational study. Crit Care Lond Engl. 201317(2):R46. This study has objectively measured the sleep quality and quantity and the factors affecting it in the ICU setting.
Pisani MA, Kong SYJ, Kasl SV, Murphy TE, Araujo KLB, Van Ness PH. Days of delirium are associated with 1-year mortality in an older intensive care unit population. Am J RespirCrit Care Med. 2009180(11):1092–7.
Girard TD, Jackson JC, Pandharipande PP, Pun BT, Thompson JL, Shintani AK, et al. Delirium as a predictor of long-term cognitive impairment in survivors of critical illness. Crit Care Med. 201038(7):1513–20.
Thomason JWW, Shintani A, Peterson JF, Pun BT, Jackson JC, Ely EW. Intensive care unit delirium is an independent predictor of longer hospital stay: a prospective analysis of 261 non-ventilated patients. Crit Care Lond Engl. 20059(4):R375–81.
Bryant PA, Trinder J, Curtis N. Sick and tired: does sleep have a vital role in the immune system. Nat Rev Immunol. 20044(6):457–67.
Born J, Lange T, Hansen K, Mölle M, Fehm HL. Effects of sleep and circadian rhythm on human circulating immune cells. J Immunol Baltim Md. 1997158(9):4454–64.
Spiegel K, Sheridan JF, Van Cauter E. Effect of sleep deprivation on response to immunization. JAMA. 2002288(12):1471–2.
Kahn-Greene ET, Killgore DB, Kamimori GH, Balkin TJ, Killgore WDS. The effects of sleep deprivation on symptoms of psychopathology in healthy adults. Sleep Med. 20078(3):215–21.
Babkoff H, Sing HC, Thorne DR, Genser SG, Hegge FW. Perceptual distortions and hallucinations reported during the course of sleep deprivation. Percept Mot Skills. 198968(3 Pt 1):787–98.
Watson PL, Ceriana P, Fanfulla F. Delirium: is sleep important? Best Pract Res ClinAnaesthesiol. 201226(3):355–66. This article links sleep deprivation to delirium in the hospital which is a marker of poor outcome.
Chen HI, Tang YR. Sleep loss impairs inspiratory muscle endurance. Am Rev Respir Dis. 1989140(4):907–9.
White DP, Douglas NJ, Pickett CK, Zwillich CW, Weil JV. Sleep deprivation and the control of ventilation. Am Rev Respir Dis. 1983128(6):984–6.
Kaneko Y, Floras JS, Usui K, Plante J, Tkacova R, Kubo T, et al. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med. 2003348(13):1233–41.
Redfield MM, Jacobsen SJ, Burnett JC, Mahoney DW, Bailey KR, Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA. 2003289(2):194–202.
Arnulf I, Merino-Andreu M, Perrier A, Birolleau S, Similowski T, Derenne J-P. Obstructive sleep apnea and venous thromboembolism. JAMA. 2002287(20):2655–6.
Hilton BA. Quantity and quality of patients’ sleep and sleep-disturbing factors in a respiratory intensive care unit. J AdvNurs. 19761(6):453–68.
Aurell J, Elmqvist D. Sleep in the surgical intensive care unit: continuous polygraphic recording of sleep in nine patients receiving postoperative care. Br Med J (Clin Res Ed). 1985290(6474):1029–32.
Freedman NS, Gazendam J, Levan L, Pack AI, Schwab RJ. Abnormal sleep/wake cycles and the effect of environmental noise on sleep disruption in the intensive care unit. Am J RespirCrit Care Med. 2001163(2):451–7.
Cooper S, Oborne J, Newton S, Harrison V, Thompson Coon J, Lewis S, et al. Effect of two breathing exercises (Buteyko and pranayama) in asthma: a randomised controlled trial. Thorax. 200358(8):674–9.
Watson PL, Pandharipande P, Gehlbach BK, Thompson JL, Shintani AK, Dittus BS, et al. Atypical sleep in ventilated patients: empirical electroencephalography findings and the path toward revised ICU sleep scoring criteria. Crit Care Med. 201341(8):1958–67.
Scoring sleep in critically ill patients. Limitations in standard methodology and need for revised criteria. Crit Care Med. 200634(12):A83.
Gehlbach BK, Chapotot F, Leproult R, et al. Temporal disorganization of circadian rhythmicity and sleep-wake regulation in mechanically ventilated patients receiving continuous intravenous sedation. Sleep. 201235:1105–14.
Mundigler G, Delle-Karth G, Koreny M, et al. Impaired circadian rhythm of melatonin secretion in sedated critically ill patients with severe sepsis. Crit Care Med. 200230:536–40.
Hetzenecker A, Buchner S, Greimel T, Satzl A, Luchner A, Debl K, et al. Cardiac workload in patients with sleep-disordered breathing early after acute myocardial infarction. Chest. 2013143(5):1294–301.
Thurnheer R. Obstructive sleep apnea and cardiovascular disease—time to act! Swiss Med Wkly. 2007137(15–16):217–22.
Dyken ME, Somers VK, Yamada T, Ren ZY, Zimmerman MB. Investigating the relationship between stroke and obstructive sleep apnea. Stroke J Cereb Circ. 199627(3):401–7.
Schober A-K, Neurath MF, Harsch IA. Prevalence of sleep apnoea in diabetic patients. ClinRespir J. 20115(3):165–72.
Punjabi NM, Caffo BS, Goodwin JL, Gottlieb DJ, Newman AB, O’Connor GT, et al. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med. 20096(8):e1000132.
Young T, Finn L, Peppard PE, Szklo-Coxe M, Austin D, Nieto FJ, et al. Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin sleep cohort. Sleep. 200831(8):1071–8.
Marin JM, Carrizo SJ, Vicente E, Agusti AGN. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet Lond Engl. 2005365(9464):1046–53.
Shah N, Redline S, Yaggi HK, Wu R, Zhao CG, Ostfeld R, et al. Obstructive sleep apnea and acute myocardial infarction severity: ischemic preconditioning? Sleep Breath Schlaf Atm. 201317(2):819–26.
Floras JS. Sleep apnea and cardiovascular risk. J Cardiol. 201463(1):3–8. This article describes the cardiovascular risks associated with sleep disordered breathing.
Patel D, Mohanty P, Di Biase L, Shaheen M, Lewis WR, Quan K, et al. Safety and efficacy of pulmonary vein antral isolation in patients with obstructive sleep apnea: the impact of continuous positive airway pressure. CircArrhythmElectrophysiol. 20103(5):445–51.
Mehra R, Benjamin EJ, Shahar E, Gottlieb DJ, Nawabit R, Kirchner HL, et al. Association of nocturnal arrhythmias with sleep-disordered breathing: The Sleep Heart Health Study. Am J RespirCrit Care Med. 2006173(8):910–6.
Kanagala R, Murali NS, Friedman PA, Ammash NM, Gersh BJ, Ballman KV, et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003107(20):2589–94.
Kasai T, Bradley TD. Obstructive sleep apnea and heart failure: pathophysiologic and therapeutic implications. J Am CollCardiol. 201157(2):119–27.
Shepard JW, Pevernagie DA, Stanson AW, Daniels BK, Sheedy PF. Effects of changes in central venous pressure on upper airway size in patients with obstructive sleep apnea. Am J RespirCrit Care Med. 1996153(1):250–4.
Yumino D, Redolfi S, Ruttanaumpawan P, Su M-C, Smith S, Newton GE, et al. Nocturnal rostral fluid shift: a unifying concept for the pathogenesis of obstructive and central sleep apnea in men with heart failure. Circulation. 2010121(14):1598–605.
Kasai T, Arcand J, Allard JP, Mak S, Azevedo ER, Newton GE, et al. Relationship between sodium intake and sleep apnea in patients with heart failure. J Am CollCardiol. 201158(19):1970–4.
Yumino D, Bradley TD. Central sleep apnea and Cheyne-Stokes respiration. Proc Am Thorac Soc. 20085(2):226–36.
Kaye DM, Mansfield D, Aggarwal A, Naughton MT, Esler MD. Acute effects of continuous positive airway pressure on cardiac sympathetic tone in congestive heart failure. Circulation. 2001103(19):2336–8.
Tkacova R, Rankin F, Fitzgerald FS, Floras JS, Bradley TD. Effects of continuous positive airway pressure on obstructive sleep apnea and left ventricular afterload in patients with heart failure. Circulation. 199898(21):2269–75.
Naughton MT, Rahman MA, Hara K, Floras JS, Bradley TD. Effect of continuous positive airway pressure on intrathoracic and left ventricular transmural pressures in patients with congestive heart failure. Circulation. 199591(6):1725–31.
Khayat RN, Abraham WT, Patt B, Pu M, Jarjoura D. In-hospital treatment of obstructive sleep apnea during decompensation of heart failure. Chest. 2009136(4):991–7.
Staniforth AD, Kinnear WJ, Starling R, Hetmanski DJ, Cowley AJ. Effect of oxygen on sleep quality, cognitive function and sympathetic activity in patients with chronic heart failure and Cheyne–Stokes respiration. Eur Heart J. 199819(6):922–8.
Franklin KA, Eriksson P, Sahlin C, Lundgren R. Reversal of central sleep apnea with oxygen. Chest. 1997111(1):163–9.
Doherty LS, Kiely JL, Swan V, McNicholas WT. Long-term effects of nasal continuous positive airway pressure therapy on cardiovascular outcomes in sleep apnea syndrome. Chest. 2005127(6):2076–84.
Haentjens P, Van Meerhaeghe A, Moscariello A, De Weerdt S, Poppe K, Dupont A, et al. The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a meta-analysis of placebo-controlled randomized trials. Arch Intern Med. 2007167(8):757–64.
Alajmi M, Mulgrew AT, Fox J, Davidson W, Schulzer M, Mak E, et al. Impact of continuous positive airway pressure therapy on blood pressure in patients with obstructive sleep apnea hypopnea: a meta-analysis of randomized controlled trials. Lung. 2007185(2):67–72.
Wang H, Parker JD, Newton GE, Floras JS, Mak S, Chiu K-L, et al. Influence of obstructive sleep apnea on mortality in patients with heart failure. J Am CollCardiol. 200749(15):1625–31.
Malone S, Liu PP, Holloway R, Rutherford R, Xie A, Bradley TD. Obstructive sleep apnoea in patients with dilated cardiomyopathy: effects of continuous positive airway pressure. Lancet Lond Engl. 1991338(8781):1480–4.
Mansfield DR, Gollogly NC, Kaye DM, Richardson M, Bergin P, Naughton MT. Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure. Am J RespirCrit Care Med. 2004169(3):361–6.
Smith LA, Vennelle M, Gardner RS, McDonagh TA, Denvir MA, Douglas NJ, et al. Auto-titrating continuous positive airway pressure therapy in patients with chronic heart failure and obstructive sleep apnoea: a randomized placebo-controlled trial. Eur Heart J. 200728(10):1221–7.
Bradley TD, Logan AG, Kimoff RJ, Sériès F, Morrison D, Ferguson K, et al. Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med. 2005353(19):2025–33.
Philippe C, Stoïca-Herman M, Drouot X, Raffestin B, Escourrou P, Hittinger L, et al. Compliance with and effectiveness of adaptive servoventilation versus continuous positive airway pressure in the treatment of Cheyne–Stokes respiration in heart failure over a six month period. Heart Br Card Soc. 200692(3):337–42.
Pepperell JCT, Maskell NA, Jones DR, Langford-Wiley BA, Crosthwaite N, Stradling JR, et al. A randomized controlled trial of adaptive ventilation for Cheyne–Stokes breathing in heart failure. Am J RespirCrit Care Med. 2003168(9):1109–14.
Cowie MR, Woehrle H, Wegscheider K, et al. Adaptive servo-ventilation for central sleep apnea in systolic heart failure. N Engl J Med. 2015373(12):1095–105. This is the most recent randomised trial which has cast doubt about the usefulness of adaptive servo ventilation for the treatment of CSA specially in those with systolic dysfunction.
McArdle N, Riha RL, Vennelle M, Coleman EL, Dennis MS, Warlow CP, et al. Sleep-disordered breathing as a risk factor for cerebrovascular disease: a case–control study in patients with transient ischemic attacks. Stroke J Cereb Circ. 200334(12):2916–21.
Sahlin C, Sandberg O, Gustafson Y, Bucht G, Carlberg B, Stenlund H, et al. Obstructive sleep apnea is a risk factor for death in patients with stroke: a 10-year follow-up. Arch Intern Med. 2008168(3):297–301.
Harbison J, Gibson GJ, Birchall D, Zammit-Maempel I, Ford GA. White matter disease and sleep-disordered breathing after acute stroke. Neurology. 200361(7):959–63.
Martínez-García MA, Galiano-Blancart R, Román-Sánchez P, Soler-Cataluña J-J, Cabero-Salt L, Salcedo-Maiques E. Continuous positive airway pressure treatment in sleep apnea prevents new vascular events after ischemic stroke. Chest. 2005128(4):2123–9.
Fletcher EC, Donner CF, Midgren B, Zielinski J, Levi-Valensi P, Braghiroli A, et al. Survival in COPD patients with a daytime PaO2 greater than 60 mmHg with and without nocturnal oxyhemoglobin desaturation. Chest. 1992101(3):649–55.
Mokhlesi B, Hovda MD, Vekhter B, Arora VM, Chung F, Meltzer DO. Sleep-disordered breathing and postoperative outcomes after elective surgery: analysis of the nationwide inpatient sample. Chest. 2013144(3):903–14.
Kaw R, Chung F, Pasupuleti V, Mehta J, Gay PC, Hernandez AV. Meta-analysis of the association between obstructive sleep apnoea and postoperative outcome. Br J Anaesth. 2012109(6):897–906. This study highlights the importance of evaluation and treatment of SBD in patients undergoing emergency or elective surgery as there is increased risk of complications.
Memtsoudis S, Liu SS, Ma Y, Chiu YL, Walz JM, Gaber-Baylis LK, et al. Perioperative pulmonary outcomes in patients with sleep apnea after noncardiac surgery. AnesthAnalg. 2011112(1):113–21.
Gross JB, Bachenberg KL, Benumof JL, Caplan RA, Connis RT, Coté CJ, et al. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: a report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Anesthesiology. 2006104(5):1081–93. quiz 1117–8.
What to Expect After 72 Hours
If you go three days without sleep, you greatly decrease your ability to think. In particular, your executive functions, including paying attention, remembering details and multitasking, will be severely affected. With this level of sleep deprivation, you can expect great difficulty completing even simple tasks.
Furthermore, your emotions are affected at this level of sleep deprivation. You will be extremely irritable. You may also experience paranoia, anxiety, or a depressed mood. Furthermore, you will struggle to read other people's emotions. One study in particular shows that participants who went 30 hours without sleep struggled to differentiate between happy and angry facial expressions.
As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.
Took a look at the study
The diffence between the people that were in the non users and heavy users is massively different. 3x higher on EVERY risk factor stroke, obese, etc.. Odd this would get so much traction with the press.. Borderline irresponsible of Harvard to publish this on their blog. Nothing here even hints at causality
here is what the experts say. Also people have been taking bendryl for 70 years, over the counter for 30 years. If this was causing dementia the rates would be increasing..
Dr. Knopman said that it was “highly unlikely” that the drugs themselves were the direct cause of the dementia, adding that the ultimate underpinnings of the article have a strong biologic basis.
Anticholinergic drugs “affect the area of the brain that facilitates learning and memory, and that’s the basis of the cholinergic model of Alzheimer’s,” he said. “That pharmacologic profile probably has negligible impact on people under 60, but with people with incipient dementia, the drug probably exacerbates the symptoms.”
Dr. Knopman said the main limitation with a prospective study is an indication bias. He suggested that the use of these drugs might be because of incipient dementia, rather than the drugs themselves causing the dementia.
Trouble sleeping, especially past middle age?
Worth considering: your body makes as much melatonin as it needs but only starts to do it after the last blue light goes away in the evening — if you let it.
Blue light has a dark side – Harvard Health
You can find yellow “bug light” bulbs cheap, or amber “turtle safe” lights.
(The blue light ‘wakeful/attention’ switch is evolutionarily very, very old. Daytime sky light color — Florida protects baby turtles so they go toward the ocean instead of toward the freeway)
— or any automotive supplier has 12-volt “clearance” amber LED lights. Remember there’s a spike of blue in even “warm white” lights. You can see it.
That’s what drives the phosphor that emits the rest of the color.
May 1, 2012 – Light at night is bad for your health, and exposure to blue light emitted by electronics and energy-efficient lightbulbs may be especially so.
My mother has taken these drugs and she has made such a turnaround since being off of them that it amazes me…..
I’ve been taking diphenhydramine for three years, and have been noticing a definite decline in short-term memory and the ability to retrieve the word I need. Have been blaming it on the job being more stressful than it seems. Stopped taking it around Valentine’s Day when I first came across the info being discussed here. Have just in the past day or so noticed a little lifting of the fog, but I also take supplements specifically for brain, and meditate. Maybe has something to do with quicker recovery. Experience has shown me DHA has the most noticeable effect, at least at short-term. For brain I also take B Vites and ginkgo. So I don’t know that everyone would feel some recovery that quickly, or that I’ll recover completely. But I think I will, and will use my newly recovered mental powers to search out ways to enhance that recovery. So good luck all you’re on a computer here, won’t find a more convenient way to research what you need now.
May I just point out that this article, as presented, is meaningless.
54 percent increase FROM WHAT? Without knowing the relative distributions of people in control and non-control groups this tells us nothing.
Was the risk 1/100 increased to 1.5 in 100? Was it 25/100 increased to 37.5/100?
Learn how NOT to lie with statistics please…
Obviously, it was not 1/100 with an increase to 1.5/100. Far more than 1% of the population acquires dementia. You make a valid point though. I was thinking the same thing you were. If 17% of the population acquired dementia without taking the suspected drugs, and 26% of those who took the suspected drugs acquired dementia, it does lead to some suspicion though. Like you said, we need to see the exact numbers.
Hi, thanks for the informative research link. There is always the risk of any medication, and it is challenging to know which poses the greater risk-allergicic reaction, untreated depression, or insomnia.
I have read too that Melatonin is also not without risk as the hormonal effects for older folks causes problems, and that is best used as a short term reset for sleep disorders.
Gloves, face masks, good sleep hygiene, and increasing activities that improve our quality of life seem all the more necessary when faced with damage from the pharmacopeia approach to allergies, sleep disorders depression, and lack of physical conditioning. Just a thought.
Thanks for a great discussion
Recently I lost my COBRA coverage. It was very expensive but they kicked me out and the only insurance I could get is MediCal. Today I met my new primary care MD (newly minted Resident). I asked for a refill of oxazepam that I have taken for 15 years without any problem. The doctor did not want to fill it. He recommended melatonin, benadryl and Elavil. So he wanted to give me a combo of anitcholinergics. I told him I have tried each in the past with poor results. I also mentioned this research as a concern. His reply, “I have read the information”. End of discussion. He suggested I might need to find another doctor unless I want to take his Rx. Disappointing.
I believe I have an early s/s of dementia caused by the benadryl and I am scared to death at this point 2/24/15. I took 200mg Benadryl for allergies in Texas (lots, lots of allergies in TX) for about 15 years. The prescription was read, Benadryl 50mg po qid. My husband is a physician, and his friend who also is a physician whote the prescription for me after seeing an horrible allergy attack and the trip to the ER for anaphylactic episode. About 5 to 6 years later I started to noticed that I was forgeting names (but could see the face of the person in mind’s eye, just can’t bring the names up), often can’t find the things. I often don’t remember what I have done minutes before I start another project thus running the car in the garage for hours… it just wanted to warm up the car before take off but changed mind to do another project. I also left house while the eggs were boiling in the kitchen… when I came home after having a lunch with friends, the house was full of the smoke… I also not showing up at the dinner party which was for my honor. They said a week before and I agreed to be there.
My family has no history of dementia.
No one told me about long term use of the dementia effect from the Benadryl. I told my FPs & other specialists (when I see them for other reasons, but they do the medication inventory on new pt) they never questioned me taking such a high doeses of the Benadryl for all these years… now what should I do? I understand this is a permanent state. No way to cure it. Please help me.
What you are experiencing is not necessarily early signs of dementia. Talk to your husband more about this. I did similar things as you when I was in my twenties and thirties. I am not in my fifties and am not any worse. There can be many reasons for forgetting. Stress, fright, ADD, and medications to name a few, can all cause this to happen. I think 200 mg of benedryl is too much though. I have severe allergies myself. The allergist said I am one of his ten worst patients. I limit the benedryl to 25 mg a day though.
I’m a White Male age 77. I’ve been taking one Benadryl and 10 mg Melatonin for sleep for the last 27 years and haven’t noticed any dementia although I do read slower to fully comprehend what I read.
I have been taking Benedryl for years for insomnia. Occasionally I will take Ambien or Melatonin. I never take more than 1/2 tablet and probably average 2-3 Tylenol PM/Alieve PM a week. Any suggestions as to what to take instead? And, at 52 years, will there still be long term affects if I stop now?
Thank you for the informative article. I am worried about the medications my husband (age 81) is taking. Both over the counter (Advil PM, contains diphenylhydramine) and the prescription drugs you mentioned. He has complained about brain fog. Will double check all his medications for interactions and/or anticholinergic actions.
I have panic attacks and allergies and the best alternative to some drugs (xanax and 12/24hr. allergy pills that didn’t work). I have been taking Benedryl almost regularly for the past 5 yrs. I would take up to 4 doses a day during my allergy season and at least 1 or 2 doses every other day! My question is since I quit taking it about 2 wks ago…..will the effects be reversed or am I simply keeping the dimentia symptoms from coming on faster and harder or whatever. Will I get better and be back to me? Or am I screwed.
For Healthcare Professionals
Applies to nortriptyline: compounding powder, oral capsule, oral solution
Frequency not reported: Alteration in electroencephalogram (EEG) patterns, ataxia, dizziness, drowsiness, extrapyramidal symptoms, extremity paresthesia, headache, incoordination, mydriasis, numbness, peculiar taste, peripheral neuropathy, seizures, stroke, tingling, tremors [Ref]
Frequency not reported: Agitation, anxiety, confusional states with hallucinations, delusions, disorientation, exacerbation of psychosis, hypomania, increased/decreased libido, insomnia, nightmares, panic, restlessness, suicidal behaviors, suicidal ideation [Ref]
Frequency not reported: Abdominal cramps, black tongue, constipation, diarrhea, dry mouth, epigastric distress, gingivitis, nausea, paralytic ileus, parotid swelling, stomatitis, sublingual adenitis, tongue edema, vomiting [Ref]
Frequency not reported: Arrhythmias, edema, flushing, general edema, heart block, hypertension, hypotension, myocardial infarction, palpitation, tachycardia
Postmarketing reports: Brugada syndrome [Ref]
Frequency not reported: Breast enlargement, delayed micturition, dilation of the urinary tract, galactorrhea, impotence, nocturia, urinary frequency, urinary retention, testicular swelling [Ref]
Frequency not reported: Alopecia, face edema, itching, perspiration, petechia, photosensitization, skin rash, urticaria [Ref]
Frequency not reported: Drug fever, fatigue, malaise, tinnitus, weakness [Ref]
Frequency not reported: Altered liver function, hepatitis, jaundice (simulating obstructive), liver necrosis [Ref]
Frequency not reported: Anorexia, elevation/depression of blood sugar levels, weight gain/loss [Ref]
Frequency not reported: Blurred vision, disturbance of accommodation
Postmarketing reports: Angle-closure glaucoma [Ref]
Frequency not reported: Gynecomastia, syndrome of inappropriate antidiuretic hormone (SIADH) secretion [Ref]
Frequency not reported: Cross sensitivity (with other tricyclic drugs) [Ref]
Frequency not reported: Increased risk of bone fractures [Ref]
1. "Product Information. Pamelor (nortriptyline)." Sandoz Pharmaceuticals Corporation, East Hanover, NJ.
2. Cerner Multum, Inc. "Australian Product Information." O 0
3. Cerner Multum, Inc. "UK Summary of Product Characteristics." O 0
How Long Should You Sleep?
According to the Centers for Disease Control and Prevention (COD), it is recommended that adults (between 18 and 60 years) need a minimum of 7 hours of sleep.
Children, depending on the age need to get anywhere between 10 and 17 hours of sleep. It could be said that the younger you are, the more sleep your body requires.
Still, the results of the COD research and survey have shown that more than 23% of adults get less than 5 hours of sleep, and over 64% of people that are 65+ receive less than 7 hours of sleep.
It is also recommended that a person shouldn’t stay awake for more than 17 hours. Anything more than that starts to take its toll and ruins our health, sometimes slowly and sometimes quickly. Sleep deprivation, as well as sleeping too much, can have their short-and long-term effects on our health.
What is the Longest Time Spent Without Sleep?
Have you been deprived of sleep for an extensive period? Did you notice any changes in the ability to function optimally? If yes, you’re not alone. Sleep is one of the most important human activities for tissue repair, memory regeneration, and recharging of batteries.
A lack of sleep has been linked with side effects that can be detrimental to your long-term and short-term health.