Thursday, January 28, 2010

4 Signs of Sleep Deprivation in Teens


4 Signs of Sleep Deprivation in Teens

Signs of insufficient sleep may include the following:
  1. Memory lapses and inattention
  2. Irritability, depressed mood, being overly emotional
  3. Falling asleep spontaneously during quiet times
  4. Needing catch-up slee on the weekends

Obstructive sleep apnea (OSA), a form of sleep-disordered breathing


OVERVIEW

Obstructive sleep apnea (OSA), a form of sleep-disordered breathing, encompasses a spectrum of breathing disturbances caused by narrowing of the upper airway. Zuid Afrikaans Sleep Centre treats a number of OSA patients each year and is a leader in research to better understand the disorder and develop new treatments.

Diagnosis

Dr Yacoob Omar Carrim's approach to diagnosis of OSA is based on advanced patient testing, examination and analysis of symptoms.

Treatment

Patients treated for OSA benefit from the combined expertise of top specialists working together across the fields of sleep medicine, otorhinolaryngology (ear, nose and throat), cardiology, orthodontics, oral surgery, endocrinology, and nursing. Each patient is unique and specialists combine their expertise to develop the best treatment plan possible.

Monday, January 18, 2010

Periodic Limb Movements during Sleep

Periodic Limb Movements during Sleep

Periodic limb movement (PLM) disorder is unique in that the movements occur during sleep. Most other movement disorders manifest during wakefulness. The condition is remarkably periodic, and the movements may cause poor sleep and subsequent daytime somnolence. PLM disorder may occur with other sleep disorders and is related to, but not synonymous with, restless leg syndrome (RLS), a less specific condition with sensory features that manifest during wakefulness. The majority of patients with RLS have PLM disorder, but the reverse is not true. Treatment involves either dopaminergic medication in an attempt to modify activity of the subcortical motor system or, more commonly, sedative medications to allow uninterrupted sleep. Many new agents are proving efficacious for treatment as well.

Symonds first described PLM disorder in 1953. The original name, "nocturnal myoclonus," does not describe the condition accurately, since the movements are slower than are those of myoclonus. The original name seldom is used today.


The etiology of the primary form of PLM disorder is uncertain. Suprasegmental disinhibition of the descending inhibitory pathways may be a factor. Because the etiology is not clear, treatment is primarily symptomatic and does not modify the disease. Studies differ regarding the frequency of polyneuropathy in cases of PLM disorder. Martinez-Mena and Pastor found that only 1 of 9 patients had signs of neuropathy.

The secondary forms of PLM disorder may be due to diabetes mellitus, spinal cord tumor, sleep apnea syndrome, narcolepsy, uremia, or anemia. Many authors report an association between attention deficit hyperactivity disorder (ADHD) and PLM disorder. Antidopaminergic, dopaminergic, or tricyclic drug therapy or cessation of treatment with barbiturates or benzodiazepines may initiate the syndrome as well. Voderholzer and colleagues noted an increased incidence of periodic limb movements during sleep in patients with Gilles de la Tourette syndrome. However, the authors emphasized that the different responses to pharmacological treatments are evidence against a pathophysiological relationship between PLM disorder and Gilles de la Tourette syndrome.

The presenting symptom may be stereotyped periodic limb movements that cause awakening during the night, but often the presenting complaint is poor sleep and daytime somnolence. Haba-Rubio et al report that sleep changes induced by periodic limb movements during sleep (PLMS) are associated with decreased physical and psychological fitness on awakening.

Occasionally, a bed partner may provide the history of limb movements.
Nozawa and colleagues studied arousal index and movement index in PLM disorder and noted that the sleep-wake disorders associated with PLM relate to threshold of awakening.
Leg movements are stereotyped and involve one or both limbs.

The movement simulates triple flexion with leg flexion, ankle dorsiflexion, and great toe extension; it lasts approximately 2 seconds and thus is not consistent with the rapid jerk that defines true myoclonus.
The periodicity ranges from 20-40 seconds with a variable duration. The movements are said to occur mainly in non?rapid eye movement (REM) sleep.

Restless Legs Syndrome

Restless Legs Syndrome

The term restless legs syndrome (RLS) was used initially in the mid-1940s by Swedish neurologist Karl A. Ekbom to describe a disorder characterized by sensory symptoms and motor disturbances of the limbs, mainly during rest. However, early descriptions date back to the 17th century. It is recognized now as a neurologic movement disorder of the limbs, often associated with a sleep complaint. Patients with RLS have a characteristic difficulty in trying to depict their symptoms; they may report sensations such as an almost irresistible urge to move the legs, which are not painful but are distinctly bothersome; this can lead to significant physical and emotional disability. The sensations usually are worse during inactivity and often interfere with sleep, leading to walking discomfort, chronic sleep deprivation, and stress. Once correctly diagnosed, RLS can usually be treated effectively by relieving symptoms; in some secondary cases, it can even be cured.


Pathogenesis of RLS is unclear. Ekbom originally proposed that it was mainly the result of accumulation of metabolites in the legs because of venous congestion. Peripheral nerve abnormalities also have been proposed, but no associated structural changes in nerve endings have been identified.

RLS also has been linked to dopaminergic or opiate abnormalities. Centrally acting dopamine receptor antagonists reactivate symptoms when given to patients with the syndrome. Results of single-photon emission computed tomography (SPECT) have suggested deficiency of dopamine D2 receptors. Sympathetic hyperactivity also has been implicated on the basis of observations that sympathetic nerve blockade relieves periodic limb movements of sleep and that alpha-adrenergic blockers improve symptoms of RLS. Studies also have suggested possible underactivity of the serotonin and gamma-aminobutyric acid (GABA) neurotransmitter systems.

The severity of symptoms in patients with RLS ranges from mild to intolerable. Although patients experience the sensations in their legs, they also may occur in the arms or elsewhere. RLS symptoms are generally worse in the evening and night and less severe in the morning. While RLS may present early in adult life with mild symptoms, usually by age 50 it progresses to daily severe disruption of sleep leading to decreased daytime alertness. RLS is associated with reduced quality of life in cross-sectional analysis.

A childhood-onset restless legs syndrome has also been described. A study published in Dec 2004 by Kotagal and Silber concluded that iron deficiency and a strong family history were characteristic of this childhood-onset presentation.

Insomnia

Insomnia

Insomnia is the most common sleep complaint. It is a perception that sleep quality is inadequate or non-restorative, despite the adequate opportunity to sleep. That insomnia is a symptom, not a disease, is important to note; it is associated with a variety of medical, psychiatric, and sleep disorders. A comprehensive history and physical examination are essential to determine the etiology of the insomnia.

The complaint of insomnia encompasses many sleep problems. These include difficulty falling asleep, sleeping too lightly, being easily disrupted with multiple spontaneous awakenings, or early morning awakenings with inability to fall back asleep. The timing of insomnia is important in determining its etiology. Therefore, having each patient define what he or she means by insomnia is essential.

To be considered a disorder, the complaint of insomnia should be accompanied by distress and/or impairment in daytime functioning.


On the basis of duration, insomnia is commonly divided into the following 3 types:

Transient insomnia lasts up to 1 week and often is referred to as adjustment sleep disorder because it most often is caused by an acute situational stress, such as a new job, upcoming deadline, or exam. It often recurs with new or similar stresses.
Short-term insomnia lasts for 1-6 months and is usually associated with more persistent stressful situational (death or illness of a loved one) or environmental (noise) factors.
Chronic insomnia is any insomnia lasting more than 6 months and is associated with a wide variety of disorders.
Insomnia usually results from an interaction of biological, physical, psychological, and environmental factors.

Although transient insomnia can occur in any person, chronic insomnia appears to develop only in a subset of patients who may have predisposing factors. Evidence for this theory includes the following:

When compared to control subjects, individual with insomnia (1) have higher rates of depression and anxiety, (2) score higher on scales of arousal, (3) have longer daytime sleep latency, (4) have an increased 24-hour metabolic rate, (5) have more night-to-night variability in their sleep, and (6) may have more beta EEG activity (an EEG pattern seen during memory processing/performing tasks) at sleep onset.
In experimental models of insomnia, control subjects deprived of sleep do not demonstrate the same abnormalities in metabolism, daytime sleepiness, and personality as persons with insomnia.
In an experimental model of giving control subjects caffeine, causing a state of hyperarousal, the control subjects did have changes in metabolism, daytime sleepiness, and personality similar to those seen in individuals with insomnia.
These results support a theory that insomnia is a manifestation of hyperarousal. In other words, the poor sleep may not itself be the cause of the daytime dysfunction but merely the nocturnal manifestation of a general disorder of hyperarousability.

Therefore, chronic insomnia is believed to primarily occur in patients with predisposing factors. These factors may cause the occasional night of poor sleep, but in general, the patient sleeps well until the occurrence of a precipitating event, such as death or other life stress. Then, acute insomnia develops. If poor sleep habits or other perpetuating factors occur, chronic insomnia develops despite the removal of the precipitating factor.

As stated previously, insomnia is a symptom; an accurate differential diagnosis is essential for the proper management of this complaint in any given patient.

Transient and short-term insomnia: Etiologies can be divided into 2 broad categories, as follows:

Environmental - Unfamiliar or unconducive sleep environment due to factors such as too much noise or light, extremes of temperature, or poor bed
Stress - Primarily life events such as new job or school, deadlines or exams, or death of a relative or close friend
Chronic insomnia: Differential diagnosis is broader and includes the following categories:

Medical disorders - Include chronic pain syndromes from any cause (eg, arthritis, cancer), advanced COPD, chronic renal disease (especially if on hemodialysis), chronic fatigue syndrome, and fibromyalgia
Neurologic disorders - Include Parkinson disease and other movement disorders, as well as headache syndromes, particularly cluster headaches, which frequently are triggered by sleep
Psychiatric disorders - Most chronic psychiatric disorders
Depression most commonly is associated with early morning awakenings and inability to fall back asleep; studies also have shown that insomnia can lead to depression. (The presence of insomnia for longer than 1 year is associated with an increased risk of depression.)
Schizophrenia and the manic phase of bipolar illness frequently are associated with sleep-onset insomnia.
Anxiety disorders (including nocturnal panic disorder and posttraumatic stress disorder) are associated with both sleep-onset and sleep-maintenance complaints.
Drug-related insomnia: Sleep disruption is common with excessive use of stimulants, alcohol, or sedative-hypnotics.
Primary sleep disorders

Restless leg syndrome (RLS)/periodic limb movement disorder (PLMD) is a sleep disorder characterized by unpleasant physical sensations in the legs, often described as a motor restlessness; relief of symptoms through movement, with worsening in a recumbent position; and occurrence only in the evening, primarily at bedtime. It is frequently relieved by movement (in the case of RLS) and is usually (but not necessarily) associated with frequent and rhythmic leg kicking once asleep (in the case of PLMD). If RLS is predominant, sleep-onset insomnia is the rule; if PLMD is predominant, sleep-maintenance insomnia or daytime hypersomnolence is more likely.
In obstructive sleep apnea, a minority of patients complain of insomnia rather than hypersomnolence. They frequently complain of multiple awakenings or sleep-maintenance difficulties.
Circadian rhythm disorders, such as sleep phase advance (patient goes to bed early and rises early) and sleep phase delay (patient goes to bed late and rises late) syndromes can present as insomnia when the patient wants to either stay in bed later or go to bed earlier but cannot and then believes he or she has a problem sleeping. Shift workers also frequently have problems with insomnia, particularly when they want to sleep during the day.
Primary insomnia: If all the disorders already discussed have been ruled out, the patient has primary insomnia. Most primary insomnia is psychophysiologic insomnia; rarely, primary insomnia is caused by idiopathic insomnia (long-standing insomnia beginning in childhood without antecedent psychiatric or medical trauma) or sleep state misperception (insomnia with objective evidence of a sleep disorder).

Psychophysiologic insomnia is a disorder of somatized tension and learned sleep-preventing associations resulting in a complaint of insomnia and daytime fatigue.
Psychophysiologic insomnia begins with a prolonged period of stress in a person with previously adequate sleep. The patient responds to stress with somatized tension and agitation, causing physiologic arousal. The bedroom and/or sleep routine becomes associated with frustration and arousal; poor sleep hygiene follows.
In a normal sleeper, as the initial stress abates, the bad sleep habits are extinguished gradually, as they are not reinforced. However, in a sleeper with a tendency toward occasional poor sleep nights, bad habits are reinforced, the individual "learns" to worry about his or her sleep, and chronic insomnia follows.
History in these patients frequently reveals excessive daily worries about not being able to fall asleep, evidence of trying too hard to sleep with apprehension if unable to fall asleep, an ability to fall asleep during monotonous pursuits (such as watching TV or reading) and in inappropriate situations (at a lecture or while driving) but not when desired, improvement of sleep in unusual sleep environments, and increased agitation and muscle tension prior to bed.