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9 Articles in Volume 9, Issue #3
Amino Acids and Diet in Chronic Pain Management
Clinical Case Study of Low-level Laser Therapy
Comorbidity of Musculoskeletal Injury Pain and PTSD
Craniofacial Pain of Cardiac Origin
Intellectual and Moral Tasks in Intersection – Part 1
Opioid Antagonists in Pain Management
Post-traumatic Headaches, Migraines, and Sleep Disorders
Restoration of Normal Cervical Lordosis
Tension Headaches

Post-traumatic Headaches, Migraines, and Sleep Disorders

Most, if not all, post-concussion symptoms are quite treatable and can often make a dramatic difference in the quality of life for a patient recovering from traumatic brain injury.

Of the post-concussion symptoms that can occur after a traumatic brain injury (TBI), headaches and sleep disorders are among the most common early features. Studies demonstrate a very high proportion of both symptoms and these require treatment to help combat the persistent disability. What is not often recognized is that the headaches often have migrainous features or are brand-new or reactivated migraine headaches. Treatment has very often simply not been offered to the patient by their physician. Similarly, sleep disorders—including initiation or maintenance of a normal sleep pattern—are quite prominent after TBI. Unfortunately, these, too, are ignored and often untreated—even years after the TBI.

Despite a high incidence per year of so-called “minor” or “mild” TBI—estimates vary but a figure of 5 million occurrences is not far-fetched—there is very little literature to document the high prevalence of headaches and sleep disorders as prominent post-concussion symptoms. In my practice—which deals primarily with headache, pain management, sleep disorders, and TBI—I have evaluated and treated over two thousand patients with post-TBI symptoms. We have found that the majority of patients complaining of these symptoms is quite in concordance with published data on post-TBI regarding headaches and sleep disorders.1-12 The total available data pool, however, is rather meager, despite the high incidence of mild TBI. Based on first-hand clinical experience, I will present anecdotal information along with recommendations for treatments of both post-traumatic headaches (PTHA) and sleep disorders using modern state-of-the-art pharmacologic strategies.

Post-traumatic Headache

It was recently published1 that 41 out of 109 (38%) of a group of VA patients with moderate or severe traumatic brain injury had acute post-traumatic headache. Of those, 20 of 41 (49%) experienced it in a frontal location, and 31 out of 41 (76%) experienced it at a daily frequency. Post-hospitalization, PTHA symptom severity declined and better individual improvement was associated with less anxiety and depression at 6-month follow-up. Almost all subjects with PTHA symptoms that persisted into the 6-month follow-up (21 of 22; 95%) continued to report symptoms at 12-month follow-up. In another recent publication2 from Spain, post-traumatic headache is one of several symptoms of the post-traumatic syndrome and therefore may be accompanied by somatic, psychological, or cognitive disturbances. PTHA can resemble a tension-type, migrainous, or cervicogenic headaches. Post-whiplash headache habitually is a pain radiating from the neck to the forehead, with moderate intensity and a benign but prolonged course. The pathogenesis of PTHA is still not well-known but might share some common headache pathways with primary headaches.

The relationship of PTHA to cognitive dysfunction after sports-related concussion is poorly understood. As shown in a recent publication, high school athletes reporting headache approximately one week after injury have significantly more of the other concussion symptoms and will perform more poorly on neuropsychological tests than athletes not experiencing headache.3 One hundred nine athletes who had sustained concussion were divided into two groups: those reporting headache seven days after injury and those reporting no headaches. The two groups were compared regarding on-field markers of concussion severity at the time of injury and symptoms and neurocognitive test results collected via ImPACT, a computerized neuropsychological test battery and post-concussion symptom scale, at a mean of 6.8 days after injury. Those reporting PTHA had significantly worse performance on reaction time and memory as measure by ImPACT neurocognitive composite scores. They also reported significantly more symptoms besides headache and were more likely to have demonstrated on-field anterograde amnesia. The authors concluded that any degree of post-concussion headache in athletes after brain injury (seven days after injury) is likely to be associated with an incomplete recovery after concussion.3

An even more recent report in 2005 from the same authors,4 studied a larger cohort of high school and college-aged athletes who had sustained concussive injuries—with and without headaches (HA) and post-traumatic migraine (PTM). In this study, 261 high-school and collegiate athletes with a mean age of 16.36 +/- 2.6 years were divided into three groups: the PTM group (74 athletes with a mean age of 16.39 +/- 3.06 years), the HA group (124 athletes with a mean age of 16.44 +/- 2.51 years), and the non-HA group (63 patients with a mean age of 16.14 +/- 2.18 years). Symptom scores were collected using ImPACT to assess sports-related concussion. Significant differences existed among the three groups for all outcome measures. The PTM group demonstrated, once again, significantly greater neurocognitive deficits when compared with the HA and non-HA groups. The authors concluded that athletes suffering a concussion accompanied by PTM should be examined in a setting that includes symptom status and neurocognitive testing to address their recovery more fully. Given the increased impairments observed in the PTM group, parents and schools should exercise increased caution in decisions about when the athlete should be allowed to return to play.

A Finnish study evaluated patients with mild head injury (MHI) in a series of 172 consecutive MHI patients admitted into the emergency room of a general hospital and who developed post-concussion symptoms (PCSs). A modified Rivermead Post-Concussion Symptoms Questionnaire was used to identify the patients with and without PCSs one month after injury. They identified 37 patients with MHI who developed PCSs (22%). Risk factors for PCSs in the MHI patients were skull fracture (OR 8.0, 95% CI 2.6-24.6), serum protein S-100B > 0.50 microg/l (OR 5.5, 95% CI 1.6-18.6), dizziness (OR 3.1, 95% CI 1.2-8.0), and headache (OR 2.6, 95% CI 1.0-6.5). Serum protein S-100B proved to be a specific, but not a sensitive predictor of PCSs. The presence of skull fracture, elevated serum protein S-100B, dizziness, and headache may help the emergency room physician to identify patients at risk of PCSs and refer them for further examination and follow-up.5

A study published in Germany in 19976 suggested that head trauma (HT) and whiplash injury (WI) is followed by a post-traumatic headache (PH) in approximately 90% of patients. The PH due to common WI is located occipitally (67%), is of dull-pressing or dragging character (77%), and lasts three weeks on average. Tension-type headache is the most frequent type of PH (85%). Besides post-traumatic cervicogenic headache, migraine- or cluster-like headache may be observed in rare cases.

Chronic Post-traumatic Headaches

Within six months, 80% of patients with post-traumatic headache following head trauma show remission, but chronic PH—lasting at least four years occurs in 20%. Unfavorable prognostic factors included age more than 40 years; a low intellectual, educational, and socio-economic level; previous HT; or history of alcohol abuse. A prolonged PH due to WI, lasting years and with an extensive decrease of mobility of the cervical spine and other associated risk factors, can be expected in patients with initially severe headache.

“...chronic post-traumatic headache is a common condition, often part of the post-concussion syndrome. The pathophysiology is not well understood but includes biological, psychological, and social factors.”

Other types of analysis7 show that chronic post-traumatic headache is a common condition, often part of the post-concussion syndrome. The pathophysiology is not well understood but includes biological, psychological, and social factors. Tension-type headache is the most common manifestation, but exacerbations of migraine-like headaches often occur. After a structural lesion has been ruled out, the treatment of post-traumatic headache is similar to that of the primary headaches. PTHA can resemble a tension-type headache [TTH], migrainous, or cervicogenic headaches. Post-whiplash headache often consists of a pain radiating from the neck to the forehead, with varying intensity and often a prolonged course. The pathogenesis of PTHA is still not well-known but might share some common headache pathways with primary headaches such as migraines.

In a European study, the epidemiological and clinical profile of Chronic Post-Traumatic Headache (CPTH) has been studied in 57 out of 130 consecutive patients hospitalized, following closed head injuries, at the Institute of Neurosurgery of the University of Milan.8 The incidence of CPTH was 44%. Age of the patients ranged between 4 and 69 years. head injuries were of a mixed degree of severity: mild, moderate and severe. Chronic muscle contraction headache was the most common clinical picture, followed by migraine. Following the head trauma, moderate correlations have been found between the severity of CPTH and disturbance of consciousness, and positive findings at CT scan. Personality profile testing (via MMPI) of CPTH (n=26) with a post-traumatic control group without headache (n=17) showed higher scores on hypocondriasis, depression, hysteria, and schizophrenia scales only in the severe CPTH group. Age of the patients, duration of unconsciousness, neurological deficits, course length and pending litigation or compensations were unrelated to the occurrence and outcome of CPTH and the findings suggest the importance of both physical and psychological determinants (social or emotional maladjustment) in the pathogenesis of CPTH.

TBI and Migraine

Although very early studies spoke to the possibility of migraine headaches occurring after TBI, several published studies more recently have speculated on the similarity or overlap of post-concussion headaches with traditional migraine presentations.10-12 One study concluded that patients suffering recurrent post-traumatic headaches or other elements of the post-concussion syndrome should be treated for migraine.9 Some authors concluded that the most common symptom in mild head injury or mild traumatic brain injury is headache which resembles migraine with unknown pathophysiology. Biochemical mechanisms believed to be similar in both conditions include: increased extracellular potassium and intracellular sodium, calcium, and chloride; excessive release of excitatory amino acids; alterations in serotonin; abnormalities in catecholamines and endogenous opioids; decline in magnesium levels and increase in intracellular calcium; impaired glucose utilization; abnormalities in nitric oxide formation and function; and alterations in neuropeptides.12 A very early paper alluded to cortical spreading depression of Leao to account for transient neurological disorders that resulted from rather mild head injuries. These events, which appeared after a lucid interval, included headache, nausea and vomiting, pallor, somnolence, irritability and restlessness, stupor, hemiparesis and aphasia.13 The symptoms were not attributable to cerebral compression but were probably due to a transient cortical phenomenon.

“There is almost no literature on specific treatment of post-concussion headaches and migraines and one exceptional paper written over ten years ago described good success with 34 patients treated with IV dihydroergotamine for post-concussion headaches.”

One study14 reported the onset of chronic paroxysmal hemicrania after TBI. Indomethacin, 75mg daily, resulted in only isolated occurrences of autonomic and aura symptoms in the absence of headache symptoms and total control on indomethacin at 100mg daily. There is almost no literature on specific treatment of post-concussion headaches and migraines and one exceptional paper written over ten years ago described good success with 34 patients treated with IV dihydroergotamine for post-concussion headaches. With this therapy, 88% achieved a good to excellent overall response.15

TBI in Children and Adolescents

The foregoing review of the literature speaks primarily to headaches and migraines occurring after TBI primarily in adults. There is a corollary body of data in children and adolescents after TBI who developed these disorders. A very early study16 grouped attacks of hemiparesis, somnolence, irritability, vomiting, blindness, and brainstem signs and related them to the head trauma. The authors felt that there may be a common underlying process related to migraines. Another early study17 evaluated 13 children and adolescents who developed transient nonconvulsive neurologic symptoms within a few hours of trivial head injury. Some of these young people were known to have migraines before and/or after these episodes. In all but one, a family history of migraine was elicited. The authors concluded that a diagnosis of migraine should be considered in children who develop delayed impairment of consciousness after head trauma—with or without convulsive phenomena or focal neurological deficits. A study from Poland18 evaluated the characteristics and persistence of post-traumatic headaches 90 days after brain concussion and 10 days after contusion in a group of 100 children (29 girls and 71 boys), aged 3-14 years old. It was the author’s observation that 83% of children had headache after brain concussion and contusion. The majority (56%) had acute post-traumatic headache, but 27% of children complained of chronic headache —mainly tension-type headache. In a more recent study, the same authors19 showed that regional cerebral blood flow measurements using SPECT, in children with post TBI headaches, showed persistent differences over time. Regional cerebral blood flow (rCBF) was assessed 10-15 days after trauma, and in cases of brain concussion three months and one year. The study looked for a correlation between changes in rCBF and the occurrence of post-traumatic headache. Thirty-two children were studied, aged 6-16, at 10-15 days, and then at 3 and 12 months after brain concussion. In all children no changes were found in CT and MRI examinations. In the early period after trauma, blood flow impairment was found in 21 children in the studied group, mostly in frontal areas. One year after trauma the rCBF improved in 11 children and, in the remaining 10 cases, the pattern was normal. In a group of four children with headache one year after brain concussion, three of them still presented with impairment of blood flow.

Another recent study investigated the prevalence and clinical features of headaches in children with mild TBI.20 Changes over time were also evaluated. 301 children who had experienced a single mild TBI were compared with a control group (301 children who had suffered from any other mild body injury without head trauma). Groups were matched according to gender and age and standardized questionnaires were sent to parents from both groups. Parents were asked about character, frequency, dizziness, and other symptoms that accompanied the headaches. 102 matched pairs were analyzed. Questionnaires revealed that, for the prior year, 114 parents indicated headaches: 64 in the TBI group and 50 in control group. Frequent (> 8 days per month) headaches prevailed in children with mild traumatic brain injury (p=0.039); however, their prevalence decreased from 43.8% to 12.5% (p=0.01) with increasing time interval between the date of trauma and the questionnaire. Thirty-three parents from the TBI group and sixteen from the control group indicated that dizziness accompanied headaches (p

Headache Discussion

In a most recent French study,21 51 such children after TBI were studied retrospectively through contact with their family. Several situations were categorized: syncope-like loss of consciousness (11 cases), seizures (6), severe headaches with neurologic signs (15), confusion (8), visual disorders (6), an amnesic ictus (5). Eleven of twenty-one children developed common migraine. The long-lasting episodes suggested a migrainous pathogenesis, perhaps at a stage where the trigger of migrainous mechanism is at a low level in the brain. I would pose one criticism of this study—and indeed of many of the others reviewed—that is that EEG data were not examined as part of the workup. I believe this to be far more sensitive in the TBI setting for documenting electrographic abnormalities that may accompany headaches, migraines, and behavioral and cognitive changes. One interesting study by one of my teachers (JCM) measured serum ionized magnesium and ionized calcium/ionized magnesium ratios in children with headaches.22 One hundred thirty-five children with primary complaints of headaches were studied and nine had a diagnosis of post-traumatic headache.

Table 1. Summary of Experience With Headaches and Migraines After TBI in Clinic Patients
# Patients Migraine/migrainous headache Tension-type headache Mixed headaches Nausea Light/ sound sensitivity Dizziness/
vertigo
2,174 1,913 263 2,170 1,739 1,810 775
  (88%) (12%) (4 without any headache) (80%) (83%) (36%)

My own anecdotal evidence—based on clinical experience in treating patients with post-concussive headaches and migraines—certainly is quite concordant with the literature reviewed. Although not formally published, my clinical observations and evaluations include over 2000 patients with TBI. The vast majority (93%) of patients evaluated suffered so-called minor or mild TBI, with most of the remaining patients diagnosed as moderately severe TBI.

Overwhelmingly, 88% of patients with post-traumatic headaches and migraines fulfilled IHS criteria for migraine or migrainous headache.23 These are well described in the latest International Classification of Headache Disorders published in 2004. I have summarized data from over 15 years of evaluation and treatment of post-traumatic headaches and migraines in Table 1.

Accumulated clinical experience shows that patients without any headache features whatsoever is extremely rare. For example, only 4 of 2174 patients did not complain of any kind of headache, either tension-type, migrainous, or migraine. The vast majority (88%) had either migraines or migrainous headaches using the IHC criteria. 12% had primarily tension type headaches without migrainous features and there was an overlap in virtually all patients with features of tension-type headache mixed with migrainous or migraine headaches. Eighty percent of patients with migraines complained of nausea and/ or vomiting. Eighty-three percent complained of light or smell sensitivity accompanying their migraines. Thirty-six percent complained of dizziness or vertigo accompanying the headache.

From this treatment perspective, a number of pharmacologic strategies were used but primarily migraine specific medications (ie, triptans) were a mainstay of therapy for post-traumatic migraines. Over 90% of treated patients in the migrainous/migraine group responded at least 50% or better to triptan therapy strategies. These medications were given with and without antinauseant medication (most often metochlopramide). As an alternative to triptan medications, dihydroergotamine (DHE) given intranasally or intramuscularly (or intravenously in the clinic) was used as a migraine-specific treatment for post-TBI migraines. At times, refractory migraines were treated with intravenous medication in the outpatient headache clinic using a number of I.V. medication strategies published recently.24 Indeed, our success rates—based on outcomes of better than a 50% reduction of the severity of symptoms—approached 98% across the board for all refractory headaches and migraines treated with I.V.25

Sleep Aberrations After TBI (16 Years and Older)

As outlined in the case of headache and migraine disorders after traumatic brain injury (TBI), the published data regarding sleep aberrations after TBI is also not very extensive. Our own data had 98% of 2174 patients reporting non-refreshed sleep and frank problems with either initiation or maintenance of sleep, or both. Daytime fatigue was likewise a very significant problem in virtually all patients.

In a very recent large study,26 452 participants, aged 16 years and older, with minor to severe TBI, answered a questionnaire pertaining to quality of sleep and fatigue. Of the sample 50.2% reported insomnia symptoms and 29.4% fulfilled the diagnostic criteria for an insomnia syndrome. In almost 60% of cases, the reported sleep problems remained untreated. Risk factors associated with insomnia were milder TBIs, and higher levels of fatigue, depression, and pain. The authors concluded insomnia is quite prevalent after TBI and requires clinical and scientific attention and may have important repercussions on rehabilitation.

Another very recent but smaller study27 evaluated 63 patients with TBI consecutively recruited after discharge from rehabilitation and 63 age- and sex-matched controls from the general community. A 7-day self-reported sleep-wake diary was used to monitor sleep and wake times, sleep onset latency, frequency, and duration of nocturnal awakenings, and daytime naps. The Epworth Sleepiness Scale was used to measure daytime sleepiness. The study showed a significantly higher frequency of reported sleep changes after TBI (80%) relative to the control group (23%) and the TBI group reported more nighttime awakenings and a longer sleep onset latency. These changes were more frequently reported by participants with TBI resulting from milder injuries. Increased levels of anxiety and depression were associated with increased reporting of sleep changes. The results confirm changes in sleep after TBI and may account for the reported increased daytime sleepiness in the TBI population. The authors felt that sleep disturbance should be addressed during rehabilitation.

These observations have been echoed across other studies spanning some 20 years in patients with sleep disturbances after TBI.28-32 One study looked at the prevalence, demographics, and causes of excessive daytime sleepiness in adults with brain injuries after the acute phase of their injury. A case series of patients enrolled consecutively in a residential rehabilitation program were studied28 and polysomnography and Multiple Sleep Latency Test (MSLT) were performed for each patient. Daytime hypersomnolence was diagnosed by mean sleep latency on the MSLT

Another study29 studied long-term effects of TBI on sleep in adolescents. Nineteen who had suffered TBI three years before the study and had complained of sleep disturbances completed a sleep questionnaire and were investigated in the sleep laboratory by whole-night polysomnographic recordings and were actigraphically monitored for five days at home. TBI was associated with lower sleep efficiency (79.8 +/- [9.8]% vs 87.7 +/- [6.8]%; P

In yet another study,30 50% of subjects had difficulty sleeping after TBI: 64% described waking up too early, 25% described sleeping more than usual, and 45% described problems falling asleep. Eighty percent of subjects reporting sleep problems also reported problems with fatigue. It was also noted that the more severe the brain injury, the less likely the subject would be to have a sleep disturbance. Subjects who had sleep disturbances were more likely to have problems with fatigue and females were more likely to have trouble with sleep. This study demonstrates the substantial prevalence of sleep disturbances after brain injury and underscores the relationship between sleep disorders and perception of fatigue.

An early study31 studied 75 subjects who had experienced a minor head injury (MHI) with a disturbance in consciousness three months prior to filling out a questionnaire. The majority were males, 16 to 30 years old, involved in motor vehicle accidents. Sleep-awake patterns following head injury differed from base-line patterns prior to head injury. Sleep interruptions per week and per night increased significantly (p

One prospective study found that 50 patients in a rehabilitation setting—evenly divided between spinal cord injury (SCI) and musculoskeletal (MSK) cases—without TBI, studied prospectively and compared with 50 consecutive post-acute TBI admissions, had poor sleep quality and insomnia in both groups. While there were definitely problems for the TBI group, the magnitude of these problems was much greater for the rehabilitation comparison group.32

Sleep Aberrations in Children After TBI

One study in children after TBI33 used prospective neurological, and electroencephalographic investigations in 98 children, 3-13 years of age, within 24 hours after the TBI and 4-6 weeks later. Inclusion criteria for mild head injury were unconsciousness

The authors discouraged the routine EEG examination in very slight head injury cases, although the reported baseline number of abnormal EEG examinations was high and no data was given for the number of abnormal EEG studies after 6 weeks. I would disagree with the conclusions of this study based on our own data. In another EEG study,34 ten patients were examined with the use of daytime routine EEG and night polysomnography. The amount of REM sleep is most sensitive to brain damage and is reduced in all patients with nonspecific epileptiform changes in the EEG. The reduction of REM sleep seems to be a sensitive marker of development of epileptiform EEG-changes and might play a predictive role in the development of post-traumatic epilepsy.

A small number of observations, largely case reports, have described unusual features for sleep aberrations after TBI. A few cases of jactatio nocturna, or night-time head banging, have been considered a sleep disorder. An analogy to somnambulism and pavor nocturnus has been suggested. One report35 observed episodes of jactatio nocturna in a patient with global encephalopathy and frontal lobe dysfunction after closed head injury and successfully treated these with imipramine. The author cautions that jactatio nocturna must be differentiated from post-traumatic seizures and may represent partial or defective arousal during light non-REM sleep.

Circadian Rhythm Sleep Disorders

Acquired circadian rhythm sleep disorders may occur after traumatic brain injury. One study36 described a 48-year-old man who presented with sleep onset insomnia and cognitive dysfunction after a car accident. A diagnosis of delayed sleep phase syndrome (DSPS) was confirmed by sleep logs and actigraphy, which revealed sleep onset in the early morning hours and awakening around noon. Another study37 described a 15-year-old girl who developed a prominent delayed sleep phase syndrome (DSPS) following traumatic brain injury. Several physiological markers of the sleep-wake rhythm: plasma melatonin, body temperature, wrist activity, and sleep architecture (EEG) were delayed. This patient returned to normal after treatment with 5mg melatonin.

Post-traumatic Narcolepsy

Although sleep disturbances following head injury are very common, post-traumatic narcolepsy has rarely been reported. A patient with all four major features of narcolepsy following significant head injury was presented.38 Tissue typing showed the HLA-DR2 which is strongly associated with idiopathic narcolepsy. Interaction between the brain injury and a genetic predisposition appears to be involved in the development of post-traumatic narcolepsy. Another study39 obtained data on nine patients, previously diagnosed with mild to moderate closed head injury, and who had unresolved sleep complaints. All patients presented with complaints of excessive daytime somnolence and/or sleep attacks. Patients also presented with a mix of cataplexy, hypnagogic hallucinations and/or sleep paralysis. The protocol utilized consisted of overnight poly-somnography with a Multiple Sleep Latency Test (MSLT) the following day. All patients’ histories were negative for narcolepsy or any other significant sleep disorders prior to the head injury. Polysomnography and MSLT data indicated a diagnosis of narcolepsy in all cases. The results of HLA typing showed that three patients were DR2 positive, two were DR4 positive and one was DQW1 positive. The conclusion was that narcolepsy may be “dormant” and that, in cases genetically at risk, even a minor injury to the CNS can cause that person to become symptomatic.

Mechanistically, hypocretin deficiency —as shown by low or absent concentrations in CSF—was found in 90% of patients with sporadic narcolepsy-cataplexy, and less commonly in familial narcolepsy. Very recent studies have pointed to the likely role of hypocretins (orexins) in the cause or genesis of post-traumatic sleep disorders.40-43 These are peptides that are produced by a group of neurons situated in the posterolateral hypothalamus and have been shown to excite many CNS areas including many neuronal systems that regulate sleep and wakefulness. The hypocretin system is influenced both neuronally (e.g. suprachiasmatic nucleus, GABAergic, cholinergic and aminergic brainstem nuclei) as well as metabolically (e.g. glucose, ghrelin, and leptin). A role in REM sleep, neuroendocrine, autonomic, and metabolic functions has also been suggested. A deficient hypocretin neurotransmission has been found in human narcolepsy and (engineered) animal models of the disorder. Animal studies indicate that hypocretins play a role in the regulation of various functions including arousal, muscle tone, locomotion, regulation of feeding behavior, and neuroendocrine and autonomic functions. A link between hypocretin deficiency and narcoleptic symptoms was first shown in canine and rodent models of narcolepsy. Low hypocretin-1 cere-brospinal fluid levels in neurologic conditions (e.g. Guillain-Barre syndrome, traumatic brain injury, hypothalamic lesions) have been shown with and without sleep-wake disturbances. Thorough reviews of the subject have been recently published.42,43

In one study, 44 consecutive patients were prospectively assessed with regard to CSF hypocretin-1 after acute traumatic brain injury (TBI).40 Compared with controls, hypocretin-1 levels were abnormally lower in 95% of patients with moderate to severe TBI and in 97% of patients with post-traumatic brain CT changes. A case report41 supported the hypothesis of an association between cranial trauma and alterations in the dopaminergic pathways represented by periodic leg movements during sleep and a sleep behavior disorder. The possibility of hypothalamic hypocretin involvement was proposed in its genesis. The patient, a 52-year-old male, had sustained TBI 24 years prior (with a two month-long coma) and had developed extremely restless sleep and excessive daytime sleepiness. Video-polysomnography showed periodic leg movements and, during REM sleep, aggressive and agitated behavior. The MSLT revealed extremely short latencies. He was successfully treated with levodopa-benzerazide, 100/25 mg, two hours before bedtime.

Conclusion

Symptoms of headache and sleep disorders are among the most common early features after a traumatic brain injury. Most, if not all, of the post-concussion symptoms—and particularly post-traumatic headaches, migraines and sleep aberrations—are quite treatable and can often make a dramatic difference in the quality of life while the patient is recovering from traumatic brain injury.

Last updated on: December 27, 2011
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