In order to make a diagnosis, a subjective evaluation and objective sleep tests are assessed. Subjective evaluations include self-report questionnaires and sleep diaries to assess the sleep pattern from the patient's perspective. Objective sleep tests include mental and physical examinations and laboratory tests to test the medical background, such as Polysomnography (PSG) and Actigraphy. It is typically not possible to assess these tests prior to an injury. Therefore, it is often not clear whether the<unk> <unk> is a result of pre-existing<unk> . Careful assessment of patients and determining the nature of their<unk> <unk> is essential for finding the most effective treatment. There is no explicit treatment for sleep<unk><unk>  TBI. Several interventions for general sleep disturbance have been tested in patients with TBI. In order to provide the proper treatment, it is best to divide the injury and its recovery in stages, given that the treatments differs in the different stages. It has been seen how a deterioration of sleep quality during the subacute phase of mTBI has been linked with the worsening of behavioural, neuropsychiatric and somatic outcomes. In general, treatment of sleep<unk><unk>  TBI can be distinguished in pharmacological and nonpharmacological interventions. Pharmacological treatments Phototherapy Pharmacological treatments have to be administered carefully. Some medication is highly addictive and the resulting withdrawal syndromes cause even more sleep disturbances, e.g. Insomnia. Possible medications are Zopiclone and lorazepam, which have been proven effective in people with TBI. Also Benzodiazepine hypnotics, Benzodiazepine-receptor antagonists, antidepressants, psychostimulants can be administered, especially in patients with insomnia. Some studies have shown negative effects of hypnotics, such as an increased risk of dementia. In patients with hypersomnia, Modafinil, Armodafinil, Methylphenidate and amphetamines are often used as a treatment for day time<unk> ss. Medication should always be prescribed by an expert to make sure that the correct medicament is taken in an appropriate dose. Nonpharmacological treatments Nonpharmacological treatments involve different interventions, starting with sleep hygiene, which includes sleep promoting activities such as maintaining a regular and strict sleep schedule and avoiding heavy meals before bedtime in order to restore the natural sleep-wake cycle. Further treatments options are phototherapy and infrared light therapy, which both, aim to treat circadian rhythm<unk>  such as delayed sleep phase<unk>  Especially in patients with hypersomnia, bright light therapy in the morning has been proven to be effective. A prolongation of slow-wave sleep increases glymphatic clearance of metabolic waste products, which can lead to improvements of sleep<unk> . Furthermore, studies showed ameliorated sleep pattern due to acupuncture of patients with TBI. Sleep apnea due to TBI can be treated through positive airway pressure, which helps with the development of a regular breathing pattern during sleep and prevents waking up. Cognitive behavioral therapy for insomnia also have been shown to effectively improve sleep in TBI patients. It aims to improve sleep habits and behaviors by identifying and changing the thoughts and the behaviors that affect the ability of a person to sleep or sleep well. The improvement of the quality of sleep and the decrease of depressive severity is associated with he use of near-infrared light for intracellular healing. Animal studies Animals studies showed that sleep deprivation prior to a<unk>  injury might have healthy effects. Five days of complete sleep deprivation in rats before the traumatic<unk>  injury, acted as protection against ischemic injury and a habitual deceased in total amount of sleep time before TBI reduced the severity. There are several theories on the protectional effects of sleep disturbances before an injury in rats. Firstly, it may alter the pattern of gene activation and deactivation. This could lead to a higher degree of neuroprotection. Lack of sleep might increase the levels of extracellular adenosine, which is also mostly neuroprotective against the TBI sequelae. Furthermore, sleep deprivation might lead to a form of “ischemic precondition” which habituates the<unk>  to the byproducts of a cellular injury. Studies have been run to assess the role of caffeine in rats with<unk><unk> . While results regarding rats studies have come out positive, in humans caffeine is believed to worsen sleep fragmentation and insomnia. Lastly insufficient quantity and quality of sleep may cause a rebound sleep post injury and increase the sleep enhanced regeneration and recovery. More research is needed to investigate how these findings can be transferred to the treatment of humans suffering from TBI.
Sleeping disorders following traumatic brain injury
Acute behavioural disturbance
Mass psychogenic illness
Post-stroke depression
Pollutant-induced abnormal behaviour
Fatal insomnia
Febrile infection-related epilepsy syndrome
Complications of traumatic brain injury