Have you ever had dreams of being chased by a monster or a wild animal with sharp teeth and/or claws, falling endlessly through a void, drowning in deep waters, being murdered in cold blood by a bullet to the head or a knife to the chest, exploring a haunted house at night with booming thunder or eerie fog, being tormented by spirits or ghosts, being paralysed or immobilised by a mysterious force, or your teeth falling off your gums for no reason? If you had any of these common terrifying dreams, they would be sufficient to wake you up screaming and sweating. You check your body for any bullet holes, lacerations or missing limbs, check your surroundings to find out you're still in your bedroom at 4am, or become aware that you are outside of your bedroom without realising you walked there still in your PJs. When dawn rises, your friend or family member informs you that they heard you talking in the middle of the night as if you were communicating with a person known to you, but there weren't actually there. Now you feel lethargic, tired, and restless after that dreadful night.
What you just experienced is parasomnia.
But what is parasomnia?
(C) Parasomnia
This family of sleep disorders concerns abnormal movements, behaviours, emotions, perceptions and dreams occurring during sleep, whilst falling asleep, between sleep stages, or during arousal from sleep.
(a) NREM-related
NREM parasomnias are arousal disorders that occur during stage 3 (or 4 by the R&K standardization) of NREM sleep i.e. slow wave sleep (SWS). It is generally triggered by physiological activation as the sleeping patient transitions out of SWS and is stuck between a sleeping state and a waking state. Bassetti et al. (2000) stated these disorders associate with the activation of the autonomic nervous system, motor system, or central nervous system during sleep or sleep-wake transitions.
https://en.wikipedia.org/wiki/Confusional_arousals
Describe the epidemiology of confusional arousal
The prevalence of confusional arousals varies depending on the year and the sample population, which is roughly 4%.
-- 4.2% in UK, 1999
-- 6.9% in Norway sample population with a lifetime prevalence of 18.5%, 2010
In UK, Germany and Italy sample population, 2000
-- 6.1%: 15–24 years old (y.o.)
-- 3.3%: 25–34 y.o.
-- 2%: 35+ y.o.
Lettieri et al. (2014) estimated the current prevalence of confusional arousals in children (3–13 y.o.) is higher and approximately 17.3%. Studies in 2007 suggested the genetics of confusional arousal is passed on through generations of the same family.
Risk factors include:
- Shift work
- Hypnagogic hallucinations
- Excessive daytime sleepiness
- Insomnia and hypersomnia disorder
- Circadian rhythm sleep disorder
- Restless legs syndrome
- Obstructive sleep apnea syndrome (OSAS)
- Bipolar disorder
- Daily smoking
- 15 - 24 years old
Precipitating factors include:
- Sleep deprivation
- Hypnotics or tranquilisers before bedtime
- Sudden awakening from sleep due to loud noise such as a ringing telephone or an alarm clock
What are the signs and symptoms?
- Accompanied by mental confusion and disorientation, lack of response to environmental stimuli, and difficulty waking up.
- Vocalisation along with coherent speech
- Feeling upset, sometimes aggressive or agitated
- Children attempting to awaken or console an adult patient may worsen agitation.
- Provini et al. (2011) found confusional arousal may occur during or following an arousal of deep sleep and upon an attempt of waking up the sleeping person in the morning.
In children:
- They usually sit up in bed, cry, moan, whimper, and speak words such as “no” or “go away”.
- Feels distressed and miserable in spite of parental efforts. Paradoxically, parental efforts may aggravate the child's agitation.
- Onset of symptoms within 2 and 3 hours of sleep onset, which last from 10 to 30 minutes.
Neurological symptoms:
- Behavioural awakening with persistent slow-wave electroencephalographic activity during Non-rapid eye movement sleep (NREM).
- The sensorimotor network is activated while non sensorimotor areas are less active during sleep.
- Hypersynchronous delta activity in network involving the frontoparietal cortices (i.e. asleep), and higher frequency activities in sensorimotor, orbitofrontal, and temporal lateral cortices (i.e. awakening).
Behaviours:
- Sleep-related violence (self-injury or injury to bed partner)
- First documented case of homicide due to confusional arousal was Silesian woodcutter Bernard Schedmaizig during the medieval times.
- Sleep-related abnormal sexual behaviours
- No specific predisposition to aggression during episodes of confusional arousal
How is confusional arousal classified?
i. International Classification of Sleep Disorders (ICSD) 2nd edition
- Confusional arousals are classified in NREM parasomnias embedded in the non-epileptic paroxysmal motor events during sleep. Those NREM parasomnias include (1) Parasomnia, (2) Sleep-related movement disorders and (3) isolated symptoms, as well as sleep terror and sleepwalking.
- More or less complex movements without leaving bed with whimpering, sitting up in bed and articulation without walking or terror.
- Age onset is generally around 2 - 5 years
- Inconsolability = Unable to be comforted or alleviated
In the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V), confusional arousals aren't recognised as a disorder, which explains its lack of research by the scientific community.
How is confusional arousal diagnosed?
Evaluation should include:
-- Comprehensive medical history
-- Physical, neurological, and developmental examination
-- Detailed description of the nocturnal events, sleep-wake schedules, and daytime behaviour
- If life history is untypical, a video-polysomnography may be needed.
- Suspicious parents can use infrared camera to record the behaviour of their child during sleep.
- Important to distinguish from epileptic seizure on the basis of clinical and electroencephalographic features.
How can confusional arousal be managed?
Non-pharmacological treatments and daily behaviours guidelines, which include safety measures and/or medications if the patient is in danger from his or her behaviour:
- Ensure regular and adequate sleep routines in order to prevent the disruption of sleep-wake cycle.
- Implement safety measures for the patient and family such as clearing the bedroom from obstacles, securing the windows, or installing locks or alarms.
- Administer medications if the patient is in danger from his or her behaviour. e.g. Imipramine or low-dose Clonazepam
— Sexsomnia (Sleep Sex)
- Also known as sleep sex, this type of parasomnia is characterised by sexual acts during NREM sleep. Not to be confused with normal nocturnal sexual behaviours, which doesn't occur during NREM sleep.
- Often diagnosed in males beginning in adolescence.
- Patients with sexsomnia tend to forget the sexual behaviours demonstrated while asleep. Therefore, their sleeping partner notices and reports their sexual behaviour.
How is sexsomnia classified?
- Under DSM-5 criteria, sexsomnia is classified under NREM arousal parasomnia.
-- Arousal disorders
-- Sleep-wake transition disorders
-- Parasomnias associated with REM sleep
What are the symptoms of sexsomnia?
Symptoms of sexsomnia include, but are not limited to:
-- Masturbation
-- Fondling
-- Intercourse with climax
-- Sexual assault or rape
-- Moaning
-- Talking dirty while asleep
e.g. In 1986, a 34-year-old male was reported to masturbate each night until climax, even after reporting to have had sexual intercourse with his wife each night before falling asleep.
A 2013 article described the eyes of an individual with sexsomnia as being open, or "vacant" and "glassy", which resembles wakefulness and consciousness, despite the individual being unconscious and oblivious of their actions.
What are the causes of sexsomnia?
Causes include:
-- Stress factors
-- Sleep deprivation
-- Consumption of alcohol or other drugs
-- Pre-existing parasomnia behaviours
- Extended periods of sleep deprivation leads to neural malfunction, which directly influences an individual's behaviour.
- Sleep deprivation impacts neural regeneration, as well as generation of new synaptic connections, etc.
- Sexsomnia can be triggered by physical contact initiated by a partner or another individual sharing the same bed.
- Individuals with a history of parasomnia during their childhood are likely to experience sexsomnia in their adulthood.
Although sexsomnia affects individuals of all age groups and backgrounds, the risk increases for individuals who experience:
-- Coexisting sleep disorders
-- Sleep disruption secondary to obstructive sleep apnea
-- Sleep related epilepsy
-- Certain medications e.g. Sedative-hypnotic Zolpidem (Ambien)
-- Behaviours such as pelvic thrusting, sexual arousal, and orgasm attributed to sleep-related epilepsy disorder.
What are the effects of sexsomnia?
Common secondary effects of sexsomnia include:
-- Anger
-- Confusion
-- Denial
-- Frustration
-- Guilt
-- Revulsion
-- Shame
- The patient's significant other, in the case of sexual intercourse, or a bystander, in the case of masturbation behaviour, tend to be the first to identify abnormal behaviour.
- The partner may not consent to these abnormal sexual behaviours, which could be defined as sexual assault.
How is sexsomnia diagnosed?
Determining factors include but are not limited to:
-- Amnesia of episode
-- Disorientation when awoken
-- Family history of somnambulism, or sleepwalking
-- Lack of regard to conceal episode
-- Nature of event compared to the individual's baseline character
-- Prior episodes of somnambulism
-- Observed confusional or autonomic behaviour
-- Trigger factors the individual possesses
Clinical tests:
-- Electroencephalography (EEG)
- Measures electrical activity and waves produced by the brain to detect any abnormalities during slow-wave-sleep (SWS), which links to episodes of sexsomnia.
- Health professionals use EEG data to determine whether the sexual behaviours are occurring during NREM sleep or if the individual is fully conscious.
-- Polysomnography (PSG)
- A PSG is not guaranteed to form a diagnosis every time it is utilised, however it can help narrow down the type of diagnoses that are relevant. Although it is a useful diagnostic tool, it doesn't substitute forensic examination.
- For instance, a PSG study may detect sexsomnia, but it can't ascertain the exact cause of that sexsomnia, whether it is due to the individual's actions or already existing during the time of an alleged crime.
- If the PSG study fails to detect sexsomnia, it does not indicate the patient never experienced it, therefore it is crucial to gather as much information from a range of sources.
- Acquiring that information requires interviews with friends, family, and significant others, as well as collecting medical records concerning the individual's sleep previous patterns.
How is sexsomnia treated?
- Prescription Medications = Benzodiapezines such as clonazepem
- Anticonvulsant therapy
- Continuous positive airway pressure (CPAP)
- Positive lifestyle changes e.g. Open communication between couples to reduce the negative emotional feelings and stress and generate a support system, or decreasing stress and anxiety triggers.
2. Sleepwalking (Somnambulism)
- Known as somnambulism or noctambulism, sleepwalking is a behavioural phenomenon featuring both sleep and wakefulness.
- A meta-analysis discovered sleepwalking affects about 5% of children and 1.5% of adults, which is at least once in the previous 12 months. Moreover, the study estimates the lifetime prevalence of sleepwalking to be 4.6% - 10.3%.
- It is reported sleepwalkers have little or no recollection of sleepwalking, due to their low consciousness in which memory recall is minimal.
- It occurs during the slow wave stage (SWS) of sleep, where consciousness is at a minimal level. Sleepwalkers tend to perform activities that are usually conducted during a state of full consciousness.
Examples of such activities include:
-- Talking
-- Sitting up in bed
-- Walking to the bathroom
-- Eating food
-- Cleaning
-- Cooking
-- Driving a motor vehicle
-- Expressing violent gestures
-- Grasping at hallucinated objects
How was sleepwalking first discovered?
- Sleepwalking behaviour has been observed for centuries, but it wasn't until the 19th century that researchers investigated and diagnosed it. German chemist and parapsychologist Baron Karl Ludwig von Reichenbach (1788–1869) was the first person to extensively investigate sleepwalking, which lead to his theory of the Odic force.
- In 1907, Sigmund Freud posited sleepwalking associated with the fulfilment of sexual desires, and the urge the sleep in the same location as the individual slept during their childhood. Furthermore, he suggested the unconscious impulse is an instinctual demand that becomes a preconscious dream, which may be manifested as mobility during sleep.
- In the 1950s, the Society for Science & the Public initially hypothesised sleepwalking associated with dreaming, before altering their theory that sleepwalking occurs during the deepest sleep stage.
- Swanson (1999) found sleepwalking is a disorder of NREM arousal, but acting out a dream is a feature of REM Behaviour Disorder.
- As of 2002, it is not known whether the phenomenon of sleepwalking is unique to humans, or is demonstrated by other animals such as non-human primates.
What are the signs and symptoms of sleepwalking?
Symptoms include:
- Partial arousal during NREM sleep, typically during the first third of the night
- Dream content that may or may not be recalled when awake
- Dream-congruent motor behaviour, either simple or complex
- Impaired perception of the environment
- Impaired judgement, planning and problem-solving.
Signs include:
- Open eyes with a glassy-eyed stare or blank expression, and dilated pupils
- Disorientation, a consequence to awakening
- Confusion and perplexed expression
- Talking, which may be nonsensical to the observer
- Amnesia, ranging from no memory to vague recall or a narrative
Associated disorders:
- Restless leg syndrome (RLS)
- Sleep-disorder breathing (SDB)
- Sleep terror = Elevated level of brief EEG arousals
- Night terrors = Distress during sleep. e.g. Attempting to run or aggressively defend themselves
- High levels of dissociation = High scores on the hysteria portion of the "Crown-Crisp Experiential Index
- Schizophrenia
- Hysteria
- Anxiety neuroses
- Migraine headaches
- Tourette syndrome
Outcomes:
- Physical injuries such as cuts or bruises
- Bone fractures, or worse, death
- Embarrassed being witnessed nude in public
What are the causes of sleepwalking?
The cause(s) of sleepwalking is/are currently unknown, with several hypotheses suggested by researchers yet to be proven.
Theories concerning the causes include:
-- Delay in the maturity of the central nervous system (CNS)
-- Longer slow wave sleep (SWS) stage
-- Sleep deprivation
-- Fever
-- Excessive Fatigue
-- Genetic link between children and parents with a history of sleepwalking
- Kales et al. (1980) posited heritable factors may predispose an individual to sleepwalking, whereas environmental factors may influence the expression of sleepwalking behaviours.
- A fruit fly study by Kucherenko et al. (2016) discovered a connection between night sleep and brain development regulated by evolutionary conserved transcription factors such as AP-2. This indicates sleepwalking is an inherited autosomal dominant disorder with decreased penetrance.
- A genome-wide multipoint parametric linkage analysis by Dogu & Pressman (2011) identified a correlation between sleepwalking and chromosome 20q12-q13.12 between 55.6 and 61.4 cM.
- Barabas et al. (2008) suggested altered metabolism of serotonin in people with migraine and Tourette syndrome, whom are more likely to experience an episode of sleepwalking.
- Schenck & Mahowald (1995) discovered fluctuations in hormone levels increased the chance of sleepwalking episodes in women, particularly before the onset of menstruation.
- Stallman et al. (2018) identified a number of medications such as (1) benzodiazepine receptor agonists and other GABA modulators, (2) antidepressants and other serotonergic agents, (3) antipsychotics, and (4) β-blockers contributed to the risk of sleepwalking. e.g. Zolpidem and sodium oxybate
How is sleepwalking diagnosed?
- Polysomnography (PSG) is the only diagnostic assessment of a sleepwalking episode, but it is expensive and sleepwalking episodes are typically rare. Therefore, specialists employ other cheaper measures such as self-, parent-, or partner-report, as well as the International Classification of Diseases (ICD-10), International Classification of Sleep Disorders (ICSD-3) and the Diagnostic and Statistical Manual.
The Diagnostic and Statistical Manual defines 2 subcategories of sleepwalking, though it doesn't need to involve the following behavioural features:
-- Sleepwalking with sleep-related sexual behaviour (sexsomnia)
-- Sleepwalking with sleep-related eating
- Likely caused by stress-related factors, sleep medication (e.g. Ambien)
- Increased risk of weight gain due to frequent consumption of high carbohydrate food.
Sleepwalking should not be confused with alcohol- or drug-induced blackouts, which can lead to amnesia for events similar to sleepwalking. Wetherill & Fromme (2016) stated that people who experienced alcohol-induced blackouts (drug-related amnesia) can actively perceive and respond to their environment (e.g. having conversations or driving a vehicle), but the brain does not create memories for the events.
-- Assessment:
- Studies highlighted an issue with the use of PSG to assess sleepwalking is due to the infrequency of the sleepwalking episodes in the sleep lab. In addition, even if an episode coincidentally occurs, it isn't as complex as the patient's usual experiences at home.
- Hublin et al. (1997) stated the diagnosis can be performed by assessing the patient's sleep history, time-course and content of the sleep related behaviours.
- Moreover, Kavey et al. (1990) suggested the use of home recordings of the patient's sleepwalking experiences in the diagnostic process.
Diagnostic assessment should include:
- Age of onset
- Timing of episode during the sleep epriod
- Frequency and duration of episodes
- Description of the episode, including behaviour, emotions, and thoughts during and after the event
- Responsiveness of the patient to external stimuli during the episode
- Level of consciousness or awareness, when awakened from an episode
- Any memory of the episode afterwards
- Triggers or precipitating factors
- Sleep–wake pattern and sleep environment
- Daytime sleepiness
- Other co-existing sleep disorders
- Family history for NREM parasomnias and other sleep disorders
- Medical, psychiatric, and neurological history
- Medication and substance use history
How is sleepwalking treated?
- Helen Stallman (2017) pointed out no clinical trials of psychological or pharmacological interventions were effective against the prevention of sleepwalking episodes. Nevertheless, various treatments have been administered to sleepwalkers.
Psychological:
- Psychoanalysis
- Hypnosis
- Scheduled or anticipatory waking
- Assertion training
- Relaxation training
- Management of aggressive feelings
- Sleep hygiene
- Classical conditioning (including electric shock)
- Play therapy
Pharmacological:
- Tricyclic antidepressants (imipramine)
- Anticholinergics (biperiden)
- Antiepileptics (carbamazepine, valproate)
- Antipsychotics (quetiapine)
- Benzodiazepines (clonazepam, diazepam, flurazepam and triazolam)
- Melatonin
- Selective serotonin reuptake inhibitors (paroxetine)
- Barbiturate (sodium amytal) and herbs
Recommendations:
- Maintenance of the safety of the sleepwalker and others
- Administration of treatments for other sleep problems
- Reassurance of sleepwalking not leading to any problems
- Hypnosis and scheduled waking times if sleepwalking causes distress or a risk of harm from it
Safety planning:
- If sleepwalking episodes are hazardous, a door alarm may be installed for protection. The loud ringing alarm is intended to fully awaken the sleepwalker and interrupt the episode, or alert their neighbour to check on the sleepwalker's wellbeing.
- Sleepwalker's bedrooms should be on the ground floor of a home, apartment, dorm, hotel, etc.
- No easily accessible weapons (loaded guns, knives) in the bedroom or any room of the house for that matter. They are recommended to be locked away with keys separated from the sleepwalker.
- If parters are concerned sleepwalkers would become violent or disturb their sleep, they are advised to sleep in another room in order to achieve better sleep quality and quantity.
3. Night terror
- Also known as sleep terror, night terror is a sleep disorder that triggers feelings of panic or dread, which usually occur during the first hours of stage 3-4 NREM sleep and last for 1 to 10 mins, perhaps longer in children.
- It typically starts in childhood and decreases as individuals' age increases. Mason et al. (2007) stated the risk factors of sleep terrors include fever, medications, intrinsic sleep disorders, sleep deprivation, stress, and young age.
- The frequency and severity varies among the patients with the interval between episodes ranging from minutes to weeks.
What are the signs and symptoms of night terror?
Symptoms:
- A universal feature is insolability, which is similar to a panic attack
- During periods of night terror, patients bolt upright with their eyes wide open and express fear and panic on their faces.
- Screaming, yelling, or trying to speak, but their speech tends to be incomprehensible.
- Sweating, rapid breathing, rapid heart rate
- Likely to demonstrate more exaggerated movements, such as thrashing of limbs, including punching, swinging, or fleeing movements.
- Protecting themselves and or escaping from a possible threat of bodily injury.
- Confusion, inconsolable and/or unresponsive to any communications from anyone, unable to recognise others familiar to them.
- When a person experiencing a night terror is awakened, they tend to lash out at the one awakening them.
- A majority of people who experienced night terror have no recollection of their actions the following day, however short dream images or hallucinations may be recalled.
- Sleepwalking is common during night-terror periods.
- Both adults and children exhibit behaviours of escape attempts, such as thrashing about, or moving out of bed and start walking or running around aimlessly while inconsolable, which increases the risk of accidental injury.
- Inadvertent provocation by adjacent people may elevate the risk of injury to others. This means efforts from nearby people to calm the individual may induce a physically violent response from the individual during their escape attempt.
- High delta (δ) activity on EEG: Increase in muscle tone and elevated heart rate
- Alpha (α) and theta (θ) activity also detected during an episode of night terror.
- Intense autonomic discharge of tachypnoea (unconscious or involuntary rapid breathing), flushing (skin reddening), diaphoresis (excess sweating), mydriasis (pupil dilation).
- Instantaneous but calmer arousal from NREM sleep, short of a complete night-terror episode.
- It was found children with night terrors experienced no increased occurrence of psychiatric diagnoses, but adults with night terrors manifested psychopathology and mental disorders.
- Post-traumatic stress disorder (PTSD) and generalised anxiety disorder (GAD)
- Several personality disorders such as dependent, schizoid, and borderline personality disorders
- Low blood sugar
- Increased symptoms of depression and anxiety.
- Thalamic lesions of the brain and brainstem
- Sleepwalking and frontal lobe epilepsy
i. Children
- Night terrors usually occur in children aged between 3 and 12 years, with a peak onset in 3.5 years.
- Approximately 1-6% of children experience night terrors, with both sexes and all ethnic backgrounds affected equally.
- Children younger than 3.5 years old may experience at 1 night terror episode a week, which is around peak frequency. On the other hand, older children may experience about 1 or 2 night terror episodes per month.
- Children likely won't recall the night terror episode the following day.
- A paediatric evaluation is recommended to exclude the possibility of the night terrors being caused by seizure disorders or breathing problems.
ii. Adults
- Adults of all age groups can experience night terrors.
- Although the symptoms are shared between adolescents and adults, prognosis and treatment qualitatively differ between them.
- If an adult consumes a poor diet, achieves inadequate high quality sleep, experiences stressful events, then he or she may experience a night terror every night.
- Adult night terrors often less frequently, and tend to respond to treatments that aim to alleviate causes of deficient quality or quantity of sleep.
- Nguyen et al. (2008) demonstrated adults with night terrors exhibited other psychiatric symptoms, which indicated some form of comorbidity.
- Julia McMillan (2006) suggested an association between night terrors and hypoglycaemia.
- Adults may run out of the house, which may result in violent actions.
- Snyder et al. (2008) discovered some adults on a long-term intrathecal clonidine therapy exhibited side effects of night terrors, such as feelings of terror early in the sleep cycle. Bevacqua et al. (2007) suggested this may be caused by changes in cervical/brain clonidine concentration.
- Guzman & Wang (2008) suggested using MRI to research any links between night terrors and neurological disease.
What are the causes of night terror?
- Researchers suggest possible congenital causes for night terrors and other parasomnias. People often report family history of either episodes of sleep terrors or sleepwalking.
- Studies estimated 1st-degree biological relatives are 10 times more likely to experience night terrors, however the exact connection to inheritance is currently unknown.
- Nguyen et al. (2008) suggested familial aggregation is an autosomal mode of inheritance. The American Psychiatric Association (2000) discovered sleep deprivation and fever increased the likelihood of a night terror episode occurring in adults.
- Other possible contributing factors include asthma, central nervous system medications, constricted nasal passage, and gastrooesophageal reflux, as well as narcolepsy.
- There is no evidence of a cultural difference between manifestations of night terrors, although the significance and cause of night terrors differ within cultures.
- Adults and older chidlren are likely to provide descriptive and accurate images from their night terrors than younger children.
- The American Psychiatric Press (2000) found female children are likely to experience sleep terrors than male children, whereas sleep terrors occurs equally across both sexes in adults.
- Poblano et al. (2008) discovered identical twins exhibited a higher concordance rate of night terror than in fraternal twins.
- Kiera Pritchard (2021) hypothesised night terrors may occur in individuals with poor diet, poor amount or quality of sleep (e.g., because of sleep apnea), or stressful events.
- Chen et al. (2010) found adults with experience of sexual abuse were more likely to be diagnosed with sleep disordrs, including night terrors.
How is night terror diagnosed?
The DSM-5 diagnostic criteria for sleep terror disorder requires:
- Recurrent periods of abrupt but not complete wakefulness from sleep, typically occurring during the 1st major period of sleep.
- Experience of intense fear with a panicky scream at the start and symptoms of autonomic arousal, such as increased heart rate, heavy breathing, and increased perspiration.
- Unable to be soothed or comforted during the episode
- Incapable of remembering images of the dream (only a single visual scene for example).
- Completely forgot the night terror episode
- Sleep terror episodes results in clinically significant distress or impairment of the person's normal functioning.
- Disturbances are not caused by the effects of a substance, general medical condition or medication.
- Coexisting mental or medical disorders have no association with the sleep terror episodes.
Differential diagnosis:
A 1993 French study stated that night terrors are distinct from nightmares. Major differences between nightmares and night terrors include:
- Lack of vocalisation or agitation
- Nightmares occur during REM sleep, whereas night terrors occur during NREM sleep.
- Individuals can completely wake up from nightmares and have vivid and descriptive memories of their dreams.
- Epileptic seizures may occur during both the night and the day, whereas night terrors only occur during the night when sleeping.
- An EEG should be utilised to confirm differential diagnosis of either epileptic seizure or night terror.
How is night terror assessed?
The assessment of sleep terrors looks at:
- When the sleep terror episode occurs during the period of sleeping
- Age of onset
- Frequency and duration of the sleep terror episodes
- Description of the night terror episode, including behaviour, emotions, and thoughts during and after the event
- Responsiveness of the patient to external stimuli during the episode
- Consciousness or awareness of the patient, when awakened from a night terror episode
- If the patient can remember the episode afterwards
- Any triggers or precipitating factors
- Sleep–wake pattern and sleep environment
- Daytime sleepiness
- Other sleep disorders that may be present
- Family history for NREM parasomnias and other sleep disorders
- Medical, psychiatric, and neurological history
- Medication and substance use history
- Other tools such as a home video and a polysomnography may be used to rule out other disorders and result in a proper diagnosis.
How can night terror be treated?
- Night terrors eventually disappear in most children, thus no treatment is required for them. However, it is worth reassuring the child and their family that they can fight against this disorder.
- If a child experiences a sleep terror episode, parents are recommended to let the episode subside and to be vigilant in order for them not to suffer injury.
- If the child demonstrates violent behaviour during a night terror episode, parents are advises to secure the environment in which their child sleeps. This includes closing windows, removing all potentially dangerous items from the bedroom, installing alarms, and placing their child in a downstairs bedroom.
- Improving a child's sleep hygiene by increasing the amount and enhancing the quality of sleep.
- Adapting a child's naps to a specific sleep period to ensure they aren't too long or too short.
- Strategies to alleviate stress combined with psychotherapy may help reduce the frequency of night terror episodes.
- If the child continues to experience night terror episodes frequently, then a polysomnography is recommended.
- Hypnosis would reduce the sleepers' sensitivity to their night terrors.
- Waking the sleeper up prior to the sleep terror may prevent from the sleep terror from occurring.
- In extreme circumstances, benzodiazepines (such as diazepam) or tricyclic antidepressants may be administered.
- Surgically removing the adenoid to widen the nasal airway may prevent sleep terrors, but a majority of patients avoid this invasive treatment.
4. Nocturnal sleep-related eating disorder (NSRED)
https://en.wikipedia.org/wiki/Nocturnal_sleep-related_eating_disorder
- Nocturnal sleep-related eating disorder (NSRED) is a combination of a parasmonia and an eating disorder.
- Although this disorder is difficult to distinguish from other similar disorders such as night eating syndrome (NES), it is specifically categorised within somnambulism or a state of sleepwalking that includes behaviours connected to a person's conscious wishes or wants.
- The first case of NSRED was reported in 1955, with a further 9 cases reported until 1991. Schenck & Mahowald (1994) found 7 of those cases were single-case studies and the remaining 2 cases were observed during objective sleep studies, all conducted by doctors and psychiatrists.
- From 1985 to 1993, Schenck and Mahowald discovered a majority of NSRED cases exhibited symptoms that were also observed in night eating syndrome (NES). Nevertheless, they reported NSRED patients were either partially or completely unaware of their actions at night while those with NES were aware. In addition, none of the patients were observed to have any eating instability before their issues occur at night while sleeping.
- In 1993, Schenck and Mahowald published their findings that stated at least 2/3 of NSRED patients were women and a majority of patients gained weight. In addition, NSRED patients' night-eating habits began as various times ranging from childhood to middle adulthood. Those NSRED patients exhibited other nighttime behaviours such as sleep terrors.
What are the signs and symptoms of NSRED?
- Partial arousals from sleep, typically within 2 to 3 hours of sleep onset
- Subsequent and rapid or uncontrollable ingestion of food
- Attempt to consume peculiar combinations of foods and potentially harmful substances such as glue, wood, or other toxic materials
- Common foods eaten by NSRED include sweets, pastas, raw, frozen, or spoiled foods, salt or sugar sandwiches, buttered cigarettes, and improper blended meals.
- Careless handling of food or opening of cans can lead to injuries to the NSRED individual
- Consumption of scalding fluids (e.g.coffee) or solids (hot oatmeal)
- Hysteric running into walls, kitchen counters, and furniture
- Significant weight gain over a short period of time, particularly in women
- Irritability due to lack of restful sleep
- Vivid dreams at night
- Symptoms are constant across weekdays, weekends, and holidays as well as the eating excursions being unpredictably distributed throughout a sleep cycle.
- A majority of NSRED patients don't have control over their unconscious appetites, therefore alternative methods are required to restrain themselves from the urge to satisfy such appetites.
How is NSRED diagnosed?
The International Classification of Sleep Disorders-Third Edition (ICSD-3) laid the following diagnostic criteria for NSRED:
- Some dysfunctional eating when the person woke up during the main sleep period
- Eating unusual or toxic food, leading to negative health consequences
- Suffered injury during these episodes
- Individual may not be conscious nor be able to recall the episode.
How is NSRED treated?
- Pramipexole was trialled to treat the symptoms of NSRED. Dr. Auger found this treatment reduced nocturnal median motor activity, and improved individual sleep quality, but the frequency and duration of waking episodes related to eating behaviours were invariant.
- An anti-epileptic drug associated with weight loss called topiramate was found to induce significant development or absolute remission of "night-eating" as well as "significant weight loss". However, this treatment is not a cure for NSRED.
- Combinations of cardibopa/L-dopa, codeine, and clonazepam resulted in a remission of NSRED. When these pharmacological treatments were combined with nasal continuous positive airway pressure (nCPAP) therapy, this resolved symptoms of NSRED as well as obstructive sleep apnoea (OSA).
- Clonazepam monotherapy reduced NSRED symptoms in patients with concurrent somnambulism.
- A combination of dopaminergic and opioid drugs, along with the occasional sedatives.
- A combination of buproprion, levodopa, and trazodone were found in patients with a history of substance of abuse (i.e. opioids and sedatives).
- Auger (2006) asserted that behavioural therapies should be included in the overall treatment plan, which includes intentional placement of food to prevent indiscriminate wandering, maintenance of a safe sleep environment, and education related to optimal sleep hygiene and street management.
(b) REM-related
1. REM sleep behaviour disorder
- Rapid eye movement sleep behavior disorder or REM behavior disorder (RBD) is a sleep disorder that involves individuals behaving abnormally during the REM phase of sleep.
- This disorder was first described by Michel Jouvet in the 1960s and 70s in his studies of brain lesions in cats that resulted in loss of atonia in REM sleep. In 1986, Schenck et al. first described RBD in Minnesota.
- RBD is a parasomnia that is categorised as either idiopathic or symptomatic. Idiopathic RBD has no link with another ongoing neurological condition, whereas symptomatic RBD is a result of an identifiable cause.
- Around 92% of patients with idiopathic RBD proceed to develop a neurodegenerative disorder such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, which are typically synucleinopathies.
- A majority of RBD patients subsequently become diagnosed with a synucleinopathy within 4 to 9 years from diagnosis of RBD, and 11 to 16 years from onset of symptoms.
Epidemiology
- As of 2017, the prevalence of RBD is estimated to be between 0.5% and 2% overall, and between 5% and 13% of those aged 60 to 99. The typical age onset is in the 50s or 60s.
- Although it is more common in males overall, it is equally prevalent between males and females under the age of 50.
- This may be due to a referral bias, as violent activity exhibited by men is more likely to lead to harm and injury and is more likely to be reported than injury to male bed partners by women. In addition, it may be a reflection of the difference in prevalence due to genetic or androgenic factors.
- RBD is observed in about 50% of Parkinson's disease patients, at least 88% of multiple system atrophy patients, and around 80% Lewy body dementia patients.
- Boot (2015) found 98% of autospies of patients with RBD (confirmed by polysomnography) showed signs of a synucleinopathy.
What are the characteristics of RBD?
- This disorder is characterised by the individual acting out their dreams, along with complex behaviours. Those dreams frequently include crying, choking, punching, kicking, flailing arms, laughing, jumping out of bed, screaming, and shouting.
- These abnormal behaviours during an episode can lead to injuries to the dreamer or their bedmate.
- The dreamer may not be aware of their abnormal movements.
- Common dreams include violent or aggressive actions as if being chased by people, animals or monsters.
- Since violent actions in dreams is more likely to be remembered, this becomes an artifact of recall bias or selection bias.
- RBD symptoms can be the earliest indicator of an underlying neurodegenerative disorder or synucleinopathy, which initiates years before the onset of another condition.
- Zhang et al. (2020) suggested symptomatic RBD may also be associated with narcolepsy, Guillain–Barré syndrome, limbic encephalitis, and Morvan's syndrome.[7]
- Arnaldi et al. (2017) discovered other RBD symptoms include diminished motor abilities, posture and gait changes, mild cognitive impairment, depression, changes in the sense of smell, impairments in colour vision, and autonomic dysfunction (orthostatic hypotension, constipation, urinary problems and sexual dysfunction).
What are the causes of RBD?
- The exact cause of RBD is currently unknown, however researchers hypothesise it may be caused by adverse reactions to certain drugs or during drug withdrawal, or is an early symptom exacerbated by synucleinopathy rather an than a separate disorder.
- This indicates impairments or damage in neural circuits of the brainstem that control atonia during REM sleep, including those in the pontomedullary brainstem and caudal brainstem structures.
- Synucleinopathy in the brainstem is associated with neurodegenerative disorders such as Parkinson's disease and other neurodegenerative diseases, such as multiple system atrophy and the Lewy body dementias, which lead to motor deficits.
- Risk factors of RBD include a family history of acting out dreams, farming, exposure to pesticides, history of head injury, low education level, drug treatment or withdrawal, depression, and use of antidepressants.
How is RBD diagnosed?
There are 2 ways to diagnose RBD:
1. Recording a history of complex, dream-enactment sleep behaviours
2. Polysomnography recording of these behaviours along with REM sleep atonia loss
- If sleep studies can't be conducted, a clinical interview as well as a number of validated questionnaires can be used to diagnose RBD.
- Examples of validated questionnaires include Rapid Eye Movement (REM) sleep Behaviour Disorder Screening Questionnaire (RBDSQ), the REM Sleep Behaviour Questionnaires – Hong-Kong (RBD-HK), the Mayo Sleep Questionnaire (MSQ) and the Innsbruck REM Sleep Behaviour Disorder Inventory.
- If RBD patients can't provide a history of dream enactment behaviour, their bed partners are consulted for their perspective.
- St Louis & Boeve (2017) stated the REM Sleep Behavior Disorder Single-Question Screen provides diagnostic sensitivity and specificity without polysomnography with one question:
- "Have you ever been told, or suspected yourself, that you seem to 'act out your dreams' while asleep (for example, punching, flailing your arms in the air, making running movements, etc.)?"
- Repetition of vocalisations and/or complex motor behaviours during sleep.
- Polysomnography (PSG) demonstrates these behaviours occur during REM sleep.
- If a record of these behaviours by PSG is not possible, they must at least be assumed to occur during REM sleep based on records of dream enactment.
- REM sleep without atonia (RWA) can be observed in polysomnographic recordings.
- Episodes cannot be explained by another mental disorder, sleep disorder, substance abuse or medication.
- Other conditions similar to RBD display excessive sleep movement and potentially violent behaviour. Such disorders include non-REM parasomnias (sleepwalking, sleep terrors), periodic limb movement disorder, severe obstructive sleep apnea, and dissociative disorders. However, polysomnography is recommended to differentiate RBD from similar conditions and confirm RBD diagnosis.
How is RBD treated?
- Common treatments of RBD include melatonin and clonazepam, but melatonin is recommended since clonazepam can lead to undesirable side effects.
- Medications that may worsen the symptoms of RBD include antidepressants, beta blockers, tramadol and mirtazapine.
- Securing the sleeper's environment requires the removal of potentially dangerous objects from the bedroom and placement of a cushion around the bed or moving the mattress to the floor for additional protection against injuries.
- In extreme cases, some RBD patients may need to sleep in a sleeping bag zipped up to their neck, wearing mittens so they're unable to unzip it until they awake.
- It is advised to avoid sleep deprivation, record any signs of sleepiness, and maintain a normal sleep schedule.
- Other treatments include moderating neurologic symptoms and treating any other sleep disorders that may interfere with sleep.
- Avoid alcohol, sleep deprivation, certain medications, and other sleep disorders.
2. Recurrent isolated sleep paralysis (RISP)
- Fleetham & Fleming (2014) described recurrent isolated sleep paralysis as an inability to perform voluntary movements at sleep onset, or upon waking from sleep. This condition is linked to sleep-related hallucinations.
- Despite the affected individual being conscious, able to recall the episode and able to breathe, they are unable to speak or move.
- Episodes last between a few seconds to several minutes and tend to disappear spontaneously.
- Sharpless & Barber (2011) estimated to be prevalent about 7% of a human's lifetime.
- Predisposing factors for the development of RISP include sleep deprivation, an irregular sleep-wake cycle, e.g. caused by shift work, or stress.
- A proposed cause of RISP is the prolongation of REM sleep muscle atonia upon awakening.
3. Nightmare disorder
- Also known as dream anxiety disorder, nightmare disorder is characterised by frequent nightmares during the sleeping period. The nightmares occur during the REM phases of sleep, which frequently depict the individual experiencing a life-threatening situation.
- Nightmare disorders should not be confused with sleep terror disorders, as individuals wake up from a sleep terror episode with more exaggerated symptoms than from a nightmare disorder, such as crying and screaming. In addition, sleep terrors occur during the NREM stages of sleep.
- Compared to regular bad dreams, nightmares are more emotionally intense, contains more events of hostility and more miserable endings.
- Nightmare disorders afflict about 4% of American adult, and up to 4 times as many women than men. Nevertheless the ratio between men and women affected by nightmare disorders decreases with age because it is less prevalent in elderly women.
- Nonetheless, it is uncertain if the discrepancy of prevalence between men and women is accurate or if the figure indicates an increased dream recall capacity of women.
- Salzarulo & Chevalier (1983) estimated children aged between 6 and 10 years are 41% more likely to experience nightmares and 22% more likely at the age of 11. Between 10% and 50% of children are known to experience persistent nightmares.
- Factors that anticipate the development of a nightmare disorder from the existence of nightmares during childhood, include the fear of falling sleep or returning to bed after a nightmare, an irregular sleep life, and the avoidance of reflecting on the nightmare.
What are the signs and symptoms of nightmare disorders?
- The sleeper may scream or yell during the nightmare.
- They are often woken up by the frightening and terrifying dreams and can vividly recall their nightmarish experiences.
- When the sleeper wakes up from the nightmare, they are more alert and adapt within their surroundings, with an increased heart rate and symptoms of anxiety, such as sweating.
- Trouble falling back to sleep due to the fear of experiencing a another nightmare.
- Disruption to daily functioning and completing everyday tasks. Anxiety and sleep deprivation due to the nightmares may hamper efficient completion of everyday tasks.
- Recurring episodes of awakening while remembering the intense nightmare manifestations, as a result of fear or anxiety, as well as anger, disgust, sadness, and other dysphoric emotions.
- A 2018 review article by the Journal of Clinical Sleep Medicine found the sleeper may experience delayed return to sleep after episodes, and/or episodes in the latter half of the sleep period.
i. Consequences
- Nightmare disorders can disrupt a person's quality of life by making the patient avoid sleep, result in sleep deprivation, which would lead to increasingly intense nightmares.
- This would lead to medical conditions associated with chronic fatigue and insomnia.
- Schagen et al. (2017) stated other negative consequences of nightmare disorders on a patient's quality of life include reduced quantity and quality of sleep, impaired cognitive and emotional functioning and well-being, as well as negative impact on the life of the bed partner.
ii. Content of idiopathic nightmares
- Physical aggression, accidents, apprehension, disasters, evil forces, failure, helplessness, interpersonal conflict, insects and environmental abnormalities.
- Common emotions include fear, anger, sadness, and confusion.
What are the causes of nightmare disorder?
- Intense pressure or irritation if no other mental disorder is diagnosed.
- Death of a loved one or a stressful life event
- Post-traumatic disorder, schizophrenia, and borderline personality disorder, as well as other psychiatric disorders can manifest nightmares.
- Medications such as amphetamines, antidepressants, stimulants such as cocaine and caffeine can trigger nightmares.
- A 2008 article by the Gale Encyclopedia of Mental Health found blood pressure medication, levodopa and medications for Parkinson's disease can cause nightmares too.
- Stress, anxiety and substance abuse, such as drugs influencing the neurotransmitters noradrenaline, dopamine and serotonin.
- Spoormaker et al. (2006) stated the link between drugs such as beta-blockers or alpha-agonists and nightmares remains unclear, thus suggested more research is required to investigate the biochemical mechanisms of nightmares.
- In 2018, the Journal of Clinical Sleep Medicine categorised nightmares as an intrusive / re-experiencing symptom in PTSD patients.
- Germain & Nielsen (2003) reported a PTSD patients experiencing nightmares would often wake up during the night and for a longer period than those with idiopathic nightmares. This resulted in insufficient sleep quantity and substandard sleep quality. In addition, nightmares associated with PTSD tend to be more stressful than idipathic nightmares.
How is nightmare disorder assessed and diagnosed?
According to the International Classification of Sleep Disorders, the criteria required to diagnose a nightmare disorder include:
- Presence of frequent nightmares indicating danger for the person and impacting mood in a negative manner.
- Alert behaviour after waking up from nightmares. This significantly impairs the patient's social, professional, or personal functioning, in behaviour, cognition, fatigue, family, mood, occupation, or sleep.
- Individuals with nightmare disorder can sign up to be a subject at a sleep laboratory that uses polysomnography.
- It's noted that an artificial lab setting reduces the frequency of post-traumatic nightmares. Therefore, the assessment of night disorders using polysomnography requires a longer period to allow the patient to become accustomed to the artificial environment.
- Self-report by a questionnaire or by a diary is a method of documenting behaviours of nightmare disorders. However, individuals filling out these questionnaires frequently underestimate the frequency of their nightmares due to forgetfulness.
- On the contrary, individuals filling out a diary daily may overestimate the frequency of their nightmares, due to their sheer focus on this phenomenon.
- Swart et al. (2013) estimated 50-70% of PTSD cases also had concurrent nightmare disorders, 17.5% had concurrent depression, 18.3% had concurrent insomnia, 16.7% had concurrent schizophrenia, and 49% had concurrent borderline personality disorder. In addition, nightmare disorders was estimated to be exist in about 29.9% of all psychiatric disorder cases.
- This associates with sleep disorders such as chronic insomnia, night terrors, and sleep-disordered breathing.
- Nadorff et al. (2014) suggested nightmares prior to trauma would increase the severity of PTSD symptoms. Moreover, there is a correlation between nightmares and elevated risk of attempting suicide and of death by suicide.
What are the treatments for nightmare disorder?
- Stress reduction techniques such as meditation, exercise or yoga. They would alleviate stress and produce a peaceful sleeping atmosphere.
- Eye Movement Desensitisation and Reprocessing (EMDR) was found to significantly decrease the frequency of nightmares, particularly for PTSD treatment. Studies found found EMDR reduced the frequency of nightmares in Vietnam War veterans, in tsunami survivors and in children. An additional benefit of EMDR is the lack of negative side-effects.
- Kartje et al. (2018) found imagery rehearsal therapy was effective in treating nightmare disorder in both PTSD and non-PTSD populations. Imagery rehearsal therapy aim to alter the nightmare's negative content by spending 10 to 20 mins a day writing a novel scenario of the nightmare with positive images to be rehearsed.
- Lynch et al. (2013) found cognitive behavioural therapy for insomnia (CDT-I) reduced nightmares in the PTSD population, which involves altering the sleep habits with the clinician's support and the use of tools such as a sleep diary.
- Nadorff et al. (2014) suggested exposure, relaxation and rescripting therapy to treat nightmares associates with PTSD, which combines Imagery Rehearsal Therapy with exposure and relaxation techniques.
- Lucid Dreaming Therapy is a type of Imagery Rehearsal Therapy that develops awareness of the individual's act of dreaming, known as lucid dreaming. If the dreamer can regulate the negative content of the dream, this reduces their anxiety, increase their controllability of the dream's content, alter their expectations, which may reduce the frequency of nightmares.
- Studies by Morgenthaler et al. (2018) and Bout & Spoormaker (2006) found Lucid Dreaming Therapy reduced the frequency of nightmares after about 12 weeks, with 80% of the cases having the nightmares disappear after 1 year.
- Kartje et al. (2018) found Systematic Desensitisation was effective in treating chronic nightmares, which involves the individual facing the frightening aspects of nightmares in a gradual manner, from the least to the most stressful. If the individual begins to feel uncomfortable, then they need to apply a relaxation technique in order to manage the stress.
- An α-blocker called Prazosin decreases tone during sleep by blocking noradrenergic receptors. Nadorff et al. (2014) found Prazosin significantly reduced the frequency of PTSD-associated nightmares, hence improved quality of sleep.
- Other pharmacological treatments include benzodiazepines, atypical antipsychotic medications, olanzepine, Risperidone, Aripiprazole, clonidine, cyproheptadine, fluvoxamine, gabapentin, nabilone, phenelzine, topiramate or trazodone. However, more research is required to understand its efficacy against nightmare disorder.
What is a nightmare?
- Nightmares are defined as an awful dream that triggers a strong emotional response from the mind, usually fear as well as anxiety, sadness or despair. Psychologically, nightmares can awaken individuals during the night, whereas bad dreams don't.
- The prevalence of nightmares in children aged 5 to 12 years is between 20 and 30%, and in adults is between 8 and 30%.
- In general language, the definition of nightmare has broadened as a metaphor to numerous negative things, such as a terrible situation or a frightening monster or person.
- The term nightmare originated from the Old English mare, which is a mythological demon or goblin who torments others with scary dreams. Note that this term is not associated with the Modern English word for a female horse.
What are the signs and symptoms of nightmares?
- Abnormal sleep structure
- Characterised by frequent nocturnal awakenings and fear of falling asleep
- Detailed recall of content of frightening dreams, characterised by threats to survival, security, or self-esteem.
What are the causes of nightmares?
- Schredl et al. (2008) found a direct correlation between nightmares and stress in children's lives. This lifestyle stress may be manifested from the death of a close friend, a family member, or a person known to them with a chronic illness.
- Patients with obstructive airways disease (OAD) and asthma reported more frequency nightmares than controls or OAD subjects without asthma. However, healthy subjects experienced more nightmares than those with sleep apnoea.
- In 1990, Stephan LaBerge believed lucid dreaming begins as an individual thought or scene, such as strolling along a dimly lit street. Since dreams are not predetermined, it is suggested the brain responds to the scenario by either imagining a positive or negative thought, and the dream framework proceeds from there. Therefore, a higher amount of negative thoughts in a dream would result in a nightmare.
4. Periodic limb movement disorder
- Periodic limb movement disorder (PLMD) is a sleep disorder that is characterised by involuntary and periodic limb movement during sleep.
- Studies estimated PLMD affects roughly 4% of adults (aged 15 - 100), with a higher prevalence in elderly females, with up to 11% experiencing symptoms.
- Montplaisir et al. (1997) found 80% of restless legs syndrome (RLS) cases have concurrent PLMS. However, a majority of PLMS cases don't have concurrent RLS.
- According to adult criteria and PSG analysis, the prevalence of isolated PLMD in children with no comorbidity was estimated to be between 1.2 and 1.5%.
- For children with more than 5 episodes of PLMD an hour, the prevalence increases to between 5.6 and 7.7%.
What are the signs and symptoms of PLMD?
- Excessive daytime sleepiness (EDS)
- Falling asleep during the day
- Difficulty falling asleep at night
- Difficulty staying asleep throughout the night
- Involuntary limb movements occurs periodic intervals between 20 and 40 seconds apart.
- Symptoms only last the first half of the night during NREM sleep stages, and movements don't occur during REM stages due to muscle atonia.
What are the causes of PLMD?
- The causes of PLMD are mostly unknown, but in numerous cases PLMD patients have other medical problems such as Parkinson's disease or narcolepsy.
- Stephany Fulda (2018) found a number of psychopharmacological drugs including serotonergic and tricyclic antidepressants, venlafaxine and mirtazapine increase the risk of PLMD.
- In women, there is a correlation between an increased risk of both PLMD and restless legs syndrome, and a number of disorders such as musculoskeletal disease, heart disease, obstructive sleep apnea, cataplexy, or a mental disorder, as well as physical activities close to bedtime.
- It is suggested PLMS is associated with increased spinal reflexes, as well as with disorders characterised by dopaminergic dysfunctions.
- Sun et al. (1998) hypothesised reduced ferritin levels may be a cause of PLMD because it associated with elevated RLS severity and elevated PLMS prevalence. Moreover, reduced iron levels may correlate with the inhibition of dopamine formation, which might contribute to PLMD.
How is PLMD diagnosed?
- In the third edition of the International Classification of Sleep Disorders (ICSD-3), PLMD is classified in the Sleep-Related Movement Disorders' section. A significant clinical impairment, rather than a simple complaint, is required for diagnosis. Fulda (2008) stated sleep impairments have to be demonstrably caused by PLMS and the symptoms have to explained solely by the PLMS.
- Since the cause of excessive daytime sleepiness and limb movements in PLMD is currently unknown, diagnosis requires not only a polysomnogram, but also a complete medical history and any other available relevant information are required.
- Video-polysomnography is recommended to distinguish PLMD from other limb movements during sleep that share similarities with PLMS in terms of duration and pattern. EMG electrodes are typically placed on anterior tibialis muscle to measure its electrical activity during PSG.
- In combination of polysomnogram, actigraphy can be worn on the wrist to record sleep and wake periods for at least a week. This evaluates whether the movements satisfy diagnostic criteria for PLMD.
- Each movement must occur within a 4 to 90 second interval from the previous movement. The periodic limb movement index (PLMI) must be more than 15 movements per hour in adults and at least 5 movements per hour in children.
- There must be evidence of a cause-effect relationship between PLMS and an observed sleep disturbance or daytime impairment (both disturbance and impairment have to be clinically significant).
- Insomnia and hypersomnia would need to be ruled out before PLMD diagnosis, particularly anxiety, obstructive sleep apnea, and narcolepsy. In addition, the observed symptoms can't be better explained by any other conditions.
- Alternating leg movement activity (ALMA)
- Hypnagogic foot tremor (HFT) events
- Excessive fragmentary myoclonus (EFM) events
How is PLMD treated?
- Dopaminergic agents (e.g. pramipexole, ropinirole, cabergoline, and rotigotine) comined with oral iron supplements was found to improve symptoms in PLMD patients with low ferritin levels. Adverse effects of these agents include the manifestation of restless leg syndrome and cortical arousals.
- It is recommended to avoid caffeine, alcohol, or antidepressants since they could worsen PLMD symptoms.
- Medications that can alleviate or eliminate leg jerks or arousals include non-ergot derived dopaminergic medications (pramipexole and ropinirole), co-careldopa, co-beneldopa, pergolide, or lisuride.
- Hornyak et al. (1998) suggested the use of magnesium for PLMD treatment due to its therapeutic effects on insomnia and RLS, however more evidence is required to substantiate this hypothesis.
5. Catathrenia
- Known as nocturnal groaning, catathrenia is a sleep-associated breathing disorder that is characterised by end-inspiratory apnoea (breath holding) and expiratory groaning during sleep.
- The name is derived from the Greek words kata (below) and threnia (to lament), which describes this condition's typical symptoms of monotonous, irregular groans during sleep.
- The first case of catathrenia was reported by De Roeck in 1983. However, the rarity of disorder makes its atypical sleep pattern unfamiliar to numerous sleep specialists and otolaryngologists.
- Øverland et al. (2012) discovered the incidence of catathrenia to be about 4 out of 1,0004 (0.4%) among patients with sleep and/or wake problems over a 12 month period.
- Jaar et al. (2009) found the incidence of catathrenia to be 25 out of 15,052 (0.17%) among patients with sleep and/or wake problems over a 10-year period.
- Diagnosis of catathrenia requires distinction from moaning during epileptic seizures, sleep-related laryngospasm, snoring, stridor and central sleep apnoea.
- A video polysomnography with audio recording is recommended to diagnose catathrenia in order to prevent errors.
- The best treatment for catathrenia is continuous positive airway pressure (CPAP), which is found to significantly reduce the sounds produced by a catathrenia patient.
What are the signs and symptoms of catathrenia?
i. Common characteristics in reported cases
- Vocal sound = Sounds are a short or long vocalisation of the same letter (mainly an [a], [e], [o] sound). It also has harmonics and more regular and similar patterns between nights.
- Onset of groanings: They first appear in childhood, adolescence, or early adulthood, between 5 and 36 years.
- Consistent symptoms every night
- Symptoms appear during expiration: The sounds appear exclusively when breathing out and are interrupted when breathing in.
- Unawareness of the disorder: Patients tend to sleep normally despite the sounds and the effort to breathe. However, these sounds disturb the sleep of bed partners and entourage, which they become concerned about the pathological meaning of the disorder.
- No predisposing factors or aetiology
- The groaning sound lasts between 2 and 49 seconds.
- Some form of stress or anxiety in patients' lives.
- Patients aren't aware of their sleep apnoea, and their unconscious mind plays a role in holding their breath.
- Participation in sports that required holding their breath during adolescence, such as swimming and weight lifting.
- Lucid or stress dreams during catathrenia episodes
- Complaints of a painful chest upon waking from sleep.
- Side effects include dizziness, fatigue, and sore throat.
- Tendency to hold breath during daily activities requiring concentration.
ii. Discrepancies among reported cases
- Although the ISCD-2 stated limits of the sound duration between 2 and 49 seconds, Abbasi et al. (2012) reported the catathrenia sound may last as long as 0.5 seconds. Montagna et al. (2008) found 2 types of catathrenia patients produced sounds that can either be short-lasting (0.5-1.5 secs) or long-lasting (2-20 secs).
- Sound intensity: A large range in sound intensity between 40 dB and 120 dB.
- Onset time of the noise during the night: ISCD-2 stated the latency of noises after falling asleep ranges from 2 to 6 hours. However, Songu et al. (2008) reported the onset time of the noises can be as short as 3 mins.
- Association with respiratory disorders
- Response to continuous positive airway pressure (CPAP) treatment: This varies depending on each respiratory disorder. For example, patients with respiratory dysrhythmia would demonstrate poor to no improvements, even in combination with drugs. However, there are patients (such as young women with catathrenia over a 5-year period, as well as those with OSA and pulmoary hypertension) whom demonstrated a positive response to CPAP.
- Predominance of REM or NREM: Catathrenia usually occurs during REM sleep, and rarely during NREM sleep. This predominance of REM or NREM sleep during which noises occurs varies from patient to patient.
6. Sleep-related painful erections
Silber et al. (2017) reported painful erection only occur during the REM phase of sleep, which occurs in men of all ages, particularly in middle-aged men. This symptom doesn't feature amy lesion or physical damage, but rather an hypertonia of the pelvic floor. Recommended pharmacological treatments include clozapine, clonapem, baclofen, propranolol, and a number of antidepressants.
(c) Others:
1. Exploding Head Syndrome
- Exploding head syndrome (EHS) is an abnormal sensory perception during sleep characterised by the experience of short, loud, and unreal noises when falling asleep or waking up.
- The first cases of EHS was first reported by Silas Weir Mitchell in 1876, who described them as "sensory discharges" in the patient.
- Otaiku (2018) suggested the biography of the French philosopher René Descartes in 1691 made the earliest written observation of EHS.
- In 1920, British physician and psychiatrist Robert Armstrong-Jones coined the phrase "snapping of the brain" when describing EHS.
- In 1989, British neurologist John M. S. Pearce published a detailed description of the syndrome and coined the name "explording head syndrome" to label the disorder.
- In 2016, Peter Goadsby and Brian Sharpless proposed renaming EHS to episodic cranial sensory shock because they argue it describes the symptoms more accurately and better attributes to Mitchell.
- Not enough studies have been conducted to determine the prevalence of EHS in the human population. Sharpless (2015) found 14% of a sample of undergraduate students experienced at least 1 episode of EHS over the coure of their lives, with higher rates in those who concurrently have sleep paralysis.
What are the signs and symptoms of EHS?
- Hearing or experiencing loud imagined noises as individuals fall asleep or wake up
- Frightened emotional reaction to the noises.
- Doesn't report significant pain
- Rare visual disturbances such as perception of visual static, lightning, or flashes of light.
- Feelings of heat
- Peculiar feelings in their torso
- Feelings of electrical tinglings that rises to the head before the auditory hallucinations occur.
- Elevated arousal - Distress, confusion, myoclonic jerks, sweating, tachycardia, feeling of shortness of breath and effort to breathe again.
- 2 or 4 auditory hallucinations followed by a prolonged or total remission, over the course of a few weeks or months before they spontaneously disappear, or they may recur irregularly every few days, weeks, or months for a majority of a lifetime.
What are the causes of EHS?
- The cause of EHS is currently unknown, thus several hypotheses were proposed to determine the possible causes.
- Common theory: Dysfunction of the reticular formation in the brainstem responsible for transition between sleeping and waking.
- Minor seizures impacting the temporal lobe
- Ear dysfunctions, including rapid shifts in middle ear components or the Eustachaian tube, or rupture of the membranous labyrinth or labyrinthine fistula.
- Stress and anxiety
- Variable and segmented sleep, correlated with a reduction in delta-wave sleep.
- Antidepressant discontinuation syndrome
- Temporary calcium channel dysfunction
- PTSD
How is EHS diagnosed and treated?
- EHS is classified under other parasomnias by the 2014 ICSD-3 and is considered an unusual type of auditory hallucination as it occurs in period who aren't fully awake.
- According to ICD-10 and DSM-5, EHS is classified as either other specified sleep-wake disorder or unspecified sleep-wake disorder.
- As of 2018, no clinical trials had been administered to determine what treatments are considered safe and effective.
- Sharpless (2014) found a number of case studies with small sample sizes that suggests clomipramine, flunarizine, nifedipine, topiramate or carbamazepine as possible treatments.
- Frese et al. (2014) suggested the frequency of EHS episodes may be decreased by education and reassurance.
- Sharpless (2018) found underreporting of EHS episodes to medical professionals.
2. Nocturnal enuresis (NE)
- Known as bedwetting, nocturnal enuresis is involuntary urination during sleep after the age at which bladder control typically begins.
- Most cases of bedwetting are due to developmental delays rather than emotional problems or physical illnesses, with only 5-10% of cases associated with a medical condition.
- Bed-wetting was first described by Lucretius in the 1st century BC in lines 1026-29 of the fourth book of his On the Nature of Things.
"Innocent children often, when they are bound up by sleep, believe they are raising up their clothing by a latrine or shallow pot; they pour out the urine from their whole body, and the Babylonian bedding with its magnificent splendor is soaked."
- Avicenna's 1025 work "The Canon of Medicine" provided a psychological perspective of bedwetting:
"Urinating in bed is frequently predisposed by deep sleep: when urine begins to flow, its inner nature and hidden will (resembling the will to breathe) drives urine out before the child awakes. When children become stronger and more robust, their sleep is lighter and they stop urinating."
- Numerous doctors often regard bedwetting as a self-limiting problem, since a majority of children tend to outgrow it as they mature.
- Nappo et al. (2002) found children aged 5 to 9 years old have a spontaneous cure rate of 14% per year, and adolescents aged 10 to 18 years have a spontaneous cure rate of 16% per year. However, the adult rates of bedwetting demonstrate little change due to spontaneous cure.
- Teenagers who are still enuretic at 18 years of age are likely to experience bedwetting throughout their lives.
- A Dutch study found 0.5% of adults aged between 20 and 79 years experience bedwetting. Hong Kong study found 2.3% of adults aged between 16 and 40 years experience bedwetting.
What are the causes of nocturnal enuresis (NE)?
- The causes of NE are currently are entirely understood, however 3 common causes have been identified: (1) bladder contractions, (2) poor sleep arousal, and (3) excessive urine volume.
- Patient history and fluid charts completed by the parent or carer can result in differentiation of the causes.
- Fritz et al. (2004) found children whose parents were not enuretic have about a 15% incidence of bedwetting, whereas children whose one or both parents were bedwetters have a 44% and 77% incidence of bedwetting respectively.
- There is conflicting evidence regarding antidiuretic hormone production in bed-wetting children, with some showing some increase and others showing no increase.
- Bedwetting is found to be associated with a higher rate of attention deficit hyperactivity disorder diagnosis.
- Urine production is increased by the consumption of caffeine.
- Chronic constipation characterised by full bowels and pressure on the bladder can lead to bed wetting.
- Less than 5% of all bedwetting and NE cases are due to infection or disease, particularly urinary tract infection.
- The increased rate of bedwetting issues correlated with more severe neurological-developmental problems. Järvelin et al. (1988) observed a group of 7-year-olds demonstrating "handicapped and intellectually disabled children" with a bedwetting rate roughly 3 times higher than "non-handicapped children" (26.6% vs. 9.5%, respectively).
- Fritz et al. (2004) found psychological issues (such as, loss of a family member, sexual abuse, bullying) as a cause of secondary nocturnal enuresis (i.e. a return to bedwetting), but rarely a cause of PNE-type bedwetting.
- In 2010, NIMH described bedwetting as a symptom of a paediatric neuropsychological disorder called PANDAS.
- Sleep apnoea caused by upper airway obstruction due to enlarged tonsils or adenoids is associated with bedwetting.
- Bedwetting can also occur during sleepwalking episodes when the sleepwalker urinates in a room that is not the bathroom, such as a closet, sofa or the middle of the living room.
- Stressful events such as parent conflict or divorce, arrival of a newborn baby, loss of a loved one or pet, or moving to a new residence leads to insecurity, which may result in bedwetting.
- NE is also associated with diseases such as Type 1 diabetes mellitus, as well as other medical conditions such as diaper candidiasis, lethargy, weight loss, polyuria, polydipsia, and polyphagia.
There are 2 known mechanisms to prevent bedwetting:
- Around sunset every day, the body releases a burst of antidiuretic hormone (or arginine vasopressin, AVP). This decreases the kidney's urine output during the night, which allows the bladder to not reach full capacity until the morning. Children usually develop this hormone cycle between 2 and 6 years, whereas others between 6 years and the end of puberty, and some not at all.
- When the person wakes up, they remain dry when their bladder is full. This mechanism develops in the same age range as the vasopressin hormone, but is separate from that hormone cycle.
Failure in the above mechanisms may result in bedwetting.
How is NE diagnosed?
i. Voiding diary
- This records and measures when and how much their child voids and drinks, as well as describes any associated symptoms.
- It records voided volume along with the time of each micturition for at least 24 hours. This associates with nocturia and frequency of voiding only.
- If other symptoms are observed, a detailed bladder diary is recommended. The bladder diary records times of incontinence episodes, micturition and voided volume, pad usage, and other information such as fluid intake, the degree of urgency, and the degree of incontinence.
ii. Physical examination
- Each child should undergo a full paediatric and neurological exam at least once at the start of treatment.
- Blood pressure is measured to rule out any renal pathology.
- Thorough examination of the external genitalia and lumbosacral spine is required to check for any spinal defects, such as dimples, hair tufts, or skin discolouration, that may be visible in about 50% of patients with an intraspinal lesion.
- A thorough neurologic examination of the lower extremities, including gait, muscle power, plantar responses, reflexes, sensation, and tone should be conducted during the first visit.
iii. Classification
- Nocturnal urinary continence depends on 3 factors: (1) nocturnal urine production, (2) nocturnal bladder function, and (3) sleep and arousal mechanisms.
- Nevéus (2011) stated that if more urine is produced than can be contained in the bladder or if the detrusor is hyperactive, it leads to nocturnal enuresis, assuming that the child is not awakened by the imminent bladder contraction.
a. Primary nocturnal enuresis
- The most common form of bedwetting that persists after the age at which bladder control typically occurs (i.e. 4-7 years), and is either leading to an average of at least 2 wet nights a week with no long periods of dryness or an inability to sleep dry without being assisted to the toilet by another person.
- Studies found anti-psychotic drug and poor diet can result in enuresis in children.
- Constipation due to poor diet can lead to impacted stool in the colon, which adds undue pressure on the bladder. This results in the loss of bladder control (overflow incontinence).
b. Secondary nocturnal enuresis
This occurs after a patient experiences an extended period of dryness at night (6+ months) and subsequently regresses to night-time wetting. A 2008 study by the University of Chicago Pritzker School of Medicine found secondary enuresis can be a result of emotional stress or a medical condition, such as a bladder infection.
c. Psychological definition
If nocturnal enuresis is found to cause the patient significant distress, psychologists can diagnose and write a prescription for diapers.
According to the DSM-IV, nocturnal enuresis is defined as repeated urination into bed or clothes, occurring twice per week or more for at least 3 consecutive months in a child of at least 5 years of age and not due to either a drug side effect or a medical condition.
How can NE be managed?
- If bedwetting is caused by a specifically identifiable medical condition such as a bladder abnormality or diabetes, then treatment is recommended to alleviate specific medical condition such as bladder abnormalities, infection, or diabetes.
- Friman and Jones (2005) found behavioural treatment of bedwetting can improve the self-esteem of children.
- Motivational therapy: This mainly involves parent and child education that aims to restrict fluid consumption 2 hours prior to bed, and to encourage the child to empty their bladder completely prior to going to bed. A diary or chart can be used to monitor progress and establish a system that rewards the child for each night of dryness. This motivates the child to clean up in the morning as a natural, lenient consequence of wetting, which is found to result in dryness in 15-20% of the younger children (< 8 years).
- Waiting: Urologists and paediatricians recommend parents to delay treatment until the child is at least 6-7 years old. If the condition is perceived to damage the child's self-esteem and/or relationships with family/friends, then physicians can administer treatment at an early age.
- Bedwetting alarms: They blast a loud tone upon the perception of moisture, which aims to condition the child to awaken at the sensation of a full bladder. Caldwell et al. (2020) suggested they may decrease the risk of adverse events than a number of medical therapies but there is uncertainty regarding alarms being more effective than other treatments. Evans (2001) detected a 29 - 69% relapse rate, which indicated the treatment requires repetition in order to be effective.
- DDAVP (desmopressin) tablets: They are a synthetic replacement for antidiuretic hormone, which is typically used in the form of desmopressin acetate that decreases urine production during sleep. Neveus et al. (2010) found DDAVP is more efficient in children with nocturnal polyuria and normal bladder reservoir function. Jain & Bhatt (2016) suggested desmopressin may be helpful in children who are unlikely to comply with alarm therapy, which may be useful for summer camp and sleepovers to avoid enuresis.
- Tricyclic antidepressants: Robson (2009) found tricyclic antidepressant prescription drugs with anti-muscarinic properties were effective in treating bedwetting, but they increased the risk of side effects, including death from overdose. These drugs include amitriptyline, imipramine, and nortriptyline.
- Diapers: Wearing a diaper can decrease the feeling of embarrassment and stress for bedwetters and facilitate cleanup for caregivers. Diapers or training pants are typically used for younger children, whereas absorbent underwear or incontinence briefs are typically used for older children and adults. It would provide benefits for bedwetting children who desire to attend sleepovers or campouts, which decreases emotional problems manifested by social isolation and/or embarrassment in front of their peers. A 2007 study by the Journal of Applied Behaviour Analysis stated extended diaper usage may disrupt severely disabled adults' learning of staying dry.
- Plastic pants: Waterproof mattress pads may be used in a few cases to facilitate clean-up of bedwetting incidents unless the moisture makes contact with the mattress, sheets, bedding or sleeping partner.
3. Somniloquy (Sleep talking)
- Known as sleep-talking, somniloquy is defined as talking aloud during sleep, which ranges from mumbling noises to loud shouts and long, frequently inarticulate speech.
- It usually occurs during delta-wave NREM sleep stages or temporary periods of arousal, as well as during the REM sleep stage.
- Reimao & Lefévre (1980) reported about 50% of young children are reported to sleep-talk at least once a year. A majority of people progressively sleep-talk less frequently after the age of 25. However, a small proportion of people with no history of sleeptalking episodes during their childhood may start to sleep-talk in adulthood.
- Less then 10% of children sleep-talk every night, and 20-25% of children sleep talk at least once a week.
- No difference was found in sleep-talking episode prevalence between gender or socioeconomic class.
- It is difficult to estimate the actual prevalence of somniloquy because the sleep-talker either doesn't remember or is oblivious of their sleep-talking behaviour.
- The age of onset of sleeptalking is also difficult to determine because early occurrences may be underreported.
What are the associated conditions of somniloquy?
Somniloquy can occur idiopathically or as a feature of another sleep disorder such as:
- Rapid eye movement behaviour disorder (RBD) – loud, emotional or profane sleep talking
- Sleepwalking
- Night terrors – intense fear, screaming, shouting
- Sleep-related eating disorder (SRED)
What are the causes of somnoliloquy?
- Sleep-talking is likely to be passed on from parents to their children, suggesting the condition is hereditary.
- However, somniloquy can occur (albeit less commonly) even neither parent has a history of sleep talking.
- It's suggested a majority of people show initial symptoms of sleep-talking later in life without any prior history of sleep-talking during childhood or adolescence.
- Although somniloquy seems harmless, it can wake others nearby and cause them consternation, particularly when they misinterpret it as conscious speech.
- If somnoliloquy is emotional, profane, or theatrical, it may indicate a sign of another sleep disorder.
- Studies suggest an association between stress or post-traumatic stress disorder (PTSD) and the prevalence of somnoliloquy.
- Other risk factors of somnoliloquy include depression, alcohol, fever, or sleep deprivation, as well as other sleep disorders such as confusional arousals, sleep apnea, REM sleep behaviour disorder, or a psychiatric disorder or nocturnal seizure.
How can somniloquy be treated?
- Treatment isn't required for sleep-talking because it generally doesn't disturb sleep or result in other medical issues.
- In 1979, Le Boeuf found sleep-talking can be alleviated by sounding a 5-second automated auditory signal to alert the person when they began talking in their sleep.
- Bruxism is defined as excessive teeth grinding or jaw clenching during sleep (nocturnal) or wakefulness (awake). Since it is an oral parafunctional activity, it is unrelated to normal function such as eating or talking.
- Around 2000 years ago, Shuowen Jiezi by Xu Shen recorded the definition of Chinese character "齘" (Xiè, bruxism) as "the clenching of teeth" (齒相切也, Chǐ xiāng qiè yě).
- In the year 610, (巢元方) Chao Yuanfang's Zhubing yuanhou lun (諸病源候論) recorded the definition of bruxism (齘齒, Xiè chǐ) as "the clenching of teeth during sleep" and suggested it was caused by Qi deficiency and blood stasis.
- In the year 978, (王怀隐) Wang Huaiyin's Taiping Shenghuifang (太平圣惠方) provided a similar hypothesis and suggested 3 prescriptions to treat bruxism.
- In 1907, Marie Pietkiewics proposed the French term "La bruxomanie", which translated to bruxomania.
- The term "bruxism" was first coined in English by Frohman in 1931.
- Between 1966 and 2007, a majority of the research published in journals were focused on occlusal adjustments and oral splints in bruxism.
- In the 1960s, a periodontist called Sigurd Peder Ramfjord suggested occlusal factors played a role in bruxism.
- It is uncertain whether there is a causal relationship between occlusion and bruxism, however more researchers propose a multifactorial, biopsychosocial model of bruxism.
Describe the epidemiology of bruxism
- Due to differences in the definition, diagnosis, and research methodologies of bruxism studies, there is a wide range of reported epidemiological data for bruxism.
- For example, a number of studies rely on patients self-reporting bruxism, but this may be a poor measure of the actual prevalence due to numerous patients being unaware of their tooth grinding and clenching habits.
- The ICSD-R reported about 85-90% of the general population experience teeth-grinding at some point during their life, despite only 5% developing a clinical condition.
- A number of mixed findings were reported with females experiencing bruxism more often than males during wakefulness, whereas males and females experience bruxism equally during sleep.
- Macedo et al. (2007) suggested sleep bruxism may occur as early as the first year of life, which lead to the overall prevalence in children being about 14-20%.
- The ICSD-R reported sleep bruxism may occur in over 50% of normal infants.
- About 13% of adolescents aged 18 to 29 years frequently develop sleep bruxism.
- The overall prevalence of sleep bruxism in adults is reported to be roughly 8%, and about 3% of people over 60 years old may experience bruxism.
- Manfredini et al. (2013) found the prevalence of awake bruxism is between 22.1 and 31%, the prevalence of sleep bruxism is between 9.7% and 15.9%, and the overall prevalence of bruxism is between 8% and 31.4%.
- Moreover, bruxism overall affects males and females equally, but less frequently elderly people.
What are the signs and symptoms of bruxism?
- A majority of bruxism patients are oblivious of their condition, either due to lack of symptoms, or the symptoms aren't understood to be associated with a clenching and grinding issue.
- Symptoms of sleep bruxism occur in an intense fashion immediately after waking, and then gradually subside. In addition, the symptoms of a grinding habit that occurs primarily during wakefulness tends to worsen through the day, and may disappear on waking.
The signs and symptoms include:
- Grinding or tapping noise sleep, which may be adequately loud and unpleasant to wake a sleeping partner.
- Cheek biting and/or lip biting, which may lead to morsicatio buccarum and/or linea alba.
- Burning sensation on the tongue (i.e.glossodynia), which may be related to a coexistent "tongue thrusting" parafunctional activity.
- Teeth Indentations in the tongue (i.e. "crenated tongue" or "scalloped tongue")
- Hypertrophy of the muscles of mastication, especially the masseter muscle.
- Tenderness, pain or fatigue of the muscles of mastication. Chewing or other jaw movements worsens these symptoms.
- Trismus = Restricted opening of the mouth
- Pain or tenderness of the temporomandibular joints, which may result in preauricular pain (in front of the ear), or pain referred to the ear (otalgia).
- Clicking of the temporomandibular joints
- Headaches, especially in the temples, which is caused by pain in the temporalis muscle.
- Excessive tooth wear, especially attrition, which flattens the occlusal (biting) surface. Other types of tooth wear may occur, such as abfraction, where notches appear around the neck of the teeth at the gumline.
- Tooth fractures, and continuous failure of dental restorations (fillings, crowns, etc.)
- Hypersensitive teeth, due to the insulating layers of dentin and enamel around the dental pulp being shed.
- Inflammation of the periodontal ligament of teeth. Biting on them would induce soreness, as well as loosen the teeth.
- Bruxism can have detrimental impacts on aspects of masticatory system, the periodontium and the articulation of the mandible with the skull (the temporomandibular joints).
i. Pain
- Bruxism patients usually don't experience pain as the level of pain doesn't necessarily correlate with the severity of grinding or clenching.
- Pain may occur in the masseter (jaw) muscles over the angle of the jaw or in the temple (temporalis), which can be described as a headache or an aching jaw.
- A majority of bruxism cases includes clenching force exerted by masseter and temporalis muscle groups, whereas other bruxism cases involve clenching and grinding only the front teeth, which doesn't involve as much action by the masseter and temporalis muscles.
- Pain may occur in the temporomandibular joints themselves, typically perceived in the front of the ear, or inside the ear itself.
- Studies suggest sleep bruxism may be a causative or contributory factor to pain symptoms in temporomandibular joint dysfunction (TMD, or temporomandibular pain dysfunction syndrome).
- However, Cawson et al. (2012) argued there is no association between TMD and bruxism, despite the symptoms of TMD overlapping with those of bruxism.
- A systematic review by Manfredini & Lobbezoo (2010) concluded there is a positive association between TMD pain and self-reported bruxism. However, under stricter diagnostic criteria for bruxism, that association between TMD symptoms and bruxism is weaker.
ii. Tooth wear
- There is debate whether tooth wear is a consequence of bruxism due to the lack of a positive correlation between tooth wear and bruxism.
- The most common type of tooth wear is caused by tooth-to-tooth contact, which is described as attrition. This sheds the occlusal surface (i.e. biting surface) of the tooth.
- The exact location and pattern of attrition is dependent on the mechanism of bruxism. For instance, the canines and incisors of the opposing arches may be forced against each other laterally by the action of the medial pterygoid muscles, This results in wearing down the incisal edges of the teeth.
- Bruxism involves grinding the posterior (back) teeth that wears down the cusps of the occlusal surface.
- When tooth wear exposes the enamel layer, it softens the dentin layer and increases its susceptibility to wear and tooth decay. This effectively weakens the tooth, and creates fractures under the increased forces that occur in bruxism.
- Neville et al. (2002) described abfraction as another type of tooth wear that is hypothesised to be caused by bruxism, despite arguments claiming the contrary.
- Abfraction cavities are thought to occur on the facial aspect of the tooth, particularly in the cervical region as V-shaped defects manifested by flexing of the tooth under occlusal forces.
- Since the tooth cavities are V-shaped, it doesn't the support the theory that it is caused by toothbrush abrasion. Moreover, several abfraction cavities occur under the gumline level, i.e., in an area shielded from toothbrush abrasion.
- Pettengill (2011) added that erosion synergistically contribute to tooth wear in some cases of bruxism.
iii. Tooth mobility
- Davies et al. (2001) suggested that increased occlusal (biting) forces trigger the periodontal ligament to resorb some of the bone of the alveolar crest, which may result in increased tooth mobility. Nevertheless these changes are reversible if there is less occlusal force.
- When the tooth move during occlusal loading, it is described as fremitus. It is known that increased occlusal forces elevates the rate of progression of pre-existing periodontal disease (gum disease), however the usual treatment is plaque control rather than elaborate occlusal adjustments.
- It is argued that tooth mobility and pathological tooth migration are more commonly attributed to periodontal disease than bruxism.
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What are the causes of bruxism?
- During sleep, the voluntary muscles are usually inactive due to physiologic motor paralysis, and the jaw can remain open.
- In some bruxism cases, patients bite in intervals ranging from 1/10s of a second to 30 seconds. In other cases, patients clench their jaw without drastic lateral movements.
- It is thought that bruxism is a disorder of repetitive, unconscious contraction of the masseter and the anterior part of the temporalis muscles, as well as the lateral pterygoids.
The causes of bruxism is relatively unknown, but researchers proposed a number of possible causes. There is debate where bruxism is either a subconscious or involuntary habit.
- Awake bruxism is believed to be semivoluntary, usually associated with stress caused by family responsibilities or work pressures. In children, bruxism may be a response to earache or teething.
- Prominent features of awake bruxism include teeth clenching and grinding, which are related to other semivoluntary oral habits such as cheek biting, nail biting, absent mindedly chewing on a pen or pencil, or tongue thrusting.
- Wassell et al. (2008) suggested sleep bruxism is associated with the central nervous system, particularly impairments to sleep arousal and neurotransmission.
- The underlying factors include psychosocial factors such as daytime stress, which may impact sleep quality.
- Lavigne et al. (2007) stated sleep bruxism is characterised by "rhythmic masticatory muscle activity" (RMMA) at a frequency of about once per second, along with tooth grinding. Furthermore, about 86% of sleep bruxism episodes were reported to occur during periods of sleep arousal.
- Lobbezoo et al. (2006) used sensory stimulation to trigger sleep arousals, which manifested sleep bruxism episodes. Moreover, they hypothesised a connection between sleep bruxism episodes and a supine sleeping position (lying face up).
- Shetty et al. (2010) described sleep arousals as rapid change in the depth of the sleep stage, which may be associated with elevated heart rate, respiratory changes and muscular activity.
- Studies indicated sleep bruxism episodes may be associated with decreased oesophageal pH (acidity), decreased salivary flow, gastrooesophageal reflux, and swallowing.
- Macedo et al. (2009) indicated that bruxism aetiology may be associated with impairments to the dopaminergic system in the central nervous system. A finding suggests dopaminergic medications, such as levodopa, amphetamines or nicotine, affect dopamine release on the activity of bruxism. It is theorised that nicotine stimulates release of dopamine in order explain the finding that bruxism is twice as prevalent in smokers compared to non-smokers.
i. Psychosocial factors
- Studies stated a number of psychosocial risk factors for bruxism, such as a stressful lifestyle, emotional stress and anxiety, however it is still uncertain whether they are causative.
- It is known that bruxism patients respond dissimilarly to depression, hostility, and stress compared to people without bruxism.
- Manfredini D & Lobbezoo (2009) stated a positive association between stress and awake bruxism, but expressed uncertainty on the association between stress and sleep bruxism.
- Shetty et al. (2010) discovered children with sleep bruxism demonstrated higher levels of anxiety than other children.
- Lobbezoo et al. (2006) stated significant correlations between bruxism and people aged 50+, singleness, high level of education, work-related stress and irregular work shifts.
- A 2009 study by the Mayo Foundation for Medical Education and Research suggested a few personality traits associated with bruxism such as aggression, competitiveness, hyperactivity, suppressed anger or frustration.
- Other factors known to worsen bruxism include stressful periods such as examinations, family bereavement, marriage, divorce, or relocation, periods of high concentration such as computer work, reading, or driving.
- A rat model conducted by Rosales et al. indicated emotional stress may manifest behaviours similar to bruxism.
ii. Genetic factors
- Macedo et al. (2007) estimated 21-50% of people with sleep bruxism have a direct family member who experienced sleep bruxism during childhood, which indicates possible genetic factors despite the lack of genetic markers identified.
- In 2001, the American Academy of Sleep Medicine stated the offspring of people with sleep bruxism are more likely to have skeep bruxism than the children of people who have no bruxism, or people with awake bruxism rather than sleep bruxism.
iii. Medications
- A number of stimulant drugs, both prescribed and recreational, were suggested to manifest symptoms of bruxism, which include dopamine agonists, dopamine antagonists, tricyclic antidepressants, selective serotonin reuptake inhibitors, alcohol, cocaine, and amphetamines.
- Buescher (2007) found selective serotonin reuptake inhibitors exacerbated symptoms of bruxism, which can be resolved by reducing the dose.
- Winocur et al. (2003) listed a number of medications known to manifest symptoms of bruxism, which include levodopa, fluoxetine, metoclopramide, lithium, cocaine, venlafaxine, citalopram, fluvoxamine, methylenedioxyamphetamine (MDA), methylphenidate, and gamma-hydroxybutyric acid (GHB) and similar gamma-aminobutyric acid-inducing analogues such as phenibut. In addition, Winocur et al. (2003) suggested excessive consumption of caffeine, mostly found in coffee, tea or chocolate, is associated with bruxism.
- Lobbezoo et al. (2006) suggested addiction to drugs such as methylenedioxymethamphetamine (MDMA, ecstasy) can exacerbate symptoms of bruxism such as tooth wear.
iv. Occlusal factors
- Occlusion is defined as the contact between teeth during biting and chewing, but it doesn't imply the presence of any disease.
- Malocclusion is defined as an abnormal alignment of the upper and lower teeth, which occurs when both the upper jaw is ideally proportioned to the lower jaw, or where there is a discrepancy between the size of the upper jaw relative to the lower jaw.
- An occlusal interference may refer to issues that impedes with the usual path of the bite, which describes a localised abnormality regarding the position or shape of a single tooth or group of teeth.
- A premature contact is referred to one component of the bite meeting sooner than other components, which indicates the remaining teeth meet later or are held open, e.g., a new dental restoration on a tooth (e.g., a crown). The new tooth would have a different shape or position to the original tooth, which results in both sets of teeth contacting too early in the biting process.
- A deflective contact interferes with the bite by altering the normal path of the bite. e.g. An over-erupted upper wisdom tooth caused by the removal of or force on the lower wisdom tooth.
v. Associations with other conditions
Numerous studies listed many conditions to be associated with bruxism, either neurologically and/or psychiatrically, but they are rarely reported with varying degrees of evidence found.
Those disorders include:
- Acrodynia
- Atypical facial pain
- Autism
- Cerebral palsy
- Disturbed sleep patterns and other sleep disorders, such as obstructive sleep apnea, and insomnia
- Down syndrome
- Dyskinesias
- Epilepsy
- Infarction in the basal ganglia
- Intellectual disability, particularly in children
- Leigh disease
- Meningococcal septicaemia
- Multiple system atrophy
- Oromandibular dystonia
- Parkinson's diseases, possibly due to long-term therapy with levodopa causing dopaminergic dysfunction
- Rett syndrome
- Torus mandibularis and buccal exostosis
- Trauma, e.g. brain injury or coma
How can bruxism be diagnosed?
- Clinical diagnosis of bruxism should be conducted as early as possible in order to avoid damage that may be induced and the detrimental effect on quality of life.
- Bruxism is usually diagnosed based on the patient's history and the presence of typical signs and symptoms, including tooth wear, tooth mobility, tongue cavities, masseteric hypertrophy, hypersensitive teeth, pain the muscles involved in mastication, and clicking or locking of the temporomandibular joints.
- Questionnaires may be used to screen for bruxism in both clinical and research environments.
- If roommates or family members living in the same household as tooth grinders, they can notify them of their recurrent grinding. If tooth grinders live alone, they can use a sound-activated tape recorder.
- Studies suggest the use of the Bruxchecker, Bruxcore, or a beeswax-bearing biteplate to verify the condition of clenching.
- The Individual Tooth-Wear Index objectively quantifies the degree of tooth wear in an individual, independent of the number of missing teeth. Nonetheless, one must understand that tooth wear can be caused not just by bruxism, but also by acid erosion due to high consumption of acidic liquids such as concentrated fruit juice, or frequent vomiting or regurgitation of stomach acid.
- One must understand that tooth wear only indicates its occurrence at some point in the past, and doesn't necessarily indicate that the loss of tooth substance is taking place. It's possible people who clench and grind minimally tend to demonstrate minimal tooth wear.
- Occlusal splints can be used not only to treat bruxism, but also to diagnose bruxism by observing whether there is any wear on the splint after a certain period of wearing them at night,
- Diagnosis of sleep bruxism requires the physician to exclude dental diseases and temporomandibular disorders, as well as the rhythmic jaw movements triggered by seizure disorders (e.g. epilepsy).
- A 2001 study recommends a dental examination, an electroencephalography to determine the presence of seizure disorder, a polysomnography to detect any increased masseter and temporalis muscular activity during sleep, as well as exclude other sleep disorders.
- People with awake bruxism may not be aware of their clenching and grinding activities, thus they are advised to re-attend their dental examination in order to be informed of such habits.
- The "Bruxcore Bruxism-Monitoring Device" (BBMD, "Bruxcore Plate"), the "intra-splint force detector" (ISFD), and electromyographic devices to measure masseter or temporalis muscle activity (e.g. the "BiteStrip", and the "Grindcare") were developed to objectively measure bruxism activity, either in terms of muscular activity or bite forces. However, there are concerns they may introduce changes in the bruxism habits, which doesn't represent the innate bruxism activity.
ICSD-R diagnostic criteria
The minimal criteria include both of the following:
- A. symptom of tooth-grinding or tooth-clenching during sleep, and
- B. One or more of the following:
- Abnormal tooth wear
- Grinding sounds
- Discomfort of the jaw muscles
- With the following criteria supporting the diagnosis:
- C. polysomnography shows both:
- Activity of jaw muscles during sleep
- No associated epileptic activity
- D. No other medical or mental disorders (e.g., sleep-related epilepsy, which may cause abnormal movement during sleep).
- E. The presence of other sleep disorders (e.g., obstructive sleep apnea syndrome).
Classification by:
i. Temporal pattern
- Bruxism is subdivided into 2 types based on the timing of the parafunctional activity: sleep ("sleep bruxism"), or while awake ("awake bruxism").
- Awake bruxism (AB) is sometimes known as "diurnal bruxism", or "daytime bruxing", whilst sleep bruxism (SB) is sometimes known as "sleep-related bruxism", "nocturnal bruxism", or "nocturnal tooth grinding".
ii. Cause
- Bruxism can be subdivided into primary bruxism (i.e. idiopathic bruxism) or secondary bruxism. Primary bruxism is not related to any other medical condition, whereas secondary bruxism is associated with other medical conditions. Furthermore, secondary bruxism includes iatrogenic causes, e.g. the side effect of prescribed medications.
- Shetty et al. (2010) divides the causes of bruxism into 3 categories: central or pathophysiological factors, psychosocial factors and peripheral factors.
- Although the World Health Organisation International Classification of Diseases 10th revision doesn't contain an entry for bruxism, it does have an entry for "tooth grinding" under somatoform disorders, nonetheless.
iii. Severity
The ICSD-R described 3 different severities of sleep bruxism:
-- Mild = Occurring less than nightly, with no damage to teeth or psychosocial impairment
-- Moderate = Occurring nightly, with mild impairment of psychosocial functioning
-- Severe = Occurring nightly, and with damage to the teeth, tempormandibular disorders and other physical injuries, and severe psychosocial impairment
iv. Duration
The ICSD-D described 3 three different types of sleep bruxism based on the duration of the condition being present:
-- Acute = Lasts for less than 1 week
-- Subacute = Lasts for more than a week and less than 1 month
-- Chronic = Lasts for over a month
Comparison between sleep bruxism and awake bruxism
How can bruxism be managed?
- So far, there is no widely accepted, best treatment for bruxism. The available treatments for bruxism typically treat the symptom of tooth wear and prevent further damage and manage symptoms.
- Since bruxism is not a life-threatening condition, and there is a lack of evidence for the efficacy of any available treatment, studies recommend only conservative and reversible treatments because they carry a low risk of morbidity.
i. Psychosocial inventions
- Since there is a strong relationship between awake bruxism and psychosocial factors, it is advised to administer treatments that may alleviate stress.
- A clinician can provide sleep hygiene education, along with a clear and concise explanation of bruxism (definition, causes and treatment options).
- Pierce & Gale (1988) discovered bruxism symptoms don't improve after relaxation and tension-reduction, but the patients' sense of well-being does improve.
- Clarke & Reynolds (1991) found hypnotherapy reduced grinding and EMG activity of bruxism patients.
- Other suggested interventions include relaxation techniques, behavioural modifications, stress management, habit reversal, hypnosis, cognitive behavioural therapy, and reminder techniques.
ii. Medications
- The common medications prescribed to treat bruxism include anticonvulsants, antidepressants, beta blockers, benzodiazepines, dopamine agents, muscle relaxants. and others.
- A 2014 systematic review by the Macedo, et al. found "insufficient evidence on the effectiveness of pharmacotherapy for the treatment of sleep bruxism."
- Greenberg & Glick (2003) found buspirone resolves the side effects of bruxism associated with use of selective serotonin reuptake inhibitors in depression.
- Buescher (2007) suggested tricyclic antidepressants over selective serotonin reuptake inhibitors in people with bruxism, which may alleviate pain associated with bruxism.
iii. Preventing dental damage
- Dental treatment in people with bruxism can be conducted when essential, since any dental work is likely to break down in the long term.
- For instance, dental implants, dental ceramics such as Emax crowns and complex bridgework are contraindicated in bruxism patients.
- A full coverage gold crown is preferable to other types of crown because they have a high degree of flexibility and has less removal (and thus less weakening) of the underlying natural tooth.
- Occlusal splints (or dental guards) are a common prescription for bruxism, however there is insufficient evidence to demonstrate their effectiveness against sleep bruxism and awake bruxism.
- They mechanically protect the teeth from wear associated with bruxism rather than decrease the bruxism habits itself. If the bruxism worsens or is unaffected by the occlusal splint, the patients' splints will have holes worn through them, rendering it useless and requires immediate replacement.
- Occlusal splints are usually composed of plastic (e.g. acrylic) that can be partial or full-coverage, worn alone, or in combination with an upper appliance. It is advised for bruxism patients to wear occlusal splints about 30 mins before going to bed in order to be able to fall asleep.
- Bruxism patients with hypersensitive teeth are recommended to apply desensitising toothpastes (e.g. containing strontium chloride) initially inside the splint in order for the material to make contact with the teeth all night.
- Splints may decrease muscle strain by facilitating efficient movement of the upper and lower jaws with respect to each other.
- A partial splint called the nociceptive trigeminal inhibition tension suppression system (NTI-TSS) dental guard aims to allow the splint to snap onto the front teeth only. Theoretically, it avoids tissue damages by decreasing the bite force from closing the jaw into a forward twisting the lower front teeth.
iv. Botulinum toxin
- Bussadori et al. (2020) found Botulinum neurotoxin (BoNT), particularly type A (BTX-A), significantly decrease pain and the frequency of sleep bruxism compared to placebo or conventional treatment (e.g. behavioural therapy, occlusal splints, and drugs), after 6 and 12 months.
- It is theorised BoNT partially paralyses the muscles by inhibiting acetylcholine release at neuromuscular junctions and reduces their ability to forcefully clench and grind the jaw, while retaining sufficient muscular function to allow normal activities such as eating and talking.
- 5 - 6 injections into the masseter and temporalis muscles, and rarely into the lateral pterygoids would take few minutes per side. The effects of the BoTox would be recognisable the following day, and may last for several months. The BoTox dose varies depending upon the person, with some with stronger muscles of mastication requiring higher doses.
v. Biofeedback
- Biofeedback is a process that makes the individual aware of, and change physiological activity in order to improve their health. Despite the lack of testing of biofeedback on awake bruxism, Wu (2015) found evidence of the efficacy of biofeedback in the management of nocturnal bruxism in small control groups.
- Nissani (2000) stated that dental appliances containing capsules that break and release a taste stimulus when sufficient force is applied can wake the sleep individual in order to avoid bruxism episodes.
The next blog post in this series will delve deep into benign sleep phenomena such as dreams.
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